Ugrás a tartalomhoz

Handbook of Dental Hygienist

Péter Vályi

University of Szeged

Lesions of the oral mucosa (Péter Novák MD)

Lesions of the oral mucosa (Péter Novák MD)

Developmental and genetic anomalies

Congenital lip pits

Aetiology:a congenital genetic anomaly which is occasionally inherited dominantly.

Symptoms and signs: occur rarely, and they mostly develop on the lower lip (vermilion border), predominantly bilaterally resulting in cosmetic disadvantages accompanied by increased salivation causing inconveniencies.

It may also develop accompanying a cleft lip or palate.

Fox-Fordyce’s granules

Heterotopic sebaceous glands located within the oral mucosa.

Symptoms and signs: small, yellowish spots which create a yellowish plaque if they are located close to each other. Predominantly, this disorder presents itself on the buccal mucosa, but it may also occur on the mucosal surface of the lips or other mucous membrane surfaces.

Differential diagnosis: leukoplakia, candidosis, morsicatio buccarum.

Upper labial frenulum hypertrophy

The enlarged upper labial frenulum causes a diastema between the incisors as it protrudes stoutly down to the palatal papilla.

Ankyloglossia

“Tongue tie” is present when the lingual frenulum pulls the tip of the tongue partially to the floor of the mouth, but in some cases the whole tongue may be completely fixed to the floor of the mouth. Its causes may be congenital or traumatic, and this disease may also occur in systemic sclerosis. It may be accompanied by disorders of speech or difficulty eating.

Congenital leukokeratosis (White sponge nevus)

It is a rare disorder which is inherited in an autosomal dominant trait.

Symptoms and signs: present as white, whitish-greyish, peeling, it is a painless and complication-free disorder on the buccal mucosa and the mucosal layers of the nose, oesophagus and the ano-genital region.

These lesions appear first at the time of birth or during childhood. This disorder occurs mostly on the loose mucous membrane of the mouth (buccal mucosa, soft palate, the ventral surface of the tongue, the mucosal surface of the lips, floor of the mouth, etc.). The gingival and the dorsal surfaces of the tongue are usually unaffected.

Differential diagnosis: leukoplakia, morsicatio buccarum, lichen oris, fungal infections.

Congenital leukokeratosis (White sponge nevus)

Lingual thyroid (Lingual goitre)

Heterotopic thyroid tissue remains in the dorsal third of the tongue, near the foramen caecum. Lingual goitres are more common in women.

Symptoms and signs: Lesions various in size and mostly of exophytic form and nodular surface can be observed on the dorsal surface of the tongue. These ectopic, purple-reddish glands may become swollen during menstruation and pregnancy, or they may even bleed.

It may become a life-threatening condition as it may result in an airway or alimentary tract obstruction.

Differential diagnosis: lingual tonsils, haemangioma, lymphangioma, tongue cancer.

Naevus flammeus (“port-wine stain”)

Symptoms and signs: congenital purplish-blue, irregularly shaped stain, which is not or barely elevated from the skin, and it is formed of flat, dilated capillaries. They may be stains of a small diameter or large plaques covering larger parts of the body as well. They may occur anywhere on the skin but most commonly in the regions of the head and neck.

The naevus may be present at birth and may grow in size later on, or may develop into a cavernous haemangioma, but it might as well fade and eventually disappear.

Differential diagnosis: Sturge–Weber syndrome.

Down’s syndrome (mongolism)

Down’s syndrome is a chromosomal disorder and not a hereditary disease. Mongolism is more common in the children of mothers delivering at an advanced age.

Symptoms and signs: short stature, brachycephaly and mental retardation are typical, as well as white spots around the iris in the eye and an expressed medial epicanthic fold.

Those suffering from mongolism are more susceptible to upper airway diseases, while mouth dryness and snoring are explained by the fact that these patients breathe through their mouth because of their nasal obstruction,

The underdeveloped upper jaw causes protruded lower jaw and malocclusions.

The tongue is frequently protruded and deeply fissured (scrotal tongue),

The lips are thicker, dry and crusted, and occasionally lip fissures may also accompany the symptoms.

The eruption of the teeth is delayed, and hypodontia, enamel hypoplasia and the morphological disturbances of teeth are also common signs.

Caries activity is low among these patients, but the progression rate of parodontal diseases is higher. Respiratory, gastrointestinal and dermal infections are characteristic accompanying symptoms of this disease.

Physical, chemical and iatrogenic oral lesions

PHYSICAL INJURIES

Mechanical injuries

The main cause of traumatic ulcers is usually a single physical damage (for example, fights, sports, epilepsy, bone, sharp, broken tooth and prosthesis, etc.), which causes yellowish, painful, soft changes various in diameter on the affected mucosal tissue. These ulcers are surrounded by a thin, erythematous halo. They heal spontaneously in 6–10 days but leave scarring behind.

Differential diagnosis: specific ulcers (tuberculosis, lues), aphtha or carcinoma.

Mechanical injuries

Epulis fissuratum (denture granuloma)

There are two major factors in the development of a denture granuloma: the pathologically mobile denture and the pressure of its edge on the surrounding mucosal tissue. An epulis fissuratum may most commonly occur in the middle third of the mandibular bones and is more common on the buccal surface than on the lingual surface. The epidermal layer of the mucosa may develop increased keratinisation. These lesions may become pale, hard and more flexible to the touch where the accumulation of connective tissue fibres is more extensive.

Differential diagnosis: gingival cancer, Hydantoin hyperplasia, epulis.

Epulis fissuratum (on the left premolar region, with denture)

Epulis fissuratum (on the left premolar region)

Morsicatio buccarum et labiorum

The cause is that nervous, anxious children and young adults may repeatedly chew or bite their facial mucosa, lips or sometimes even their tongue as a bad habit. This constant mechanical trauma causes white desquamation of the effected epithelium, with erosions or even ulcers to develop mainly in the line of dental occlusion and buccal mucosa. This bad habit is commonly accompanied by bruxism.

Differential diagnosis: leukoplakia, candidiasis, ulcers caused by inflammations and cancer.

Morsicatio buccarum et labiorum

THERMAL INJURIES

Combustion (burning, hot surfaces)

Any combustion injury is influenced by the degree and the duration of the thermal contact. Burn injuries may be caused by hot meals, cigarettes, tobacco pipes, hot dental surgery instruments or imprinting materials. Damage to the epidermis, oedema, erythema, peeling and pain (first degree burn) may develop, or in more severe cases blisters may appear which leave crusting when they burst, but no scars when they are healed. A longer lasting burn may heal leaving scars behind (third degree burn).

Differential diagnosis: chemical injuries, hypersensitivity.

CHEMICAL INJURIES

Chemical poisoning occurs (sodium hydroxid, trichloroacetic acid, Aspirin, carbolic acid, silver nitrate, sodium bicarbonate, hydrogen peroxide, etc.) when these materials get onto the mucosa in higher concentrations during mucosal or dental treatment accidentally or for therapeutic purposes. Erythematous, yellowish-white fibrinous pseudomembrane covered lesions and painful ulcers can occur in the mouth.

Differential diagnosis: sore, allergic stomatitis, white lesions.

IONISING RADIATION

Radiogenic mucositis

Radiotherapy applied as part of a treatment for malignancies may cause early and late onset action depending on the dose and duration on the oral mucosa as well as on the skin.

Among early onset reactions, one must mention erythemas, oedemas, hyperpigmentation appearing on the skin in the first two or three weeks after irradiation, whereas the oral mucosa may develop erythemas, oedemas, ulcers and painful lesions covered by yellowish-whitish pseudomembranes beside a dry mouth. All these may cause problems with eating and swallowing. The patient may lose his sense of taste for a longer period (2–6 months) after these ulcers heal (2–3 weeks). The ulcers heal slowly, leaving a sensitive, atrophic oral mucosa and scarring behind as late manifestations. Xerostomia developed as a result of the irradiation damage of the salivary glands (sensitivity to radiation) may predispose the patient to bacterial (pyostomatitis), fungal (candidiasis) or viral (herpes) infections. Malignancies may evolve on the atrophic, scarred mucocutaneous surfaces.

Differential diagnosis: exfoliative leukoedema of the oral mucosa, herpetic and aphthous gingival stomatitis or allergic stomatitis.

ORAL REACTIONS DUE TO DRUGS

Cytostatic drugs

Erythematous and ulcerative alterations covered by fibrous pseudomembranes (lichenoid reaction) may develop on the oral mucosa following chemotherapy (cytotoxic effects) of patients suffering from cancer. Erosions and ulcer are usually diffuse and multiple. They may occur anywhere but must commonly on the lips, buccal mucosa and the tongue. Symptoms of mucositis are the most severe in the period of 10–15 days after chemotherapy and may persist for weeks. These lesions may be a result of toxic pharmaceutical effects, but mostly they are the results of secondary neutropenia or thrombocytopenia (bleeding).

Differential diagnosis: allergic stomatitis, pseudomembranous candidiasis.

Lichenoid reaction

This lesion may be caused by several drugs (anti-diabetic drugs, anti-hypertensive drugs, beta blockers, penicillamine, allopurinol, non-steroidal anti-inflammatory drugs and anti-malaria medication), chemotherapy, some metallic fillings non-metallic materials used in dental treatment (amalgam) as well as by graft-versus-host reactions.

These reactions resemble true lichen, vulgar pemphigus, pemphigoid and lupus erythematous oral symptoms very much. The oral mucosa develops erythemas, and multiple erosions, burning, painful ulcers covered with fibrous pseudomembranes may evolve. Metallic and newly introduced composite dental materials and prosthesis structures may cause lichenoid lesions on the oral mucosa. After the cessation of the use of these drugs, the lesions may heal, but exchanging the fillings involved may not always yield proper results.

Differential diagnosis: contact allergy, chemical and drug-induced injuries.

FOREIGN BODY INJURIES (METAL TATTOOS)

Amalgam

The most common among these alterations are amalgam tattoos, which are created when corrosion, diffusion or a trauma causes metallic particles to diffuse into the mucosa. It is more common on the mandibular gingival surface than on the maxilla or around the alveoli.

Differential diagnosis: mucocele, haemangioma, malignant melanoma.

Infectious diseases

BACTERIAL DISEASES

Folliculitis

Pathogen: Staphylococcus aureus

Superficial pyoderma of the hair follicles is frequent on the skin.

Symptoms: the yellowish pustule is pierced through by a hair. Superficial folliculitis is not surrounded by an inflammatory ring, while deeper ones have a red, hyperaemic, painful base. It is frequent on markedly hairy skin that is prone to irritation. It heals without leaving a mark or a scar.

Differential diagnosis: Furunculus, acne.

Furunculus

Pathogen: Staphylococcus aureus

Frequently painful, deep pyoderma developing in hair follicles. Clinically, the yellowish pustule is pierced through by a hair.

Symptoms: face, upper lip, nape, perianal region. Squeezing the upper lip is strictly prohibited. After healing a mark or a scar is usually left behind.

Differential diagnosis: Furuncle, phlegmon, actinomycosis.

Acute necrotising ulcerative gingivostomatitis

See in Chapter 2.15.4. Acute periodontal diseases

Tuberculosis (TB)

Chronic infectious disease

Pathogen: Mycobacterium tuberculosis

Primary tuberculosis is rare in the oral cavity.

Symptoms: it is most frequent on the tongue, palate, cheeks or on the lips. Apparently it is an excavated ulcer with irregular, undermined edges, covered with a greyish-yellow fibrinous pseudomembrane. The erythematous, solid ulcers with prominent edges are usually painless.

The final diagnosis is set up on the basis of sputum culture, chest X-ray, PCR and histological examination. As a consequence of lymphogenic spread, regional lymphadenomegaly is an accompanying symptom.

Differential diagnosis: Lupus erythematous, syphilitic ulcer, tumorous ulcer, aphthous ulcer (Sutton).

Primary syphilis (lues)

Sexually transmitted disease.

Pathogen: Treponema pallidum

Bacterial invasion takes place in the genital area but sometimes on the lips or the oral mucosa as well, as a consequence of oro-genital intercourse.

Symptoms: after 3-5 weeks of incubation, a primary lesion (primary chancre) develops on the lower lip, tongue, palate, tonsil or other parts of the oral mucosa. At the site of the invasion, first dark red erythema (1-2 cm in diameter), then a brownish-red papule develops. The primary painless, solid, dark red ulcer (ulcus durum) is usually solitary, but might be multiple, too. The evolved ulcus durum heals spontaneously with scar formation after 4-6 weeks. Painless regional rubbery lymphadenomegaly (indolent bubo) is present.

The diagnosis is based on dark field and fluorescent microscopic examinations (smear). Serological examinations are needed.

Differential diagnosis: Herpes, aphtha, tuberculosis, carcinoma.

Secondary syphilis

Between 6 weeks and 6 months after the infection, the second phase of syphilis develops.

The first and the second phases are the early stages of syphilis. As a consequence of bacterial dissemination, secondary syphilis is characterised by generalised dermal and mucosal signs and generalised lymphadenomegaly.

Symptoms: multiple, slightly prominent, initially dark red roseolas on the oral mucosa are typical. Later they transform into papules and then into opalescent, greyish white mucous patches with a red base. The most common sites are the tongue, palate, angle of the lips.

Serological examinations are positive.

There are many bacteria in the dermal and oral lesions; as a consequence, the lesions are highly contagious.

Differential diagnosis: Candidosis, allergic stomatitis, stomatitis aphthosa-herpetica, oral pemphigus, lichen oris.

Tertiary syphilis

Late syphilis evolves 3-10 years after the initial infection.

Symptoms: painless solid gumma infiltrating the dermal or deeper tissues is characteristic. This is a special granuloma that can appear on the skin, mucus membrane, bones, blood vessels or in the nervous system, too. The size of the gumma varies from some millimetres to some centimetres and they can be solitary or multiple. The typical saddle nose develops due to the destruction of nasal cartilage and bones. The filiform and fungiform papillae become atrophic and the tongue becomes “smooth”.

Gummas rarely contain Treponema bacteria, thus, they are less dangerous from the point of view of infection. They finally heal with scarring.

Differential diagnosis: pernicious anaemia, carcinoma.

PROTOZOAN DISEASES

Toxoplasmosis

An infectious disease caused by the protozoan Toxoplasma gondii.

Toxoplasma can mainly be found in cats, rodents and birds, and it gets into the human body with food contaminated with the faeces of these animals. Human Toxoplasma infection is common; however, it rarely causes clinical symptoms and actual disease. The disease mainly affects children and young adults.

Symptoms: the onset may be slow with hardly any general symptoms; only a painless swelling of the lymph glands draws the attention to the disease. In acute cases; however, solitary or generalised lymphadenopathy is preceded by fever, headache, sore throat and muscle weakness. On rare occasions, blisters, papules and ulcers may present on the oral mucosa. The disease may be self-limiting with a slow course, but it can lead to severe complications as well (uveitis, myocarditis, and encephalitis). Toxoplasmosis in pregnant women may cause foetal damage, including chorioretinitis and consequential blindness.

Differential diagnosis: Infectious mononucleosis, leukaemia, Hodgkin’s diseases.

VIRAL DISEASES

Recurrent herpes simplex infection (herpes labialis, cold sore)

Pathogen: Herpes simplex virus

After the primary infection, the virus becomes latent in the epithelium and in the ganglia of the trigeminal nerve.

Symptoms: it usually affects the lips or the boundary between the lips and the skin. Predisposing factors include exposure to sun, fever (fever blisters), upper respiratory tract infections, pneumonia, malaria, meningitis, physical or emotional stress, menstruation, dental treatment, stress, gastroenteritis, AIDS, pregnancy, trauma, local irritation, etc.. Before the development of blisters, fever and enlargement of lymph glands may develop. At the onset of the disease an itchy, burning sensation (prodrome) and redness are present. A few hours later clusters of vesicles are formed, which are 1-3 millimetres in diameter. Vesicles become coalesced, and after two or three days they rupture and become ulcerated with yellowish crusts. The surrounding skin is erythematous. Skin lesions usually heal in 8-10 days without scarring. Sites and frequency of recurrences vary from patient to patient.

Differential diagnosis: Herpes zoster, pemphigus.

Herpes labialis

Primary herpetic gingivostomatitis

See in Chapter 2.15.4. Acute periodontal diseases

Herpes zoster (Shingles)

Pathogen: Herpes virus varicellae.

Shingles typically affects adults and the elderly. Children rarely develop shingles.

In case of endogenous or exogenous (salivary droplet) re-infection, the latent virus is re-activated due to various causes, such as immunosuppression, carcinoma, trauma, corticosteroids, cytostatic drugs, Hodgkin’s disease and leukaemia.

Symptoms: herpes zoster frequently affects the orofacial area, along the first (eye) or the second or third (oral mucous membrane and face) branches of the trigeminal nerve. Fever, headache and enlarged regional lymph glands are common. Pain can be mild, but mostly it is excruciating (neuralgic). The affected mucous membrane becomes erythematous. Typical signs and symptoms include unilateral, very painful, vesicular skin and oral mucosal lesions. The ulcerations heal in 5-10 days without scarring.

Differential diagnosis: Herpetic gingivostomatitis, aphthous stomatitis, allergic stomatitis.

Infectious mononucleosis (Pfeiffer’s disease)

Pathogen: Epstein–Barr virus.

This acute infectious disease is most common in adolescents and young adults.

The infection is typically transmitted through direct contact with saliva – especially kissing can spread the virus (it is also called “kissing disease”) – and through salivary droplet infection.

Symptoms: headache, fatigue, fever, pseudomembranous angina, primarily cervical, postauricural and generalised painful lymphadenopathy and hepatosplenomegaly. Maculopapular skin rash similar to the spots in measles, rubella and scarlet fever may occur. Intraorally, erythema, purpura and petechiae (diagnostic) develop on the uvula and on the soft palate. Uvular oedema, gingival bleeding, ulceration and painful aphthous ulcers can also occur. Pharyngitis and tonsillitis also contribute to the clinical picture.

Complications may include hepatitis, myocarditis, haemolytic anaemia, splenic rupture, encephalitis, neuritis and sialoadenitis.

Differential diagnosis: Aphthous and herpetic stomatitis, secondary syphilis, AIDS, leukaemia.

Morbilli (measles or rubeola)

Pathogen: morbilli virus (paramyxovirus).

It is transmitted through salivary droplet infection.

Symptoms: highly contagious infection that causes a range of symptoms including fever, chills, malaise, cough, conjunctivitis and rhinitis after a two-week incubation period. Then, maculopapular, grey-reddish exanthemas appear on the face, neck (behind the ears), trunk and extremities. Irregular, small (1-3 millimetres in diameter) lesions develop on the erythematous oral (buccal), genital and conjunctival mucosa. Oral lesions usually precede skin lesions. Bilateral cervical lymphadenitis is also characteristic.

Complications may include otitis media, bronchial pneumonia, and in severe cases subacute sclerosing panencephalitis. The most effective form of prevention is vaccination.

Differential diagnosis: Infectious mononucleosis, herpetic and aphthous stomatitis, white lesions.

Verruca vulgaris (common wart)

Pathogen: human papillomavirus (HPV) – a member of the papovavirus family.

The wart occurs less frequently in the oral cavity than on the skin, but more commonly than previously believed.

Symptoms: they usually appear on the lips, tongue and palate, but any other location in the oral cavity may occur. They appear abruptly and grow rapidly (viral origin), they are broad based and have a whitish-grey, papillary surface (usually feel hard on the skin).

Verrucae may appear as multiple and confluent lesions.

Differential diagnosis: Papilloma, verrucous leukoplakia.

Wart on the upper lip

Rubella (German measles)

It is a moderately infectious viral (RNA virus) disease usually transmitted by salivary droplets and affects primarily children and young adults.

Symptoms: may begin with milder symptoms (fever, headache, common cold and general malaise). Swollen, tender lymph nodes, usually in the back of the neck (cervical), behind the ears (retroauricular) or in the suboccipital area are characteristic. A maculopapular skin rash appears on the face and spreads downward to the trunk. Erythematous, red, petechial spots occur on the palates and the pharynx, especially on the soft palate.

In the first 16 weeks of pregnancy, rubella infection may trigger congenital rubella in the developing foetus (resulting in heart, eye, ear and brain damage).

Differential diagnosis: Morbilli, infectious mononucleosis, scarlet fever.

AIDS (Acquired Immune Deficiency Syndrome)

HIV (Human Immunodeficiency Virus) retrovirus is transmitted through infected bodily fluids.

High-risk groups include homo- and bisexual men, heterosexual women and men, (intravenous) drug users and people with haemophilia.

Symptoms: the disease does not have any characteristic symptoms. Initial symptoms include swollen lymph nodes (generalised lymphadenopathy), weight loss, fatigue, diarrhoea and night sweats. All types of infections may occur in the oral cavity, including fungal (acute pseudomembranous candidiasis, acute atrophic or chronic hyperplastic candidiasis), bacterial (periodontitis, necrotising ulcerative gingivitis), viral (herpetic stomatitis, herpes zoster, verruca vulgaris and condyloma acuminatum) and protozoan (toxoplasmosis) infections. Furthermore, non-Hodgkin’s lymphoma and carcinoma may also develop. Two of the pathognomic oral symptoms of AIDS are diagnostic: hairy leukoplakia and Kaposi’s sarcoma.

Differential diagnosis: Hairy leukoplakia has to be differentiated from real leukoplakia, lichen planus, cheek chewing, while Kaposi’s sarcoma from malignant melanoma and hemangioma.

Varicella (Chickenpox)

Chickenpox is an acute, highly contagious, generally mild disease in children, which occurs mainly in autumn and winter.

Pathogen: herpesvirus varicellae.

Chickenpox is a salivary droplet infection.

Symptoms: the disease begins with nasopharyngitis, headache, fever and pain in the extremities, followed by itchy maculopapular exanthemas and vesicles on the trunk, extremities, face and scalp. The disease usually heals in 7-10 days without a skin mark. The ruptured vesicles on the skin form scabs and scale off, but in case of secondary bacterial superinfection pustules, and after healing small, round scarring may develop. The lesions mainly affect the hard and soft palates and the lips, but the tongue, the gingival and other mucosal areas are also at risk. Complications may include pneumonia, bilateral parotitis, TB activation and encephalitis.

Differential diagnosis: Herpetic and aphthous gingivostomatitis, infectious mononucleosis, herpangina.

Epidemic parotitis (Mumps)

Pathogen: mumps virus – a member of the paramyxovirus family.

The acute infection spreads through salivary droplets.

Mumps mainly affects children, it rarely occurs in adults.

Symptoms: the parotid gland gets painfully swollen. Trismus sometimes develops. Swelling might be unilateral, but in most cases (70%) it affects both sides. Depending on the severity of subsequent xerostomia, fungal, viral or bacterial infection may appear in the oral cavity. The orifice of the parotid duct may swell and become red (papillitis), but no pus can be squeezed from the parotid gland. Complications may include meningitis, nerve palsy, pancreatitis, orchitis in men and oophoritis in women.

Differential diagnosis: Acute bacterial parotitis, sialolithiasis, parotid tumor.

FUNGAL DISEASES

Acute pseudomembranous candidosis (thrush)

The commonest Candida albicans-caused oral disease.

Predisposing factors: inappropriate oral hygiene, heavy smoking, xerostomia, radiotherapy, the administration of antibiotics, corticosteroids or cytostatic drugs, diabetes mellitus, chronic systemic diseases, autoimmune diseases, leukaemia, AIDS, immunosuppression. It mostly presents in newborns and children suffering from chronic illnesses.

Symptoms: the appearance of cream-coloured or pearl-white, bluish-white plaques which leave a slightly burning, erythematous surface if wiped off is characteristic of this type of candidiasis. Predilection sites include the bucca, the palate and the tongue. It is common in newborns and infants. In case of acute pseudomembranous candidiasis in adults, an underlying systemic disease has to be considered.

Differential diagnosis: Lichen, leukoplakia (cannot be wiped off), morsicatio buccarum, allergic stomatitis.

Acute pseudomembranous candidosis (thrush)

Acute atrophic candidosis

Untreated pseudomembranous candidiasis can turn into the atrophic form, but the latter can develop independently as well, without a previous pseudomembranous-type candidiasis.

Acute atrophic candidiasis is the commonest type of candidiasis in the oral cavity.

Predisposing factors: overuse of antiseptics or wide-spectrum antibiotics (topical or systemic), cytostatic and immunosuppressive drugs and HIV infection.

Predilection sites: the dorsum of the tongue, but it can present anywhere in the oral cavity.

Symptoms: the mucous membrane becomes oedematous, smooth (atrophy), erythematous, painful, and a burning sensation develops. In comparison with other clinical types, only acute atrophic candidiasis causes pain.

Differential diagnosis: Pernicious anaemia, iron-deficiency anaemia, Sjögren’s syndrome, chronic atrophic candidosis, migratory glossitis.

Chronic atrophic candidosis (denture stomatitis)

It is a common chronic disease of the mucous membrane especially in patients wearing upper dentures.

Tight fitting dentures provide favourable circumstances: they practically function as a substrate for the growth of Candida.

Symptoms: well-circumscribed, red, oedematous, sometimes eroded mucous membrane corresponding with the plate of the upper denture is characteristic of the disease. Chronic atrophic candidiasis is symptom-free.

Differential diagnosis: contact allergy of the palate.

Chronic atrophic candidosis

Immune-based diseases

Seborrheic eczema

The same allergen can cause allergic dermatitis in acute cases, and eczema in chronic cases.

Eczema might run in the family. Seborrheic eczema is usually based on sensibilisation due to microbes (bacteria, fungi) and chemicals. It is a frequent dermal disease.

Predilection sites: the forehead, the edge of the scalp, the perioral, perianal, periauricular and presternal regions, but it might also be present on the lips.

Differential diagnosis: herpes simplex.

Urticaria

Urtica (nettle rash) is the oedema of the upper part of the dermis as a consequence of increased vascular permeability. Drugs (penicillin, non-steroidal anti-inflammatory drugs, sulphonamides, salicylates, and opiates) usually play a role in the development of acute allergic urticaria.

Symptoms: the skin is highly itching when pink or white nettle rashes or nodules with a sharp edge appear on its surface. Diameter from some millimetres to some centimetres.

Differential diagnosis: lip furuncle.

Quincke’s oedema (angioneurotic oedema)

The disease has two forms, hereditary (rare) and non-hereditary (acquired).

The latter one is an early type of a hypersensitivity reaction caused by a drug, food, endocrine disorder, focal infection, insect bite or emotional stress, but in most cases the origin remains unknown.

Urticaria and its “giant” form (urticaria gigantea), Quincke’s oedema can develop.

Symptoms: swelling of the face, eyelids, lips, tongue, soft palate and pharynx. The swelling has a normal or slightly pink colour and might suddenly, unexpectedly increase in size. Sometimes it may cause burning, or slightly itching sensation. In severe cases the oedema of the epiglottis or that of the larynx may lead to dyspnoea (suffocation, death). Angioneurotic oedema might also turn into an anaphylactic shock.

Differential diagnosis: granulomatous cheilitis, glandular cheilitis, lymphoedema.

Allergic contact stomatitis

Metal

The contact allergy of the oral mucous membrane is less frequent than that of the skin, because allergens can act only for a shorter time due to the cleaning effect of the saliva. Not physical, but immune reactions account for contact allergic reactions. The metal bridge of the partial prothesis may induce contact allergy on the hard palate resulting in bright red oedematous enanthemas, sometimes erosions. Foreign body sensation, impaired gustatory sense and burning, itching sensation are among the subjective complaints. Nickel, cobalt, chromium, copper and gold tend to trigger contact allergy. Among these, nickel is the most frequent sensitising agent.

Differential diagnosis: candidosis (atrophiac).

Acrylate denture

True allergy to acrylate denture is rare. The mucous membrane turns red and oedematous according to the denture, besides the patient complains of a burning sensation.

Differential diagnosis: atrophic candidosis.

Drug-induced allergy (stomatitis medicamentosa)

After drug administration (hypnotics, analgesics, antibiotics, etc.), a bulla is developed, and later an erosive allergic enanthema accompanied by diffuse erythema and subepithelial burning sensation. The lips, the tongue, the palate and the gingiva are the predilection sites of allergic reactions.

Differential diagnosis: acute pseudomembranous candidosis, chemical injuries, white lesions, pemphigus.

Recurrent oral ulcers

Recurrent aphthous ulcer (Mikulicz’s aphtha; minor aphtha)

The aetiology is not yet explained. It might be an autoimmune, viral, bacterial (Streptococci), genetic (familial) or allergic disease or could be influenced by mechanical injuries, gastrointestinal diseases (Crohn’s disease), psychic stress, menstrual cycle (hormonal factor), walnut or chocolate consumption, etc., or by hypovitaminosis (B12, folic acid).

It is the most frequent disease of the oral mucous membrane. Recurrent aphthae are more frequent in adulthood and in women. It is rare among smokers (mucosal hyperkeratinisation).

Symptoms: initially erythema and oedema develops on the corresponding area, accompanied by a nipping, burning sensation or by paraesthesia. It can be either solitary or multiple. The development of ulcers is not preceded by vesicle formation. Well-demarcated lenticular (3–10 mm) painful ulcers on erythematous bases, covered with yellowish fibrous pseudomembranes are present. After 1 or 3 weeks, they heal without leaving scars. They might persist for years, but their frequency varies from person to person. They might be accompanied by lymphadenomegaly, too. Predisposed areas are the vestibular surface of the lips, the floor of the mouth, the ventral surface of the tongue and the cheek (non-keratinized mucosal epithelium). It is rare on the hard palate, the gingiva and the back of the tongue; these areas are usually affected by gingivostomatitis herpetica.

Differential diagnosis: herpetic stomatitis, allergic stomatitis.

Recurrent aphthous ulcer

Major aphtha (Sutton’s aphtha)

Recently major aphthae have been considered to be the rare severe form of aphthous ulcer.

Symptoms: 1–4 cm in diameter, usually solitary, but might have multiple forms, too (giant aphtha). Very painful crater-like ulcers of variable depth, covered with yellowish-grey fibrous pseudomembranes. The lesion usually heals with deforming mucosal scarring after epithelisation. Women are usually more affected. Predilection areas are the oropharyngeal region, the soft palate, the cheeks and the tongue. It causes severe pain, fever, trismus, lymphadenitis and difficulties in swallowing or eating. It may persist for several months or even for one or two years and tends to recur. Biopsy is mandatory.

Differential diagnosis: tumorous ulcer, decubital ulcer, specific ulcer: TB, lues.

Sutton’s aphtha

Systemic autoimmune dermal and oral diseases

Lupus erythematosus

The aetiology has not been fully revealed, but it is mostly regarded as an autoimmune disease. More women are affected, and untreated lupus erythematosus might lead to death after a shorter or longer time.

Two types:

  • -systemic lupus erythematosus (SLE) includes both mucocutaneous and internal symptoms,

  • -discoid type (DLE) is a local dermal and oral disease.

Symptoms: cutaneous symptoms: symmetrical butterfly-shaped red plaques on the face, maculopapular exanthemas, plaques, petechiae, vesicles, pigmentation on the thorax, arms, hands and nail folds and alopecia. Fever, leucopenia, thrombocytopenia, anaemia and other internal signs (nephritis, myocarditis, polyarthritis, lupoid hepatitis, epilepsy, etc.) might also accompany the disease. Sjögren’s syndrome or Raynaud’s syndrome might be secondary to lupus. The seriously ill patients with SLE die of renal, cardiac or pulmonary dysfunction.

The discoid form usually affects the lips and the cheeks, while the systemic form is more frequent on the hard palate and the cheeks. The slightly prominent, bright red, painful plaques appear on the erythematous mucous membrane; they might transform into erosions or ulcers. There are whitish hyperkeratotic ray-like striae on the slightly prominent edges of the plaques. Lupoid oral signs are spot-like and usually bilateral, contrary to lichen oris, where the lesions are more diffuse and symmetrical. Lupoid foci heal with atrophic scar formation.

The disease is lethal in 15% of the cases.

Differential diagnosis: erosive lichen oris, erythroplakia, erosive leukoplakia, pemphigus vulgaris.

Sjögren’s syndrome

It is a chronic and systemic autoimmune disease, which causes the destruction of exocrine salivary glands. It is accompanied by xerostomia and keratoconjunctivitis sicca (primary form, or sicca syndrome).

The disease is of unknown origin, but the factors may include genetic susceptibility, environmental predisposing factors, pathologic immune reaction, viruses and sex hormones.

Symptoms: during its progression, the tissue of salivary glands is destroyed by the increasing lymphocyte infiltration. Raynaud’s phenomenon (whitened and cold fingers), lymphadenopathy, vascular purpura and complications affecting the kidneys or lungs may also coexist. Predominantly it affects middle-aged women. Increased dryness of the mouth is often accompanied by (unilateral or symmetrical) rarely painful swelling of the large salivary glands, especially the parotid ones. Xerostomia may cause circular caries. The tongue is pale or red, atrophic, and lobular. The red and painful, in patches eroded or ulcerated tongue is often infected by Candida. Dryness of the eyes may bring about conjunctivitis.

The diagnosis is helped by the examination of saliva secretion, sialography, scintigraphy, histopathology (lip and bucca biopsy), ophthalmologic (Schirmer test), haematological and immunologic examinations as well as sonography, CT and MRI.

Differential diagnosis: pernicious anaemia, iron-deficiency anaemia, atrophic candidosis, diabetes mellitus, irradiation, mumps, inflammatory diseases and tumours of the salivary glands.

Vesiculobullous, granulomatous skin and mouth diseases

VESICULOBULLOUS SKIN AND MOUTH DISEASES

Pemphigus vulgaris

Pemphigus vulgaris is a chronic, life-threatening autoimmune skin, mouth and other mucous membrane disorder characterised by blistering of the skin and oral mucosa. Sometimes pemphigus appears in reaction to a viral infection, certain drugs (D-penicillamine, antihypertensive Captopril), thymoma or myasthenia gravis.

Symptoms: it usually affects elderly women. Blistering starts intraepithelially, the surrounding mucosa is not erythematous. The thin-walled intraoral bullae easily burst leaving painful erosions covered with whitish-grey fibrinous diphtheroid coating. The erosions may also bleed. Painful erosions may cause difficulty swallowing and eating and increased salivation. Erosions heal without scarring. Sites of greatest involvement include the buccal mucosa, tongue, palates and the gingiva. Nikolsky’s sign is positive (when the surface of the unaffected skin and oral mucosa is rubbed, and the skin and mucosa separate easily).

The diagnosis is established on the basis of skin symptoms and the histopathological examination.

In order to adjust the drug therapy, hospitalisation is necessary.

Differential diagnosis: herpetic gingivostomatitis, erosive lichen oris, aphthous stomatitis.

Pemphigus vulgaris

GRANULOMATOUS SKIN AND MUCOSAL DISEASES

Hand-Schüller-Christian disease (Langerhans cell histiocytosis)

The disease is one of the histiocytosis X syndromes. It is a chronic disease that is manifested in three classical signs in 25% of the cases: osteolytic bone lesions (“cloudy skull”), diabetes insipidus and unilateral or bilateral exophthalmus.

The aetiology of the syndrome is not clear.

Symptoms: may begin to develop in childhood, but the severe complaints appear only in older ages and mainly in male patients. It may be accompanied by fever, lymphadenomegaly, otitis media, brown scaly papules on the skin (mainly on the head, trunk, and on the anogenital area) and other internal signs. Oral symptoms are frequent, and the most characteristic sign is the destruction of the alveolar process of the jaw resulting in loose teeth or in the loss of teeth. The wound of extraction heals very slowly. Painful, bleeding, necrotic ulcers covered with fibrous pseudomembrane evolve usually on the gingiva, on the alveolar mucus membrane or on the palate, or sometimes on other neighbouring mucus membranes. It may be accompanied by fetor ex ore.

The diagnosis is set up by X-ray imaging (skull, long bones, and jaw) and by histological examination.

Differential diagnosis: malignant primary and secondary carcinoma.

Foreign body granuloma

Any insoluble, non-absorbable foreign body (metal, wood, thread, talcum, bone, glass, etc.) that gets into the skin or into the oral mucous membrane (injury, operation) causes smaller or larger brownish-red nodules (giant cell granuloma).

Differential diagnosis: tumour, sarcoidosis.

Oral manifestations of systemic diseases

ENDOCRINE DISEASES

Hyperthyroidism

It is the hyperfunction of the thyroid gland.

Symptoms: the enlargement of the thyroid gland (goitre), a staring gaze, protruding eyes (exophthalmus), increased heart rate (tachycardia), weakness, sweating, loss of weight, nervousness, diarrhoea and shaking. It is more common among women than men. No specific oral symptoms are observed. It may present with shaking and burning sensation in the tongue accompanied by the early eruption of deciduous and permanent teeth. Swelling of the gingiva may also be a common symptom.

Differential diagnosis: thyroid tumours.

Hypothyroidsism

It is the hypofunction of the thyroid gland.

Symptoms: it causes cretinism in infancy and myxoedema in childhood and adulthood. Congenital hypothyroidism causes severe mental and physical retardation, neonatal jaundice and a characteristic, hoarse crying of the infant, apart from these, wide, flat facial appearance and macroglossia (the tongue protrudes from the mouth), thick skin, delayed dental eruption and the dysplasia of the dental enamel. In adulthood, mucopolysaccharide infiltration causes macroglossia, macrocheilia and dry, reddish mucosa. The enlarged tongue makes speech and feeding more difficult. The face may become swollen as well. The appearance of the skin is determined by the myxoedema, the skin becomes dry and yellowish due to carotin deposits. Mental retardation, bradycardia, sensitivity to cold or hypothermia and the predisposition to ischemic cardiac disease are also typical. Hypothyroidism may be accompanied by chronic mucocutaneous candidiasis.

Differential diagnosis: amyloidosis, acromegaly.

Diabetes mellitus

Hyperglycaemia develops due to the decreased insulin production of the beta cells within the islets of Langerhans of the pancreas. Recently this disease has been considered a metabolic disorder.

Symptoms: apart from the dry skin being more susceptible to bacterial infections (furuncles, carbuncles), xerostomia (dry mouth), glossodynia and disorders of taste sensation are characteristic. Chronic candidiasis and angular cheilitis are also common in patients with diabetes. Swollen parotid glands (sialosis) and gingival (gingivitis, parodontitis) anomalies, as well as itching of the gingival may develop. Lichen oris and lichenoid reactions (caused by antidiabetic drugs) are also common.

Differential diagnosis: candidosis, Sjögren’s syndrome, disorders of the salivary glands.

VITAMIN DEFICIENCIES, NUTRITIONAL AND METABOLIC DISORDERS

Riboflavin (vitamin B2) deficiency

Causes: may be malnutrition, malabsorption, alcoholism, conditions leading to protein malnutrition. This deficiency is most common among children not consuming any milk.

Symptoms: the most common oral symptom is angular cheilitis. Seborrhoeic dermatitis may develop on the skin of the face, on the nasal apertures and within the nasolabial folds. In the beginning, the corners of the mouth are covered by yellowish, scaly crusts, and then they become red, deeply and painfully fissured (pebbly appearance) and they bleed easily. Apart from that, the tongue becomes atrophic, red in colour, painful and fissured as well.

Differential diagnosis: anaemia caused by iron deficiency, candidiasis (chronic, atrophic).

Niacin, nicotinic acid (vitamin B3) deficiency (pellagra)

Deficiency of the vitamin group B3 used to be caused by nutrition poor in proteins, but it is most commonly caused by gastroenteritis, anacidity, congenital metabolic disorders and chronic alcoholism nowadays.

Symptoms: may be loss of appetite, weakness, and irritability. In more evolved cases dermatitis, diarrhoea, or dementia may occur. The filiform papillae of the tongue become atrophic, the tongue becomes swollen, painful, resembles burning red “raw meat”. Thick, greyish coating may appear on the dorsal surface of the tongue. The gingiva may become swollen, ulcerated and erythemas may also appear on it. Increased salivation is also characteristic, and the inflammation may develop into ulcerative, necrotic stomatitis or gingivitis.

Differential diagnosis: pernicious anaemia, anaemia caused by iron deficiency, Sjögren’s syndrome.

Folic acid deficiency

The lack of folic acid damages protein synthesis and cell division. The primary cause of folic acid deficiency is imbalanced nutrition (vegetables and fruits); however, malabsorption (coeliac disease), alcoholism, anorexia, cancerous diseases, pregnancy, haemolytic anaemia, medications (contraceptives, phenytoin, anticonvulsive drugs) may all result in folic acid deficiency.

Lack of folic acid on its own is uncommon, as this deficiency is mostly accompanied by lack of vitamin B12 as well.

Symptoms: it commonly causes erythemas and painful, atrophic lesions (filiform and fungiform papillae disappear) on the tongue, as well as aphthous ulcers, similarly to the symptoms of vitamin B12 deficiency. Angular cheilitis may also be a characteristic symptom.

Differential diagnosis: anaemia, other vitamin B deficiencies.

Vitamin C deficiency (scurvy)

This deficiency is most commonly caused by insufficient nutrition (due to poverty, elderly age or chronic alcoholism).

Scurvy, the disease caused by vitamin C deficiency, is now quite uncommon.

Symptoms: the classical clinical symptoms of scurvy are hyperkeratotic hair follicles and perifollicular bleedings. Occasionally, ecchymoses may appear on the skin. The oral symptoms are most significant in case of patients with bad oral hygiene. The gingiva of these patients becomes extremely swollen, it may cover most of the dental crown and may very easily, even spontaneously bleed. Pain in the mandibular bones is quite common. Necrosis may develop on the site of gingival bleedings. An unpleasant oral odour and severe fusospirochetal stomatitis may also accompany this disease. Any inflammation caused by bacteria in vitamin C deficiency may cause rapid periodontal destruction and thus loss of teeth due to disturbances in connective tissue regeneration. Due to the haemorrhage of the temporomandibular joint, opening the oral cavity is painful.

Differential diagnosis: ulcerative and necrotising, or herpetic gingivostomatitis, leukaemia, agranulocytosis.

LIVER DISEASES

Hepatitis C viral infection

This type of viral hepatitis is mainly transmitted by transfusions, but needle pricks and dental treatments are less common causes of transmission than in the case of hepatitis B infections.

Since hepatitis C viral infections are in more than 60% of the cases accompanied by atrophic and erosive lichen lesions, today it is a recommended procedure to examine patients with erosive lichen for hepatitis C virus. According to some authors, other types of lichen alterations (reticular, bullous, plaque lichen, etc.) may refer to hepatitis C viral infections in the background as well. Chronic hepatitis C viral infections may eventually cause cirrhosis or even hepatic cancer.

Differential diagnosis: lupus erythematosus, lichenoid reaction, erythroleukoplakia.

Hepatic cirrhosis

Symptoms:typical symptoms are hepatomegaly, jaundice, later splenomegaly, ascites, fever and encephalopathy. Patients with hepatic cirrhosis may develop gastrointestinal bleeding, spider naevi, suggillations and hyperpigmentation on the skin (hepatic chloasma). Haemorrhagic tendency is caused by the metabolic disorders of vitamin K due to liver damage. Bleeding tendency demands careful, prudential surgical interventions. Typical oral symptoms are atrophic, smooth (“lacquered”), painful, red alterations of the tongue and angular cheilitis, which are due to the decreased protein intake, chronic gastritis (consequent vitamin B-12 and folic acid deficiency) and mainly vitamin B deficiency of alcoholic patients. The absorption of iron is also affected, which may also cause aphthous stomatitis. Patients suffering from hepatic cirrhosis often complain about halitosis (hepatic fetor). The atrophy of mucosal tissue may cause leukoplakia and carcinoma. Hepatic cirrhosis is often accompanied by sialadenosis (sialosis). The development of hepatic cancer is more common among patients suffering from hepatic cirrhosis.

Differential diagnosis: acute or chronic atrophic candidiasis, pernicious anaemia and anaemia caused by iron deficiency.

DISORDERS OF THE CARDIOVASCULAR SYSTEM

Varicosity of the tongue

It is a diffuse dilation of the veins occurring in an elderly age (varix). The dark blue varicosity on the ventral surface of the tongue or sometimes on the floor of the mouth is often called caviar lesion. The varicosity of the tongue is most common among patients suffering from cardiopulmonary diseases. Due to its tumour-like surface, it may cause cancerophobia.

Differential diagnosis: haemangioma, Kaposi’s sarcoma, malignant melanoma.

Varicosity of the tongue

DISEASES OF THE AIRWAYS

Bronchial asthma

The pathogenesis of this disease is still not clear, and allergic, non-allergic, physical, chemical and psychoneurotic factors are involved.

Bronchial asthma is characterised by cough and dyspnoea with a sudden onset during which the alterations of the bronchial and pulmonary capillaries and the thickening of the walls of the bronchioles cause deficiencies in the oxygen supply of the blood (cyanosis). Chronic asthma will cause elevated pulmonary blood pressure, hypertrophy and insufficiency of the right cardiac ventricle, and eventually, cor pulmonale.

DISEASES OF THE UROGENITAL TRACT

Uraemia

Patients suffering from severe acute or more commonly, chronic renal diseases (glomerulonephritis, pyelonephritis) may develop increased levels of serum uric acid.

Symptoms: general symptoms of uraemia (nausea, vomiting, breath smelling like urine, hypertension anaemia (pale skin), infections, bleeding, and prolonged wound healing). A characteristic, brownish-yellowish-faint colour (xanthochromia) appears on the skin, especially in the facial region. The sclera has a yellowish discoloration. Erythematous, pseudomembranous ulcerations and hyperkeratotic alterations may appear on the oral mucosa. Stomatitis accompanying uraemia (erythematous, pseudomembranous or ulcerative) as well as the white lesions respond well to dialysis. Apart from the symptoms mentioned above, xerostomia, taste deficiencies, oropyrosis, metallic taste sensation, gingival bleeding, purpuras (hemorrhages) of the oral mucosa, bacterial plaques, candidiasis, lingua pilosa, cheilitis, angular cheilitis and hairy gingival hyperplasia may occur. Salivary glands may become swollen as well. Due to anaemia, the oral mucosa and facial skin become pale. Hyperpigmented lesions may also occur on the oral mucosa.

Differential diagnosis: leukoplakia, morsicatio buccarum.

DISEASES OF THE GASTROINTESTINAL SYSTEM

Gastroesophageal reflux disease

Primary motility problems of the oesophagus are common.

Symptoms: apart from acidic regurgitations, patients complain of heartburn, chest pain, cough and nausea. Due to irritating chemical effects, the oral mucosa of the pharynx and the posterior dorsal lingual surface become erythematous and atrophic. The tongue of patients suffering from reflux becomes coated (whitish-yellowish), and hairy tongue may also accompany this condition. Patients often complain about burning sensation in the oral mucosa (oropyrosis) and the tongue (glossopyrosis). Permanent dental erosions (damage to the enamel and dentin) may also evolve apart from the symptoms of the oral mucosa.

Differential diagnosis: acute atrophic candidiasis, anaemia, Sjögren’s syndrome

Crohn’s diseases

It is a chronic, inflammatory, presumably immunopathological disease with unknown origin which may affect the entire digestive system from the oral cavity to the rectum, but extraintestinal, metastatic Crohn’s disease may also occur. This disease primarily affects the ileum.

Symptoms:apart from internal symptoms (enteritis, diarrhoea, constipation, malabsorption, anaemia, arthralgia). Periorificial erythema may occur on the face. These alterations may develop anywhere on the oral mucosa but most commonly on the bucca. The mucosa becomes erythematous and swollen, and the surface is ulcerative, deeply fissured. Diffuse, red, indurated and granulomatous nodules evolve on the lips (especially on the upper lip) and gingiva. Multiple fissures may develop on the lips. Granulomatous cheilitis may be the first sign of Crohn’s disease; therefore, if swelling of the upper or lower lip occurs, examination of the intestinal system may be recommended. Aphthous ulcers may occur on the oral mucosa, most commonly on the palate. Angular cheilitis may occur in the commissures.

Differential diagnosis: granulomas due to candidiasis, Quincke’s oedema, granulomatous cheilitis.

Coeliac diseases (enteropathy caused by sensitivity to gluten)

This disease is caused by the pathological function, malabsorption and motility disorders of the small intestine. This disease is explained by genetic factors, gluten toxicity, intestinal peptidase deficiency and immune response.

Symptoms: characteristically, gastrointestinal protein loss, vitamin deficiencies and the malabsorption of lipids, carbohydrates, water and iron are common. Usually it begins in childhood, however, its symptoms may persist in adulthood as well. Symptoms associated with this disease are anaemia (usually microcytic, hypochromic), anorexia, sore bones, eczema of the skin, bleeding tendency and finger clubbing. Symptoms affecting the oral mucosa are aphthous ulcers mainly due to iron and folic acid deficiency. Small aphthas may also accompany this disease. The tongue becomes erythematous, atrophic and painfully burning. Angular cheilitis is another common symptom. Coeliac disease in childhood causes dental hypoplasia.

Differential diagnosis: anaemia, vitamin deficiencies.

ORAL SYMPTOMS OF HAEMATOLOGICAL DISEASES

Iron deficiency anaemia

Anaemia is a decreased amount of haemoglobin and of red blood cells within the circulation.

This disease is caused by extensive loss of blood, decreased iron intake or iron absorption. The idiopathic form of the disease is called Plummer–Vinson syndrome.

Symptoms:anaemia, dysphagia, broken, concave fingernails (koilonychia), glossitis and cheilosis. It is more common among women. Patients suffering from iron deficiency are usually listless, pale, their hair is turning grey, and they tend to have headaches. The tongue becomes atrophic, pale or sore, red, enlarged and smooth. Sometimes the surface of the tongue is fissured. The oral mucosa is pale. Painful erosions, angular cheilitis may also accompany this disease. Aphthous ulcers are more common on the oral mucosa. The resistance to infections decreases, therefore, osteomyelitis is more common after a tooth extraction. The lips become thin. The tongue of the patient suffering from iron deficiency is more likely to develop candidiasis and leukoplakia, which may even transform into a malignancy.

Differential diagnosis: pernicious anaemia, Sjögren’s syndrome, acute atrophic candidiasis.

Pernicious anaemia

Anaemia which is caused by the lack of vitamin B12 or folic acid and the lack of intrinsic factor required for the absorption of vitamin B12.

Symptoms: pallor, fatigue, breathlessness, tachycardia, palpitations, diarrhoea and paraesthesia of the extremities are common. Apart from these, headaches, vertigo, nausea, weight loss, yellowish, pale, dry skin, nervous system problems, such as paraesthesia, or the numbness of the limbs may be the accompanying symptoms. The most characteristic oral symptom is Möller–Hunter glossitis, which involves the atrophy of lingual papillae, thus, the tongue becomes smooth and reflective. The tongue of these patients is “beefy red” and the painful tongue may develop paraesthesia or may become lobulated (due to decreased muscle tone) later on. The tongue resembling “cobble-stone appearance” is similar to the lingual alterations that can be observed in patients suffering from Sjögren’s syndrome. The oral mucosa becomes pale and yellowish, disturbances of taste sensation, xerostomia, burning oral sensation (oropyrosis) may also occur. Chronic mucocutaneous candidiasis, angular stomatitis, leukoplakia, or carcinomas are also possible complications. Recurrent aphthous ulcers may develop.

Differential diagnosis: iron deficiency anaemia, acute atrophic candidiasis

Haemorrhagic diatheses

Von Willebrand’s diseases

Clinical symptoms resemble haemophilia rather than thrombocytopathy. This disease is inherited in an autosomal, dominant trait. The disease occurs in childhood and affects girls mostly, which is not characteristic of haemophilia. Apart from the pathologic alterations of factor VIII and the capillaries, the functional disorders of thrombocytes and thromboplastin secretion are also typical. Bleeding petechiae, purpuras and bleedings (hematomas) occur on the oral mucosa.

Symptoms: petechiae and minor ecchymoses appear on the bucca and on the lips. Purpuras are mostly located on the hard and soft palates. Gingival bleeding is more common than one would expect during gingivitis. Prolonged and severe bleeding should be expected after tooth extraction. Apart from oral symptoms, only this latter one requires any therapy, and this symptom is alleviated by proper oral hygiene and the cessation of gingivitis.

Differential diagnosis: haemophilia.

Haemorrhage caused by anticoagulants

Anticoagulant treatment is common among patients receiving renal dialysis, or suffering from thromboembolic diseases, myocardial infarction, etc. Patients taking anticoagulants containing cumarin (e.g. Syncumar) and indandione compounds may develop haemorrhagic purpuras on the oral mucosa. The continuous monitoring of prothrombin time is required during oral surgical interventions.

Differential diagnosis: Werlhof’s disease, Osler’s disease

Diseases of the lip (Péter Novák MD)

Exfoliative cheilitis (“cracked lips”)

Symptoms: exfoliative periods alternate with erosion. The lips become dry, swollen, erythematous, and in rare cases painful vertical fissures occur. Scaling, yellowish-brown crusts recur periodically in stressful conditions. This chronic disease usually affects adolescent girls and women. Predisposing factors include licking and biting of the lips, irritation caused by protruding maxillary incisors, fever, nervous tongue protrusion, tension of the lips, and cold or extremely hot weather. Licking of the lips may cause perioral inflammation and secondary bacterial or fungal infection. In some cases, the cause of the disease remains unidentified.

Differential diagnosis: acute and chronic actinic cheilitis and cheilitis glandularis.

“Cracked lips”

Angular cheilitis (perlèche)

In children and young adults Staphylococcus or Streptococcus infection results in pyoderma of the labial commissure.

Symptoms: the condition causes maceration fissures and burning, painful, red infiltration. Later, greyish-white, hyperkeratotic thickening occurs on the denuded areas. The lesions may spread to the surrounding skin and honey-coloured crusts, similar to those seen in impetigo, appear. The disease may persist for months or years. Adults and the elderly are primarily infected with Candida albicans (Candida-associated angular cheilitis). It may also develop due to iron deficiency anaemia (perlèche), vitamin B12 deficiency, Plummer-Vinson syndrome, pellagra, diabetes mellitus and malnutrition. Other risk factors include overbite, congenital lip fistula, increased salivation (ptyalism), sagging face in the elderly, edentulous persons, deepened labiomandibular fold due to a decrease in the proper vertical dimension of the teeth among denture wearing patients, which may be accompanied by maceration caused by saliva and secondary Candida infection. Secondary Staphylococcus aureus infection may exacerbate the condition.

Differential diagnosis: pemphigus vegetans.

Angular cheilitis

Cheilitis glandularis

Cheilitis glandularis is a relatively uncommon and chronic lip disease, which affects middle-aged men more frequently than women. The aetiology of the disease is poorly understood, familial predisposition may occur, and trigger factors possibly include exposure to sun, emotional stress, tobacco smoking and poor oral hygiene.

Symptoms: primarily the lower lip is affected. Red spots appear mainly on the vestibular surface of the lips and the ductal orifice of small mixed salivary glands. Chronic inflammation and the hyperplasia of the salivary glands cause swelling of the lip and drooling due to increased salivation,. The dilated ductal orifices pose a high risk of pyogenic infections, which are characterized by suppuration of the salivary glands (suppurative cheilitis glandularis), and the swollen, infiltrated lip becomes painful, ulcerated and crusty (apostematous cheilitis glandularis) with mucinous purulent secretion expressible from the ductal openings. The lesion can be considered as a potential predisposing factor for the development of lip cancer.

Differential diagnosis: granulomatous cheilitis, chronic cheilitis, Quincke’s oedema and Crohn’s disease.

Fissured cheilitis

The cause of the disease is not clarified, but different exogenous predisposing factors such as tobacco smoking, mouth breathing, climatic factors, Crohn’s disease and Down’s syndrome may play a role.

Symptoms: men are more frequently affected than women. Painful, denuded fissures appear on the lower and upper lips, which heal with difficulty. The lesions are mostly infected with Staphylococci.

Differential diagnosis: mechanical injury.

Acute actinic cheilitis

Acute actinic cheilitis is an acute inflammation of the lips caused by exposure to strong sunlight (“solar cheilitis”). Acute cheilitis frequently develops on the beach („summer cheilitis”), during skiing, and among people with light complexions. Photoallergic and phototoxic cosmetics (lipstick cheilitis) or medications may also cause acute contact cheilitis.

Symptoms: swollen, oedematous lips, redness, tension and itchy sensation. Single sun exposure results in vesicular-bullous, painful, oozing lesions, ulcers, followed by brownish-red drying crusts appearing mainly on the lower lip.

Differential diagnosis: exfoliative cheilitis, eczema, chronic actinic cheilitis and lip cancer.

Cheilitis due to diabetes

Chronic, unhealing, burning, distending cheilitis or a lip wound may indicate diabetes. In such cases, a laboratory test may confirm the diagnosis. Chronic ulcer may mimic lip cancer, thus a biopsy is necessary.

Differential diagnosis: chronic cheilitis.

Diseases of the tongue (Péter Novák MD)

Median rhomboid glossitis

The disease used to be classified as a developmental disorder (the persistence of tuberculum impar), but today the role of chronic Candida infection and decreased vascularity is emphasized. It is common among smoking men and among diabetic patients. The lesion occurs more frequently in denture-wearing patients.

Symptoms: an oval or rhombic, red, smooth, non-protruding or verrucous, prominent lobulated patch with a depapillated surface presents in the middle of the back of the tongue, in front of the foramen caecum. It is usually asymptomatic, except for patients wearing full upper dentures.

Differential diagnosis: Tongue cancer, migratory glossitis, verrucous leukoplakia.

Median rhomboid glossitis

Allergic glossitis

Various local (dental materials, medications – drug-induced glossitis) and systemic factors (medications, alimentary factors, etc.) may cause vesiculobullous lesions on the tongue that later turn into painful ulcers covered with a whitish-yellowish, fibrinous pseudomembrane.

Differential diagnosis: Migratory glossitis, decubital ulcer, pemphigus vulgaris, or atrophic candidiasis.

Coated tongue

A coating (epithelial cells, neutrophil granulocytes, mucin, fibrin and food remnants) of various colour and thickness develops together with changes in the condition of the filiform papillae of the tongue. Possible causes include upper respiratory (tonsillitis) and lung diseases, smoking, febrility, gastrointestinal and liver diseases, inappropriate oral hygiene, soft foods, denture wearing and oral diseases (e.g. stomatitis). It can be an accompanying symptom of glossitis and it may develop as a result of decreased salivation, too. The colour of the coating may vary from white to brown (smoking, tea, coffee, etc.).

Differential diagnosis: Leukoplakia, candidiasis.

Lingual papillitis

The red lesion presents in elderly, denture-wearing patients and involves the inflammation and hypertrophy of the papillae, first on the tip of the tongue, then at the back of the tongue as well. The fungiform papillae appear in the form of red spots.

Symptoms: inflammatory papillitis causes a burning sensation and moderate pain.

Vitamin deficiency (A,B,C), iron deficiency, alcohol consumption, smoking, hot and spicy foods and mechanical irritation may also play a role in the development of the disease.

Hypertrophy of the circumvallate papillae

The epithelium of the circumvallate papillae contains many taste buds, thus these papillae play a significant role in the sense of taste. The circumvallate papillae are situated on the posterior third of the back of the tongue, resembling the limbs of a letter V inverted.

Symptoms: in case of inflammatory hypertrophy, the papillae protrude more than normal and become lumpy, red and moderately painful during eating or swallowing. Frequently recurring upper respiratory infections or chronic irritation contribute to the inflammatory hypertrophy of the papillae, and even doctors or dentists might be deceived by the nodular-appearing ’tumour-like’ lesion. Such lesions on the tongue often lead to the development of cancerophobia.

Differential diagnosis: benign and malignant tumours, or median rhomboid glossitis.

Geographic tongue

The cause of the disease is not clarified; familial predisposition , psychological factors, vitamin deficiency, malnutrition, exudative diatheses and endocrine disorders may play a role in the development of the lesion.

It can be an accompanying symptom of psoriasis, reactive arthritis and diabetes mellitus.

Symptoms: Red patches of round, oval or indeterminate shape appear on the tongue (or rarely on the lips, bucca or gingiva) and migrate (“wander”) to other locations after some time, or occasionally persist at the same place for a longer period. Filiform papillae disappear but fungiform papillae persist at the site of the red patch, which has a diameter ranging from a few millimetres to some centimetres. The patch is bordered by a white, hyperkeratotic, zigzag-like and elevated margin. The condition can develop at any age. It often coexists with fissured tongue and might be accompanied by a stinging, burning sensation. Patients suffering from benign migratory glossitis are not uncommonly mentally unstable and cancerophobic.

Differential diagnosis: Leukoplakia, oral lichen planus, secondary syphilis, annular lichen planus of the mouth, or candidiasis.

Geographic tongue

Lingua villosa (hairy tongue)

The condition is considered to be a multi-aetiological disease, which presents more frequently in elderly denture-wearing patients. Hairy tongue is often idiopathic, but it can also be triggered by antibiotics, corticosteroids, vitamin A or B deficiency, radiotherapy, chemotherapy, inappropriate oral hygiene, emotional stress, Candida albicans, heavy smoking, gastrointestinal disorders or hydrogen peroxide.

Symptoms: the hairy surface is caused by the elongation, thickening (hypertrophy) and keratosis of the filiform papillae. The yellowish-greenish, brownish-black colour can be explained by the presence of pigment-producing bacteria and Aspergillus species (not Candida albicans), foods, medications, consumer goods and smoking.

Differential diagnosis: Coated tongue.

Lingua villosa (hairy tongue)

Glossodynia

In the majority of the patients organic changes cannot be detected on the tongue, so probably psychogenic causes lie in the background of the unpleasant tongue burning.

Symptoms: the condition is more frequent in women and it presents mostly during menopause. In some cases, the fungiform papillae are slightly elevated on the tip of the tongue and they become erythematous. Burning and itching develops mainly on the tip and lateral border of the tongue, but it can present on other mucous membranes as well. Glossopyrosis is often accompanied by cancerophobia.

Glossodynia may also present in iron-deficiency and pernicious anaemia, xerostomia, candidiasis, geographic tongue, lichen planus, herpes simplex, allergic reactions, diabetes mellitus, gastro-oesophageal reflux disease and hypertension.

Diseases of the salivary glands (Péter Novák MD)

Sialolithiasis

Salivary calculi develop mostly inside the submandibular or sublingual glands or within Wharton’s duct.

Salivary calculi may be composed of calcium (phosphorous or carbonic acid) compounds, bacteria, epithelial cells, foreign bodies or thickened saliva.

The development of calculi is uncommon in the parotid and minor oral salivary glands. It is more common among men than women.

Symptoms: complaints are due to the calculi partially or completely obstructing the aperture. Pus may be evacuated through Stenson’s duct when applying pressure to it. Before meals, but especially during eating, bursting, intense pain occurs due to increased saliva production, the affected glands become swollen and tender. Salivary calculi within Wharton’s duct on the floor of the mouth are easily palpable, furthermore, the swollen gland becomes visible.

Differential diagnosis: ranula, tumours of the floor of the mouth.

Recurrent parotitis in childhood

The causes of this disease are unclear, however, apart from otitis or tonsillitis, some researchers presume that allergic or mycotic factors may also play a role in its development.

Symptoms: the disease starts with uni- or bilateral, painful parotid swelling, which may be accompanied by swollen lymph nodes , fever or subfebrile periods. When pressure is applied to the parotid glands, purulent or white, thick saliva empties from Stenson’s ducts. Recurrences may occur on a monthly or yearly basis. Relapses spontaneously cease after puberty.

Differential diagnosis: epidemic parotitis, salivary calculi.

Sialoadenitis of the submandibular gland

Inflammation of the submandibular salivary gland may be caused by direct bacterial infections, salivary calculi or tumours. Bacterial sialoadenitis may be caused by staphylococcus or streptococcus infections, but dental, periodontal or mechanical irritation of the orifice (denture) may also play an important role.

Symptoms: the salivary gland becomes painfully swollen and swallowing causes pain as well. The swelling of the salivary glands may become permanent as a result of long-term involvement due to fibrosis.

Differential diagnosis: sialolithiasis, dermoid cysts, metastases.

Xerostomia

Xerostomia is not a disease but a symptom. Xerostomia may be caused by a wide range of conditions, the main cause being temporary or permanent cessation of salivary secretion.

Causes: xerostomia most commonly presents as an adverse effect of pharmaceuticals (minor and major tranquillisers, antihistamine products, antihypertensive drugs, Parkinson’s medication, cytotoxic pharmaceuticals, cytokines, narcotics, retinoid drugs, sympathomimetics and other anticholinergic drugs). Apart from these, xerostomia may be caused by congenital anomalies of the salivary glands or dehydration (diabetes mellitus or insipidus, vomiting, diarrhoea, bleeding), elderly age (menopause), psychogenic conditions (depression), salivary gland conditions (Sjögren’s syndrome), iron deficiency anaemia, irradiation, etc.

Symptoms: the oral mucosa becomes dry and red while the epithelial tissues themselves become atrophic. Patients suffering from these symptoms usually complain of swallowing, eating, speaking and tasting difficulties, as well as a burning sensation of the tongue (glossodynia) and the mouth (oropyrosis). The predisposition to caries and oral candidiasis is also increased.

Dry and shiny tongue of patient with Xerostomia

Oral symptoms of neurological and psychiatric diseases (Péter Novák MD)

Trigeminal neuralgia

Facial pain may be an accompanying symptom of some underlying diseases (multiple sclerosis, tumors of the brain stem, etc.), or may be of idiopathic origin as well.

Symptoms: sudden, flash-like, paroxysmal, sharp and stabbing, intense facial pain is also characteristic, and it may be provoked by touch, facial mimics, eating, toothbrushing, cold air or draught. As the disease progresses, attacks of radiating pain occur more frequently and spontaneous remission becomes increasingly rare. Symptoms are unilateral and usually affect areas served by the second or third branches of the trigeminal nerve.

Differential diagnosis: toothache, pain associated with herpes zoster.

Bell’s palsy (idiopathic facial palsy)

The paralysis of the facial nerve may be idiopathic or it may occur due to inflammation in the area of the stylomastoid foramen, or due to inflammation, tumour, trauma or vascular spasms within the osseous facial canal. In the past few years, the role of herpes simplex and zoster-varicella viral reactivation, draught or cold trauma have been considered as trigger factors; however, idiopathic forms of the disease occur as well.

The disease may be accompanied by hypertension, diabetes or lymphoma and may develop due to lower peripheral nerve block anaesthesia before tooth extraction. Facial palsy may be preceded by mandibular pain and numbness of the tongue on the affected side. Facial palsy usually develops suddenly, the patient feels stiffness in the face, one side of the face may be drawn, the commissure becomes loose, the closure of the ipsilateral eyelid may be compromised, the corneal reflex is missing and patients complain of increased (unilateral) lacrimation during meals (“crocodile tears”). Typically, the eyeball deviates upwards when the eyelids are closing. When patients attempt to smile, the commissure of the lips on the affected side is drawn downwards instead of upwards, and periorbital wrinkles do not appear on the paralytic side. Disturbances of taste sensation, difficulties with eating, speaking, whistling may accompany the disease, the paralysis may persist for several days or weeks or sometimes it may even become permanent.

Oropyrosis (oral dysaesthesia)

Burning sensation (stomatopyrosis) or pain (stomatodynia) inside the oral cavity may affect the tongue alone (glossopyrosis, glossodynia).

The patients are commonly middle-aged or elderly women, who experience dysaesthesia on waking up, and this sensation progresses over the course of the day. Affected patients often have cancerophobia or other causes of anxiety.

The symptoms are more common after menopause. The complaints may be caused by localised, systemic, neurological or psychiatric factors. The common local causes include geographic tongue, fissured tongue and medial rhomboid glossitis. According to some experts, candidiasis may be the most common cause, especially when it is accompanied by excessive smoking or alcohol consumption.

As a general cause, vitamin B deficiencies and consequent pathological conditions may be considered, such as pernicious anaemia, hypoacidity, gastro-oesophageal reflux disease, iron deficiency anaemia, diabetes mellitus, oral lichen planus or long-term treatment with antibiotics or other pharmaceuticals (ACE inhibitors). Xerostomia is a common predisposing factor. Unilateral symptoms suggest neurological conditions. If there are no evident local, systemic or neurological underlying causes, the diagnosis is idiopathic glossodynia. In such cases depression, cancerophobia and neurosis may be the explanation of these complaints.

Traumatic dental injuries (Ildikó Pinke DMD)

Traumatic dental injuries affect mainly the front teeth and may occur with high frequency in preschool and school age children and young adults (comprising 5% of all injuries for which people seek treatment).

Luxations are the most common traumatic dental injuries in the primary dentition, whereas crown fractures are more commonly reported for the permanent dentition. Dental traumas are often accompanied by soft tissue and other associated injuries, which may require other surgical intervention. Injuries may involve the teeth, lips, jaws, tongue, gum, cheeks (rarely the roof of the mouth, palates, neck, or tonsils).

PATIENT EXAMINATION:

  • Where did the injury occur? – the possibility of contamination

  • When did the injury occur? - the extraoral storage condition (avulsion)

  • How did the injury occur? – any sign of child abuse

  • Was there a period of unconsciousness and how long? – Amnesia, nausea and vomiting are all signs of brain damage.

  • Is there any reaction in the teeth to cold and/or heat exposure? – exposed dentin or pulp

  • Is there any disturbance in the bite? – any alveolar fracture, jaw fracture or a fracture of the condylar region

DIAGNOSTIC SIGNS

Visual signs

  • not displaced (concussion, subluxation)

  • appears elongated (extrusion)

  • displaced in palatal/ lingual or labial direction or axially

  • visible fracture line

Percussion test

  • tender to touch or tapping (concussion, subluxation)

  • tenderness (extrusion, crown-root fracture)

  • ankylotic sound (lateral luxation, intrusion)

  • not tender ( infraction, enamel fracture)

Mobility test

  • no increased mobility (contusion)

  • immobile (intrusion)

  • increased mobility (subluxation)

  • excessively mobile (extrusion)

  • normal mobility (infraction, enamel fracture)

  • coronal fragment mobile (crown-root fracture)

Pulp sensibility test – cold test and/or electric pulp test

The purpose of the test is to determine the condition of the pulp. Extrusion, intrusion and lateral luxation injuries have high rates of pulp canal obliteration (PCO). PCO occurs more frequently in teeth with open apices which have suffered a severe luxation injury.

  • Usually a negative result: contusion, subluxation, extrusion, intrusion, root-fracture

  • Usually a positive result: infraction, enamel-fracture, enamel and root -fracture

Radiographic test

  • No radiographic abnormalities: contusion, subluxation, infraction

  • Periapical enlargement of periodontal space: extrusion, lateral luxation,

  • No periodontal ligament space: intrusion

  • The fracture line is usually visible

The diagnostic protocol can be seen on the next figure (Fig.2.23.)

Diagnostic protocol of the traumatic dental injuries

TREATMENT

Avulsion

Treatment guideline for permanent teeth depends on

  • extraoral dry time:

    1. extraoral dry time

    2. extraoral dry time longer than 60 min. Delayed replantation has a poor long-term prognosis.less than 60 min.

  • storage media (tooth has been kept in physiological storage media or osmolality balanced media as milk, saline, saliva or Hank’s Balanced Salt Solution)

  • maturation of tooth (open apex or closed apex)

Splinting (Fig. 2.24.)

Short-term, non-rigid splints (usually orthodontic arches) are used (passively) in luxated, avulsed and root-fractured teeth. The duration of splinting is significantly related to healing outcome of the pulp (2 to 4 weeks). The splint may maintain the repositioned tooth in correct position, provide patient comfort and improved function.

Fixation of injured tooth with flexible fiber-reinforced composite splint

Restore with resin composite and/or glass-ionomer

In case of enamel fracture, enamel-dentin fracture

Antibiotics

Use of antibiotics is limited

  • use of systemic antibiotics is recommended in the management of avulsion (the first choice is Doxycycline 2x per day for 7 days in appropriate dose for patient age and weight; in young patients Amoxicillin in appropriate dose for age and weight)

  • there is no evidence that antibiotic therapy is effective in root fractured teeth.

Patient Instructions

  • a flexible splint for 2 weeks to stabilise the tooth;

  • brush your teeth with a soft toothbrush after each meal;

  • oral hygiene and rinsing with an antibacterial solution (alcohol free chlorhexidine gluconate 0.1%) for 2 weeks;

  • patient compliance with follow-up visits and home care contributes to better healing;

  • advise regarding care to patients and parents of young patients of the injured tooth/teeth for optimal healing;

  • follow-up controls are required to make a pulpal diagnosis;

  • prevention of further injuries (avoidance of participation in contact sports or mouth guards should be worn as an oral protector by the players).

Dental Box

Utilizing for the emergency care of acute dental emergencies. It can be used quickly and easily in the care of fractured teeth, subluxations, luxations, avulsions, dry sockets, deep caries, loose appliances and bleeding mucosa. Contents can be seen on the next figure (Fig. 2.25.)

Contents of Dental Box

Save-A-Tooth

It is a kind of emergency tooth preserving system. Use of this appliance increases the survival rate of a knocked-out tooth. Ingredients: water and Hank’s Balanced Salt Solution (active ingredients)

Deposits forming on the teeth (Zsuzsanna Tóth DMD - Péter Vályi DMD)

For several centuries, the importance of good oral health has been emphasised in the literature. There is mediaeval evidence originating from more than 5,500 year old findings of the Babylonians on the removal of deposits formed on the teeth. The role of the deposits causing periodontal diseases and caries are proved by scientific studies. A wide variety of materials of different hardness, colour and adhesiveness originating from the oral milieu can be deposited on the natural and artificial hard surfaces in the mouth:

  • acquired pellicle

  • dento-gingival plaque

  • calculus

  • debris

  • materia alba

The dental plaque is a strong adhesive layer on the surface of the teeth, restorations and dentures, which develops by the help of acquired pellicle, and it can be removed only by rubbing and not by mouth rinsing or water jet (Figure 2.26.). The main components of the dental plaque are bacterial strains colonising in the intercellular matrix, which are located in the biofilm (See Chapter 1.8). The supragingival plaque adheres above the gingival margin, and the subgingival plaque adheres under it.

Dental plaque (from Prof. S. Kneist)

The materia alba is a greyish-white-yellow soft layer that is clearly visible also by the naked eye on the hard surfaces. It is less adherent in comparison with plaque, and it can be removed using a water jet. Its main mass contains bacteria, salivary proteins, detached epithelial cells, disintegrated leukocytes, and often food remnants as well.

Debris may be found on the teeth, between the teeth, and possibly also on the surface of soft tissues, which is food remnant in the mouth washable by water, but usually they are removed by the mechanical effect of muscle function and salivary flow.

THE ROLE OF DENTAL PLAQUE IN GINGIVITIS

There are bacterial colonies organized in a biofilm, as members of the natural bacterial flora are present in the healthy oral cavity without causing any disease. Small amounts of bacteria causing diseases can often be detected, but in healthy conditions the human organism’s defence mechanisms are able to maintain a balanced state without any damage to the tissues. Due to strengthening of the bacterial effects or weakening of the body's defence mechanisms, the balance will be tilted and pathological changes, pathoses occur.

The biofilm forming microorganisms can be classified as symbiotic (apathogenic) and pathogenic microorganisms. Against the members of the symbiotic flora the organism will not trigger the tissue destruction causing, damaging defence mechanisms. The members of the pathogenic flora cause inflammation and promote the development of disease characterized by direct and indirect (inflammatory and immunological) damage of tissues. Certain risk factors influence the development and the process of the pathosis significantly (see chapter 2.15.1.).

The increase in the amount of dental plaque results in gingivitis. Gingivitis without any treatment will be followed by periodontal disease. In most of the cases the regular and efficient dental plaque removal prevents or heals the gingivitis. Frequently experienced gingivitis in pregnant women developing as a result of the hormonal changes is of great importance, but it is also related to the formation of dental plaque.

According to the non-specific plaque theory of Loesche W. (1976) and Theilade (1986) the quantity of accumulating dental plaque is the cause of the consecutive gingivitis. In larger amount of dental plaque more harmful bacterial decomposed products will be produced leading to inflammation of gingival tissues and growing worse to inflammation of periodontal tissues. In some cases however excessive mass of dental plaque of the neglected mouth does not result in serious medical consequences. Therefore scientific examinations have focused on the bacterial composition of the dental plaque, and it was found that certain well-defined pathogenic strains can be isolated, which have important role in the periodontal pathological processes, they cause disease and their removal causes the healing. That is the explanation also for the experience whereas the same large amount of plaque in the oral cavity of neglected patients can cause inflammation of different stages: mild or quite severe as well. According to the specific plaque theory (Loesche W. 1979) the disease of the periodontium can be explained not by the quantity of the dental plaque, but by the presence of some pathogens. Among the disease causing parodonto-pathogen bacteria there are only a few species, which can not be found or only in trace amounts (exogenous pathogens) in the healthy mouth. Bacteria also of the healthy organism cause very often opportunistic infections due to a change in circumstances (constitutional factors, quantitative and qualitative changes of the composition of dental plaque, risk factors etc.). This is the endogenous infection, which plays an important role in the development of inflammatory and destructive disease of the periodontal tissue (Wirthlin and Armitage, 2004).

There is not still correct answer received what a role is played by the mostly obligate anaerobic parodonto-pathogen bacteria strains in the aetiopathogenesis of the disease, since they can not be the initiators of the disease because of their nature, they are likely responsible for the progression of the disease.

Formation and properties of dental plaque see in chapter, 1.8.

THE ROLE OF DENTAL PLAQUE IN CARIES

In the chapter on biofilm is already mentioned that the composition of various colonies found on the different surfaces, mainly due to the different environmental conditions is significantly varied. While the bacterial strains at the gingival margin and below them play a role in the inflammatory processes of gingival and deeper periodontal tissues, the bacteria of dental plaque accumulating on the smooth surfaces and in pits and fissures of the coronal part of the teeth are the etiological factors of dental caries. The metabolism of cariogen plaque’s components produces acidic milieu which initiates demineralization. If they can not be neutralised and compensated by remineralizing processes, the dental hard tissue will be damaged.

The role of dental plaque bacteria in caries aetiology detailed can be found in the next chapter.

THE FORMATION OF DENTAL CALCULUS

In mature dental plaque accumulating on the surface of the teeth mineral salts can be precipitated and calcifying the plaque forming supra- and subgingival type of dental calculus.

The supragingival calculus

In the beginning the supragingival calculus is a yellowish-white porous deposit above the gingival margin (Figure 2.27.). The characteristic places are the predilection sites, where they appear very early and easily. Typical localization of dental calculus formation is as follows: the opposite tooth surfaces of the salivary glands’ outflow, for example lingual surface of the lower front teeth, and vestibular surface of upper molars. Typical experience is, that in neglected subjects chewing only on one side (unilateral chewing), also the occlusal surface of the teeth of opposite side will be covered by calculus. Without any oral hygiene deposits can be formed not only on the surface of the teeth, but on the surface of the restorations and dentures, prosthesis as well. The cleaning of the dental calculus can not be perfect, because of its rough outer layer. At first it is porous, but in the course of time it will be harder and harder, its removal needs considerable effort. Its colour can vary regarding the meals and beverages and depending on the by-product of bacterial metabolism originated on its surface developing plaque. Its colour can vary from yellowish-white to dark brown or black. Note that the role of dental calculus is determining in the process of development of periodontal diseases because it is an important plaque-retentive factor. Beside this it widens the gingival sulcus that is why the forming of subgingival biofilm will be possible. The bacterial toxins originated from the plaque of the calculus surface cause pathological tissue destruction. Every roughness of the tooth surface promotes the formation of dental plaque and calculus. In addition the accumulation will be facilitated by gaps, leakage, margins of fillings, restorations, prosthesis and orthodontic appliances beside the original dental conditions.

The subgingival calculus

Subgingival calculus can be formed only in the gingival sulcus of inflamed gingiva. There is no predilection place for its development, but there is no subgingival calculus below the healthy gingival margin (Figure 3). In case of thin gingival margin its dark bluish purple discolouration is visible also by naked eye. Its diagnosis is possible by periodontal probe, by removal of inflamed marginal gingival with air, and its interproximal localization is visible in the X-ray picture as well. Subgingival calculus develops due to the mineralization of subgingival dental plaque, its colour is black, and its surface is very rough. Its calcifying is originated from sulcus secretion and blood, that is why the supragingival calculus is from saliva and contrast with it subgingival calculus is originated from the gingival sulcus. It adheres very strong to the tooth, stronger than supragingival calculus. It can be explained by the roughness of the root surface and by the fact, that not only dental plaque but also the acquired pellicle will be mineralized.

Supra- (yellowish-white) and subgingival (brownish-gray) calculus

In the inter-bacterial matrix of dental plaque some components (proteins, fats) are centres of crystallisation, here starts the crystallisation from the supersaturated salt solution of the saliva. Dental calculus mostly contains inorganic salts (octa–calcium-phosphate, tri-calcium-phosphate, magnesium- carbonate, sodium carbonate) and later hydroxyl-apatite crystals. Supragingival calculus has a layered structure, the mineral content of the layers are different but the average value is lower than in case of subgingival calculus.

The supra- and subgingival calculus should be fully removed from the tooth surface. In case of subgingival calculus, frequently, it cannot be performed only with the accidental attenuation of the root cement.

Dental caries (Zsuzsanna Tóth DMD)

DEFINITION OF CARIES

Caries is damage to hard tissue in the presence of cariogenic microorganisms on erupted tooth surface covered by dental plaque. The chronic process is reversible in the initial stage but will be irreversible following cavitation. It extends from the coronal enamel surface towards pulp as a result of demineralising and remineralising processes depending on the frequency of the carious attacks. As a result of aging and recession of the gingival, caries can develop on the cementum and on the nude dentin as well. Over time the deep penetrating destruction results in pulp pathosis.

EPIDEMIOLOGY OF DENTAL CARIES

Epidemiology as part of medical sciences deals with pathological changes and epidemic diseases occurring on a large-scale. The existence, severity, frequency, development, spread and conditions of diseases are investigated regarding different parameters. These parameters can be e.g. the following: age, sex, occupation, qualification, behavioural and dietary habits, and geographical, social and economic conditions. After the evaluation of statistical data we may come to a conclusion about pathological factors, risk groups, therapeutical and preventive options, and about the effectiveness of therapy and prevention. Discovering the caries preventive effect of fluorides is also a result of epidemiological investigation.

Dental caries –besides inflammatory diseases affecting the periodontium – is the most frequent chronic disorder. Its therapy is expensive for the society although only a few patients visit their dentist regularly. The right solution is prevention.

Dental caries has been present since the start of human history. Its prevalence has increased to 90-100% nowadays. In the 1970’s and 1980’s in some industrialised countries the increase stopped and then decreased, e.g. in the US, in western European countries, in New Zealand and in Australia. The decline can be attributed mostly to the presence of fluoride in the drinking water and later in the products of oral hygiene, first of all in toothpastes. Dental caries is a civilisational disease. In developing countries there used to be generally low values which rapidly increased with civilisation. There is a close correlation between disadvantageous dental caries conditions and dietary and oral hygiene habits.

Epidemiological survey

The participants in epidemiological studies are the population. Caries frequency (caries prevalence) shows the percentage of persons with carious teeth. The number of diseased teeth is expressed by caries intensity (caries experience). Horizontal or cross-sectional surveys provide information about the actual conditions, in a follow-up survey, or data of a longitudinal study are registered periodically (in case of caries: yearly) in the same way. The changes in caries conditions can be determined. Caries increment reports new carious lesions, caries incidence indicates the number of persons with a new carious lesion.

DMF scores are individual quantitative data regarding caries; DMF index shows data of a group. It is a quotient: the sum of all DMF scores in the group should be divided by the number of subjects. DMF is an acronym, D means decay, M means missing and F means filled. DMF-T index (T means tooth) refers to carious teeth, DMF-S (S means surface) refers to tooth surfaces. The increasing depth of caries in the enamel is indicated by D1-D2 scores, dentinal lesions are indicated by D3-D4 scores. For primary teeth the nomination is the same but it is written with lower case letters: dmf-index. The indices df and def are widespread; in the second one e means deciduous tooth indicated for extraction. The df-t index refers to teeth and df-s index refers to tooth surfaces.

In comparative epidemiological caries surveys the data of the same age groups will be compared. Successful prevention and conservative therapy result in more remaining teeth in elderly patients although they have more periodontally involved teeth. The frequency of root caries on the exposed tooth neck is increasing due to gingival recession. RCI, root caries index expresses the quotient of carious root surfaces and exposed root surfaces. Recent epidemiological studies demonstrate an increasing number of root caries depending on age and remaining teeth. Root caries is more frequent in males and in lower teeth with the exception of the incisors.

DENTAL NOTATION

There are many nomenclatures in the literature for the definite identification of the 20 primary and 32 permanent teeth. In Hungary the Zsigmondy system is used the most frequently: the teeth are put in the Zsigmondy-cross. The patient is sitting opposite the dentist, the mouth is divided into four quadrants and each permanent tooth is assigned a number from 1 to 8 starting at the midline.

Each primary tooth is numbered similarly but with Roman numbers from I to V starting at the midline.

Notation of teeth by Zsigmondy-system

In scientific publications the two-digit notation of the World Dental Federation, FDI (Federation Dentaire Internationale) is adopted.

FDI notation of teeth (ISO system by WHO)

In the US the teeth are numbered simply following the quadrants clockwise from the upper right side numbering them continuously:

Universal numbering system "American method"

AETIOLOGY OF CARIES

Hundreds of theories explaining the development of caries have developed in the past centuries, many of which contain plausible mechanisms according to our present knowledge.

Modern theory of caries development

Dental caries is a disease of dental hard tissues with a multifactorial aetiology. Besides the four essential (primary) factors, secondary factors (e.g. biological, environmental, geographical, socio-economic, etc.) play an important role in the development of tooth decay.

The primary conditions for the formation of dental caries are (Figure 2.31.):

  1. The surface of erupted tooth in the oral cavity

  2. The microbial flora adhering on it

  3. The substrate providing nutrients for microorganisms

  4. The time factor

The primary factors for the development of dental caries

Tooth surface as host indicates the importance of systemic factors. The outer cover of the crown, the enamel is the hardest tissue of our body, but it is still susceptible to environmental harmful effects. The enamel is of ectodermal origin, has an acellular structure, no circulation, and it is unable to defend itself or to reverse already existing tissue damage. In the oral cavity after eruption, the tooth surface as host is covered by a biofilm (dental plaque). The dental plaque is a strongly adhesive bacterial aggregate on the surface of oral structures which can only be removed by intensive mechanical cleaning. In the dental plaque there are microorganisms and nutrients as well.

Biochemical reactions taking place between the enamel and the dental plaque are in a dynamic equilibrium. This balance is disturbed during food intake. After carbohydrate intake (carious attack) microorganisms produce organic acids (such as lactic acid) by the degradation of carbohydrates. This decreases the pH of dental plaque.

The mineral components of hard tissue (e.g. calcium, phosphate) are dissolved, this process is called demineralisation. With the disappearance of carious attacks under the influence of saliva, pH is increased and remineralisation processes predominate. By the diffusion of calcium and phosphate (mostly in the presence of fluoride) the demineralised surface is remineralised.

Demineralisation and remineralisation processes occur many times a day. The frequency of carious attacks leads to a dominance of demineralisation, to macroscopic lesions and irreparable cavitation (Figure 2.32.).

Carious cavity on the upper left wisdom tooth buccal surface

The significance of the time period is closely related to frequency. The more often the surface is exposed to carious attacks, (demineralisation) (e.g. due to frequent snacking), the less time is available for remineralisation (Figure 2.33.).

Changes of dental plaque pH according to the frequency of food intake (Bánóczy , 1990).

In addition to primary aetiological factors, many biological, behavioural, environmental, geographical, socio-economic factors play a role in influencing the likelihood of caries development

Microbiological background of caries

The complex and dynamic relationship between bacterial plaque, host and diseases in the oral cavity is the result of a working ecological system. The oral microflora of a toothless baby is poor, it will be rich in the presence of teeth, but under elderly edentulous circumstances the situation is similar to childhood. Only a limited number of bacteria of the 400-500 types existing in the oral cavity have an important role in caries development (cariogenesis). Dental plaque accumulates on the tooth surface in a determined sequence. Most of the microorganisms leave the mouth by swallowing and only a few of them are able to stay and adhere to soft and hard tissues. At different places of their retention there are different complex colonisations. That is why it is hard to prove the direct casual relation between the caries process and one single pathogen, but the role of Streptococcus mutans and Lactobacilli is definitive in caries development and progress.

The shape of the tooth is important in dental plaque formation and in caries development. In retention places of grooves, pits and fissures dental plaque adheres very easily, but plaque removal is complicated, and these retention places are harder to assess for the rinsing and protecting effect of saliva. Saliva is a very important endogenous factor against caries development. In case of dental congestion, there are hardly any places that can be cleaned effectively, and these are optimal for plaque retention. The role of dental plaque is dominant in caries development and do not forget its important role in the aetiology of periodontal diseases.

Formation of the dental plaque (see under II. Pathology, in chapter 12. Deposits forming on the teeth)

The dental plaque adheres to undisturbed surfaces, where the cleaning effect cannot operate due to the movement of soft tissues while chewing. In caries aetiology the supragingival plaque has special importance.

Dental plaque in the development of caries

The dental plaque is an ecological community: if it produces mostly organic acids, under it caries will develop. Initially the composition of the dental plaque is rather aerobic, and has low pathogenicity. The maturation process results in a mostly anaerobic combination. Carbohydrates metabolised to organic acids cause significant and long lasting decrease in pH. At pH between 5.0 and 5.5 demineralisation starts in the enamel: under the clinically intact enamel surface the subsurface mineral content decreases, becomes porous. After drying its appearance is chalk-white and opaque (incipient caries). This stage is still reversible, and in the presence of fluoride the enamel can be remineralised, which results in a hard and acid-resistant enamel surface, more resistant than the original was. The dental plaque is different in caries free and caries active individuals. In caries-resistant persons fasting pH is higher. If the plaque-pH remains under the critical pH of 5.5 for a period of 20-50 minutes after a single sucrose intake, it is called caries active. The acid production of the caries active plaque is twofold than the acid production of caries inactive one. Note that the consumption of sweets between main meals results in a constant acidic attack on the tooth surface.

The role of saliva in the development of caries

Saliva is particularly important in cariogenesis. The water and mucin content of saliva moistens the mucous membranes and helps taste and swallowing. An adequate amount of saliva (appropriate level of flow rate) cleans the oral cavity from a significant part of food remains, microorganisms and dissolved metabolites by its mechanical washing and diluting effect. This role inhibits the development of caries. The lubricant components of saliva facilitate speaking. Mucin and mucoid content increases viscosity and thereby facilitates the formation of dental plaque and consequently, the formation of caries as well. Enzymes of the saliva already start to digest nutrients in the oral cavity; carbohydrate breakdown results in an acidic pH in the mouth promoting caries development. In contrast to this, however the caries inhibitory properties of saliva predominate. The high number of bicarbonates has a buffering effect; its efficiency is enhanced by phosphate and to a certain extent by the protein buffer system as well. The antibacterial activity of saliva is provided partly by immune proteins and enzymes. Growth factors in saliva promote wound healing; inorganic ions (calcium, phosphate, fluoride) promote the remineralisation of enamel. Decreased salivary secretion (xerostomia) reduces the amount of protective proteins (protective function) and reduces acid and carbohydrate clearance. A decreased salivary flow rate is a physiological phenomenon of aging, menopause, symptoms of some diseases, for example psychic disorders, autoimmune diseases of the salivary glands (e.g. Sjögren's syndrome) or diabetes mellitus. It can be associated with anaemia, dehydration, vitamin deficiency or pregnancy as well, and can also occur as a result of drugs. The reduced production of saliva leads to caries increment.

Nutrition and caries

Food intake is of crucial importance in dental caries and in periodontal diseases because it provides the essential nutrients for the microorganisms in the dental plaque. The composition and consistency of food, the way, the quantity, the frequency of food intake and the duration of residence in the mouth are all important factors. Its effect can work in two ways:

  • praeresorptive effectprevails in the oral cavity before the absorption in contact with teeth and other oral surfaces during chewing.

  • postresorptive effectis a systemic effect after absorption, as in the developmental period of teeth before eruption (praeeruptive).

Other factors affecting caries development

In addition to the primary factors in the aetiology of dental caries there are also non-negligible secondary factors playing a role in the process, for example macroscopic and microscopic properties of the teeth, physique (genetic background), age, sex, hormonal and immunological factors, and some geographical, social and economic factors.

THE LOCATION OF CARIES

Caries develops if in the presence of bacteria, the balance of demineralisation and remineralisation processes is upset, leading to increased demineralisation. The anatomical location of caries is on the crown and on the root. Morphological and histological differentiation is based on enamel, dentin and cement tissue. Predilection sites are areas susceptible to caries development. The predilection sites are the non- self-cleaning surfaces, so-called habitually unclean areas. As a result of self-cleaning, the dental plaque disappears from tooth surfaces which are in contact with the lips, tongue, and bucca due to speaking and chewing or due to the abrasive effect of food. To clean the non- self-cleaning or habitually unclean areas is often very difficult. The caries susceptible predilection sites are as follows (Figure 2.34.):

  1. pits, grooves, fissures,

  2. smooth surface interproximally below the contact point,

  3. smooth surface at the gingival border,

  4. root surface.

Caries predilection sites (Wannemacher 1963)

Crown caries

Crown caries means circumscribed carious lesions developing on the tooth crown in pits, fissures or on the smooth surface (Fig. 2.35.).

Fissure caries

To clean deep and narrow fissures is often impossible; in this case fissure sealing in due time is possible to prevent caries formation (Fig. 2.36., see under IV. Prevention, in chapter 5. Fissure sealants). Pits and fissures are to be found on the occlusal surface of premolar and molar teeth and on the palatal surfaces of the upper incisors (foramen caecum).

Fissure sealing

Areas between the gingival margin and equator of the crown are not self-cleaning smooth surfaces, although it is easy to clean them because of good access. Caries in these areas draws the dentist’s attention to the lack of oral hygiene or disorder of saliva production (Figure 2.37.).

Caries at the gingival margin

The approximal smooth surface of the teeth below the contact point belongs to habitually unclean areas. The cleaning of this area requires some manual skill and the use of tools for oral hygiene besides the tooth-brush (e.g. dental floss, interdental brushes) (Fig. 2.38.).

Approximal caries

Root caries

Nowadays more and more elderly people have their own teeth, but often the root surface is exposed. This area is not self-cleaning, plaque formation is promoted also by the decreased saliva flow rate. Due to the deterioration of manual skills, cleaning is problematic. At the enamel cement junction a soft, irregular, often discoloured lesion develops and extends relatively quickly.

THE EXPANSION OF CARIES

Dental caries is a pathological process extending from the enamel (root cement) surface through the dentine toward the pulp into the depths. Because of the prismatic structure and the different formation of enamel prisms, the cross-section of fissure caries and smooth surface caries are different in the enamel. There is no difference in the dentine, which has a tubular structure, and in both cases the cross-section is similar (Fig. 2.39.).

Smooth surface caries and cross-section of groove

Primary dental caries (caries primaria) occurs on an intact tooth surface which is not self-cleaning. Secondary caries (caries secundaria) develops along the margin of crowns, fillings or inlays placed in the teeth. In the stage of caries incipient the enamel surface is carious without any clinically or histologically macroscopic cavity formation. There is a chalky white spot on the tooth surface, and it becomes porous (Fig. 2.37.). From the occlusal surface at the bottom of the fissure, developing incipient caries appears to be a dark or an opaque area. The therapy of incipient caries is remineralisation. Superficial caries is a cavitated lesion progressing to the dentine. Caries media extends to the dentine, the deepest part of the process is far away from the pulp chamber. The differences in colour, transparency and the changes in the surface and the contour are visible to the naked eye as well, the break in continuity is tactile by a dental probe. Caries profunda is an extensive carious process, at this stage there is only a thin intact dentin layer between the pulp chamber and the carious process. In the case of caries penetrans the carious process has extended into the pulp, which communicates with the oral cavity. The contamination of the pulp leads to inflammation.

THE TIME COURSE OF CARIES

Dental caries is a chronic disease. Between the incipient stage and the clinically diagnosed cavitated the development takes about 18 ± 6 months. The process extends faster in the pits and fissures than in the smooth surface. If poor oral hygiene is connected with snacking, the frequency of daily carbohydrate intake is high, incipient enamel caries can develop in three weeks. X-ray irradiation leads to xerostomia, which can cause dental caries in three months. In healthy subjects the development of caries is slower. Depending on the time, an acute and a chronic type of caries can be distinguished despite the chronic character of the process. The disintegration of the enamel and cavity formation in children develops rapidly; it is caries rapida (florid, or rampant caries). The lesion is white coloured (caries alba), it is filled with crumbly pasty mass (caries humida). At older age, when the dentinal tubules are narrower due to calcification, the process advances more slowly (caries tarda). The lesion itself is drier and harder (caries sicca), and the area has a dark brown or black discolouration (caries nigra). Stationaer or chronic caries means a carious process, which does not show further progress after the cessation of the cariogen attacks (insistens caries, arrested caries). During remineralisation, the enamel surface gets dark brown and black due to exogenous discolouration.

The acid solubility of the enamel will be reduced, its surface will be more acid resistant compared to the original condition if remineralisation occurs in the presence of fluoride. This situation can be seen, for example in approximal caries after the extraction of the adjacent tooth. Latent or hidden caries is difficult to diagnose. In this case the carious lesion involves the dentine as well, and the process extends into the depth although the enamel surface has been remineralised due to the fluoride content of oral hygiene products. In the case of a cavity, which is to be found under an extensive occlusal caries, the intact enamel does not have enough support and may break due to chewing forces. The softened carious dentine becomes exposed, and in the course of time it can be worn off by intensive chewing. Due to the increasing tubular obliteration of the dentine, a smooth, hard surface is formed (dentinal sclerosis).

CARIES DIAGNOSIS

In the earlier history of dentistry caries diagnosis was the disclosure of a carious cavity, and the only therapeutic option was filling. Nowadays we know a lot about the complex pathological process, about the extent of caries risk, so we can determine the appropriate treatment planning and methods of prevention as well. Caries diagnostics is part of the patient’s medical examination. In the case of dental caries, symptoms may include sensitivity to sweet, cold, interapproximally inserted remains of food, gingival papilla bleeding, discolouration, cavity formation, damaged aesthetics, bad taste or unpleasant odour. For the oral examination and treatment the supine position is used. The dried tooth surface has to be investigated under appropriate illumination by inspection and palpation with a dental probe. The sensitivity of the tooth has to be tested with thermal or electrical stimuli. Do not forget to take an X-ray if it is needed.

Pulp and periapical diseases (Zsuzsanna Tóth DMD)

PATHOLOGICAL CHANGES IN THE DENTAL PULP

Pulp diseases can be caused by the following aetiological factors:

  • microbial irritants / infections most commonly due to decay (Figure 2.40.),

  • mechanical / physical irritants, for example damage due to preparation without coolant,

  • chemical irritants, for example due to cavity cleaning with alcohol.

Extensive caries refers to bacterial irritation of the pulp

Injury of the pulp by these irritants may cause inflammation. There is no possibility for dilatation of the inflamed tissue encased in rigid walls in the cavity system of the tooth; therefore, significant pain can develop. From a clinical point of view, it is important to know whether the health of the pulp can be completely restored or not. The exact condition of the dental pulp and the seriousness of physiological and pathological lesions can be determined only by histological examination.

The vitality of the pulp means that pulp is a living tissue, which can be proved by the vitality test. The vitality test should be called correctly sensibility or sensitivity test, because it results in information about the condition of the pulp and not only about its living or necrotised character. The most common sensitivity test is carried out by a small, hard cotton pellet soaked with a drop of ethyl chloride. First, an isolated healthy tooth should be examined at the tooth neck as reference, and after that the questionable tooth to compare the results. If the tooth responds to cold stimulus, the pulp is living. In addition to the cold stimulus by heat and electrical stimulation, or by drilling test-cavities, it is possible to collect some information about the status of the pulp.

The clinical experience does not correspond unambiguously to the histological condition. The task of the dentist is an effective therapy. Treatment planning is related to the diagnosis. The diagnosis is based on the patient’s complaints, symptoms, and the results of the clinical investigations. The diseases of the pulp can be classified as follows:

  • Reversible pulpitis

  • Irreversible pulpitis

  • Hyperplastic pulpitis (pulp polyp)

  • Pulp necrosis

  • Pulp calcification

  • Internal resorption.

In case of reversible pulpitis, the inflammatory process is reversible, and the circulation of the pulp can become settled after the interruption of damaging stimulus (caries). If the stimulus is answered by the development of localised, sharp but only transient pain, the pulp is vital and sensible. There is no percussion tenderness, and tooth decay can be seen in the X-ray without any periapical lesion. The proper treatment is the removal of the carious tissue and restoration.

In the case of irreversible pulpitis, the pulp suffers permanent, irreversible damage. In the closed pulp chamber, intense sharp or dull pain can be generated by stimuli (e.g. cold stimulus) or even spontaneously, continuing for minutes or even for hours. The localisation of the pain is often very difficult because of its diffuse character. If the pulp chamber communicates with the oral cavity, the process is asymptomatic or only mild pain is reported.

The pulp is in vital condition, and as the inflammation is limited to the pulp, there is no percussion tenderness. There is no periapical lesion in the radiogram, but caries or deep filling can be seen. While the integrity of the pulp is impossible to recover, the correct therapy is root canal treatment or tooth extraction. The root canal filled tooth should be checked by X-ray after half a year, and then annually for 4 years. By systematic check-ups, we can intervene in due time in case of the development of apical lesions to avoid the possibility of focal infection.

In hyperplastic pulpitis (pulp polyps), the damaged pulp tissue of deciduous molars with good blood flow and circulation, and the first permanent molars in development increases and occupies the carious cavity. There is chronic inflammation, the tissue bleeds immediately but the inflammatory exudates can leave, thus, the asymptomatic disease, which might even be long-term, is discovered accidentally. Rarely signs of irreversible pulpitis with remaining pain can be found. The pulp is tender, inflammation is limited to the pulp, no percussion tendernness or a periapical lesion can be found, but caries can be visualised in the X-ray. While it is impossible to maintain the health of the pulp, root canal treatment or the extraction of the tooth is the correct therapy. In the case of permanent immature molars, pulpotomy can be performed.

Collapse of the circulation originated from inflammation, or damage of blood vessels supplying the pulp due to trauma (accident, aggressive orthodontics) results in pulp necrosis. The case can be characterised by sensitivity to heat, and later discolouration of the tooth, but pulp necrosis is poor in symptoms. Regarding multi-rooted teeth, a diagnostic mistake can be made if a canal has necrotised pulp, but another one contains vital tissue. Neither percussion tenderness is detected, nor a periapical lesion is seen in the X-ray, the adequate alternatives for the therapy are endodontic treatment or the tooth should be removed.

Pulp calcification may develop with ageing, or due to long lasting low grade irritation in the pulp. The fibrous elements are accumulated, the number of cell elements is reduced, the circulation is low, and the chance of healing in pulp damage is significantly lower. In case of extensive diffuse calcification, the crown of the tooth has yellowish discolouration. Pulp stone or denticulus may also develop freely in the pulp, respectively fixed to the dentin wall. These are asymptomatic conditions. The reaction after a stimulus is decreased, however, the pulp is vital. There is neither percussion tenderness detected, nor a periapical lesion found, and sometimes pulp stone can be recognised in the X-ray picture. Irritants should be removed, and no other treatment is needed. If the root canal of the tooth should be treated for other reasons, calcification and pulp stone can make it complicated.

In case of internal resorption, the pulp tissue is transformed into granulation tissue, and because of the dentinoclast activity, the hard tissue of the root canal will be resorbed advancing from the centre to the periphery. The pulp tissue is vital. The highly vascularised pulp involving the pulp chamber seems to have a pink spot. The progressive process may be clinically asymptomatic, but discolouration of the tooth, or a round shadow in the X-ray or an unexplainable fracture can help us in setting up the correct diagnosis. As soon as possible, preferably before the root perforation, endodontic treatment should be performed, but it has a dubious outcome in advanced stages.

The pulp is spread without any anatomical limit to the apical periodontium. Therefore, the pulp inflammatory processes through bacteria, respectively toxins can spread quickly into the periapical space across the apex. In contrast to the poor circulation of the pulp, the periapical space is rich in blood and lymphatic vessels. It favours the development of protracted, indolent chronic processes, which are poor in symptoms. An acute periapical process is characterised by its rush evolution, by pain that spreads quickly and swelling, and sometimes it is also associated with general malaise. Classification of the periapical diseases is the following:

  • Acute apical periodontitis,

  • Chronic apical periodontitis,

  • Condensing osteitis,

  • Acute apical abscess,

  • Chronic apical abscess.

In the case of acute apical periodontitis, pulpal inflammation spreads into the periodontal space and causes intense pain during biting, but it also happens if the tooth is only touched or pressed. The tooth seems to be elongated because of the production of inflammatory exudates, and that is why the occlusion is painful. The pulp is non-vital, but because of the expansion of gases in the root canals, heat sensitivity can be possible. Similar symptoms may be caused by instruments, irrigants and root canal filling materials, and also due to a flare-up of existing chronic apical periodontitis. Periapical radiographic examination shows thickened periodontal ligament space or a frank periapical lesion according to the chronic inflammation, and coronally caries, deep filling, crowns, or another restoration. The process may be accompanied by swollen lymph nodes, shivering or fever. Root canal treatment or tooth extraction can be the appropriate therapy. After obturation of the root, the tooth is to be controlled regularly. An acute abscess or a chronic lesion can develop without appropriate treatment, depending on the intensity of the infection and the resistance of the organism.

Depending on the type and number of pathogenic bacteria, the infected root canal flora causes smaller or larger periapical lesions, which refer to the development of chronic apical periodontitis. Balance is established between the organism and the infection. This condition is poor in symptoms, the tooth is often discoloured, does not respond to cold, but may respond to heat stimulus, and the patient may describe a slight discomfort feeling. Percussion causes some pain, the X-ray shows either thickened periodontal ligament space or a significantly large radiolucency (Figure 2.41.).

Chronic apical periodontitis with significant periapical radiolucency at 46 tooth before treatment and one year after healing

The periapical lesion is a granuloma or a cyst lined by epithelium. The correct differential diagnosis is possible based only on histological findings. Treatment of the disease can be root canal treatment or extraction. In the case of a cyst, after root canal treatment, additional apical surgery has to be done and regular control has to be performed.

Condensing osteitis presents with a characteristic radiopaque lesion which may develop either from irreversible pulpitis or from pulp necrosis. Inflammation results in enhanced osteoblast activity, and therefore, bone formation. Because of the necrosis, the calcification of the periapical lesion will cause a similar circular radiopaque phenomenon. Symptoms develop according to the pathological origin with painful or painless tooth, positive or negative response to thermal stimuli. Its therapy is the endodontic treatment (or extraction) with regular control after the obturation.

Acute apical abscess is accompanied by a severe general condition due to bacterial infection. It can develop directly from acute apical periodontitis, but more frequently is it produced by a flare-up of the chronic apical periodontitis as it is confirmed by the X-ray findings. The patient presents with malaise, has fever and a characteristic swelling on the face (Figure 2.42.). The necrotised tooth will be raised, it is loose and painful during biting or even if it is touched.

Acute apical abscess of the 26 tooth with swelling of the face

Inflammatory exudates can be cleared and solved by tooth extraction, but in order to save the tooth, root canal treatment should be performed. If exudates are not excreted via root canal, an incision should be performed and/or antibiotics may be administered, and daily inspection is needed. In case of deterioration in the condition, institutionalised oral surgery care is needed.

In chronic apical abscess or suppurative apical periodontitis a fistula develops more frequently after the occurrence of chronic apical periodontitis, which has formed an abscess. There is pressure and pain until the inflammation product, the pus, breaks to the surface (Figure 4), and leaves through the fistula. When the fistula can be localised by inserting a gutta percha point before taking an X-ray, and the problematic tooth can be identified. The evidence of a successful root canal treatment is that the fistula is closed.

Chronic apical abscess of the 21 tooth

Periodontal diseases (Péter Vályi DMD - László Párkányi DMD)

Aetiology of periodontal diseases

Periodontal diseases are mainly inflammatory diseases. If only the gums are affected, it can be reversible, but if it proceeds to the supporting structures, the process becomes irreversible (in part). The aetiology is diverse, but the main reason of cause is bacterial infection. The following figure (Fig. 2.44.)summarizes aetiological factors of periodontitis:

Ethiopathogenesis of periodontal diseases (Modified from Wolf HF.)

As far as we know today, excessive tissue destruction is not the direct effect of bacteria, but the destructive effect of proteolytic enzymes released as a course of immune reaction. Different alterations in the immune system can be spotted either in defects of the neutrophil defence line, which is reversible, or by infection related, excessively released inflammatory cytokines induced over reaction processes. Both situations result in tissue destruction and pocket forming, which provides favourable circumstances for sub-gingival Gram negative anaerobic bacteria. These lead to further progression, which was well demonstrated by the Offenbacher (1996) model on the pathogenesis of periodontitis:

Pathogenesis of periodontitis (modified from Offenbacher 1996)

The processes above are modified by genetic and non-genetic factors as well, as we described earlier. The complex process is demonstrated in the image below:

Current model of periodontal disease (modified from Page and Kornman 1996)

In the following, we will examine the role of each factor in the process.

Direct damaging effect of bacteria

Destructive processes of bacteria are the result of the release of proteolytic enzymes and harmful metabolic products. Damage affects the tissues (connective tissue fibres, fibrin, fibronectin), the components of the immune system (immunoglobulins, complement system), and structural proteins of soft tissues. Endotoxins of Gram-negative bacteria disturb blood clotting, damages the bone and complement system.

Indirect damaging mechanisms of bacteria

Bacterial toxins can force cells to produce cytokines directly. However, their endotoxins (lipo-poli-sacharides - LPS), and cell wall antigens (gingipain, fimbrillin, or stress proteins) can initiate pronounced immune reactions. Proteolytic enzymes released by PMN cells cause tissue destruction. This is followed by epithelial in-growth and granulation tissue forming, which is rich in plasma cells at the destructed area. Plasma cells continuously release inflammatory cytokines, which leads to further destruction. Enzyme release of PMN cells can be inhibited by alpha-2-macroglobuline and alpha-1-antitripsine, but a bacterial antigen of Porphyromonas gingivalis called gingipain can even destroy enzyme inhibitor proteins.

Role of cytokines in periodontal destruction

Cytokines are small molecule weight glycoproteins. Their role is information flow among cells, immune response, cell differentiation, and regulation of growth. A mediator released by a specific cell can affect neighbouring cells (paracrine) or even itself (autocrine). Cytokines can be either proinflammatory, anabolic cytokines or growth factors. The same cell is capable to produce both, depending on the triggering effect. Specific receptors are responsible for their effect.

Inflammatory cytokines express adhesion molecules, which help PMN cells migrate towards the inflammation, and fixate macrophages and lymphocytes in the connective tissue matrix. Their role is to initiate the immune response. They also play a major role in connective tissue and bone catabolism. Bone resorption is activated directly and indirectly: PGE2 production, macrophage transformation into osteoclasts, stimulating collagenase MMP enzyme production. They also inhibit new bone formation. Further cellular effects are the stimulation of T-cell and macrophage response, increasing the number of circulating PMN cells, promoting their chemotaxis, and stimulating MMP production.

Anabolic (anti-inflammatory) cytokines basically unite innate and adaptive immune subsystems by modulating T-helper cells. They reduce macrophage activity, and their production of cytokines. Anabolic cytokines also block phagocytosis and intracellular destructive processes, and antigen presentation. Through T-helper cells, they can inhibit inflammatory cytokine production, cytotoxic T-cells, and chemotactic function of the rest of T-helper cells. However, they promote activated B-cell growth and differentiation.

Growth factors play a role in the healing processes, attract differentiating cells (fibroblasts, mesenchymal cells, osteoprogenitor cells), promote differentiation, increase collagen, glucose-amino-glycane and other growth factors production and secretion. If these reparative procedures overweigh destructive procedures, regeneration (tissues as original) or reparation (tissues replacing original) takes place.

Products of the arachidonic acid cascade

As a result of insults damaging the membrane, phospholipids of the membrane are transformed into arachidonic acid by phospholiase-A2 enzyme. This metabolises further into leukotrienes (lipoxigenase), prostaglandines and tromboxanes (cyclooxigenase/COX). Enzyme COX-1, is responsible for protective measures (protection of mucosa, blood clotting). The other COX enzyme (COX-2) is responsible for pain sensation by releasing prostaglandins, and for fever, by affecting the heat control centre of the hypothalamus.

Prostaglandins induce oedema by vasodilatation, potentiate the effects of cytokines, stimulate MMP production, cause bone resorption in a direct and indirect way, and reduce the production of antibodies. Patientsh a hyper-reactive monocyte genotype are prone to extensive prostaglandin release, even under low bacterial insult.

Role of cellular elements

The main role of PMN cells is to eliminate opsonized material by phagocytosis. In order to achieve this, it has to react adequately to chemotactic stimuli, move through blood vessels, exit the blood stream, and destroy the opsonized foreign material by phagocytosis at the location of immune response. Any functional disorder can lead to severe periodontal destruction. Hyper-reactive PMN genotype comes with increased release of proteolytic enzymes, which ends up in severe tissue destruction.

More types of macrophages take part in the defence mechanisms of the periodontium. Some examples are the myeloid originated Langerhans-cells, and lymphoid originated natural killer (NK) cells. They play an important role in adaptive immune response. They use phagocytosis and proteolytic enzymes for antigen elimination. Besides bacteria, they eliminate decomposed cells, too. They bind to immunoglobulins and complement proteins with surface receptors. They also produce inflammatory anabolic cytokines, prostaglandins, and leukotrienes.

Periodontal bone loss

A continuous remodelling takes place in bones: building and resorption are in balance. This makes it adaptive to altering loading forces (occlusial, orthodontic forces). The main cells in this process are osteoblasts and osteoclasts. Activated osteoclasts induce reapportion, which stimulates osteoblasts to rebuild bone. Systemic (Vitamin-D, parathormone), and local hormonal factors modify these processes. In a paradox way, osteoblasts are also responsible for bone resorption by producing RANKL (receptor activator ligand), which activate osteoclasts. This process is inhibited by osteoprotegerin (binding to RANK receptor, taking the place of RANKL), which synthesises in both osteoblasts and gingival fibroblasts. The RANKL-OPG connection is regulated indirectly through cytokines. This determines whether resorptive processes dominate, or there is a stable balance. Inflammatory cytokines promote RANKL production.

Several locally produced paracrine growth factors influence bone formation, matrix formation, and mineralising procedures. These factors are PDGF, IGF, TGF-beta, FGF, BMP, and EMD.

RISK FACTORS IN THE AETIOLOGY OF PERIODONTITIS

Role of plaque microorganisms in periodontal diseases

In Chapter 2.12., the role of plaque bacteria has been mentioned in the aetiopathogenesis of periodontal diseases. From oral cultivated bacteria, 12 species have shown connection with periodontal diseases. Bacteria are considered to be periodonto-pathogenic, if they fulfil the Koch-postulates modified by Socransky:

Connection – has a greater probability of existence in periodontal patients

Eliminating – eliminating the bacteria causes remission

Host response – provokes immune response, serum and salivary antibodies are increased in number

Virulence factor – production and facilitation of enzyme production, which make changes in the function of immune system elements

Animal study model – proven disease inducing effect, bacteria can be found in case of experimentally induced destruction.

The figure below describes periodonto-pathogenic bacteria and their relationship with aetiopathogenesis of periodontitis (Fig. 2.47.):

Causal relation between an infectious agents and disease (modified from Wolf HE)

Besides the mentioned Streptococcus milleri can be found in a greater amount during the progression of the disease. Pink coded ones resemble close relationship, while yellow code stands for a more distant relationship with the disease.

Another group of bacteria can also influence periodontal diseases. These bacteria are not part of the natural oral flora and sub-gingival plaque (enteric bacteria, staphylococcus), but can be the initiators or contributors of periodontal diseases. They can be found in those who did not receive or did not react well to treatment (Klebsiella pneumoniae, Klebsiella oxytoca, Enterobacter agglomerans, and staphylococci).

We are deliberately speaking about microorganisms as the causes of disease. Recently viruses have been found to influence periodontitis. Viruses (Herpes simplex, Epstein-Barr, Human Cytomegalovirus and Papilloma virus) can alter the host response to sub-gingival plaque bacteria. They can be found more frequently in the periodontally compromised than in healthy patients.

The elements of sub-gingival flora are not randomly distributed, they are well organised spatially. Socransky and co-workers examined more than 13000 plaque samples to determine the spatial orientation of bacteria in the sub-gingival plaque. They were divided into colour coded groups named complexes.

Microbial complexes in subgingival plaque (Socransky 1992)

Members of the blue, yellow, green, and purple complex are called early colonising bacteria. Gram-negative bacteria of the orange and red complex can bind to them.

Pathogenic effect of bacteria is influenced by the effectiveness of oral hygiene, plaque retentive factors, smoking, hormonal changes, and diet.

Genetic factors

Monogenicly transmitted, autosomal dominant and recessive illnesses, which come with PMN function disorder, or collagen metabolism disturbances, can be the cause of rapidly progressing, severely destructive periodontitis.

In case of aggressive periodontitis, no systemic background can be revealed, and the family history is positive for the disease. Genetic polymorphism is a common sequential alteration in the genome structure. It can be the result of the transition of a base or insertion, deletion. Periodontitis is a multifactoral disease; therefore, several genes play a role in its development, both environmental and behavioural factors. These gene alterations are not always manifested, only a connection between the disease and the gene alteration can be discovered. Cytokines (IL-1, IL-6, TNF), HLA-antigens, Fc-receptors and structural protein coding genes can be made responsible for the altered immune reactions. Genetics can explain the differences in likeliness of periodontal diseases among the various races.

Hormonal factors, smoking, systemic diseases influencing periodontitis have been discussed in Chapter 5.13.

Other risk factors

The beginning of this chapter, the immune status of the body has already been discussed. In case of occlusal overloading, it has to be mentioned that it cannot cause attachment loss by itself, but it can change the resistance to plaque in the periodontium, and increase in damage and tissue destruction of the inflammatory process.

Regarding nutrition, some nutrition deficiencies can only influence plaque induced illnesses: protein, Vitamin-D, calcium, Vitamin-C withdrawal can be mentioned as risk factors.

Psychological conditions: Indirectly, depression can cause negligence of oral hygiene, and antidepressant drugs can induce mouth dryness. Cytokines isolated from the saliva proved the influencing effect of negative stress in the pathogenesis of periodontitis.

In poor social status population, several risk factors are combined (environmental and behavioural), therefore being influencing factors of periodontal diseases. Low degree of education comes usually with poor oral hygiene; however, high degree education does not necessarily come with appropriate oral care.

Classification of periodontal diseases

Until the 1920s, periodontal diseases were classified by clinical signs and symptoms. Later, till 1977, the classification was based on classical pathological point of view. In this aspect, periodontal diseases were classified as inflammatory diseases (gingivitis, periodontitis), degenerative processes with severe hard tissue loss (parodontosis), atrophy, hypertrophy, and periodontal trauma.

The rationale behind modern classification is the aetiopathogenesis of the disease. Miller, W.D. suspected irritating factors, host predisposition, and mixed infection in the background of periodontal diseases, but his theory was not approved at his time, in 1880. In the mid-1960s, a study on experimental gingivitis (Löe, H., Theilade, E., and Jensen, S.B), in the mid-1970s the infection-host response principle, and the discovery of leukocyte dysfunction (Page, R.C., Schroeder, H.E) led to the classification of our days. Classification today considers the role of immune status, immune responses, and even behavioural factors linked to the disease. Classification in the 1980s recognized the following groups of diseases:

Classification of periodontal diseases in the 1980's years

These classifications did not cover all pathological conditions, but the main issue was the classification of periodontitis. On the one hand, classification according to the patient’s age is not very fortunate because both typical cases of periodontitis can develop in any age, even if most cases are covered by the above mentioned criteria. On the other hand, it is hard to determine the development of the disease because many patients only come in contact with the specialist years after developing the disease.

The latest classification from 1999 tried to fix the problems mentioned above and classified diseases as follows:

  • restricted to gums or affecting periodontal apparatus

  • relationship with plaque or not

  • separate groups:

    1. abscesses

    2. endodontic lesions

    3. developmental and acquired diseases

  • can local factors give an explanation for it?

    1. chemical, physical, thermal insults

    2. occlusal trauma

    3. developmental or acquired defects, conditions

    4. endodontic lesions

    5. allergic factors

  • in relationship with systemic factors?

    1. endocrine factors internal diseases (endocrine, haematological)

    2. dermal and mucosal deformities

    3. genetic factors, syndromes

    4. infectious diseases by specific germs

New classification, 8 classes:

Main groups of classification of periodontal diseases, AAP 1999

Diseases of the gums, further classified:

Diseases of gingiva

This is followed by the two main types of periodontitis: chronic and aggressive forms. Periodontitis with systemic background also stands for several diseases:

Periodontitis as a manifestation of systemic diseases

The fifth group involves acute diseases. These are acute necrotising ulcerative gingivitis, or if the bone is affected, acute necrotising ulcerative periodontitis. Abscesses of the periodontium are gingival abscess, periodontal abscess and pericoronal abscess. The seventh main group contains endo-periodontal lesions. The last group also covers several deformities:

Developmental and acquired periodontal lesions

Though the classification above has received many critiques from its first moments, it can be stated that it is evidence based. It means that every disease has been classified based on the aetiology of the disease, which can be a great help in the treatment plan provided the correct diagnosis has been established.

Diseases of the gingiva

Gingival diseases can be divided into two groups based on plaque being an aetiological factor or not. Plaque induced gingival diseases can be further divided, based on plaque being the only reason of diseases, or other factors (systemic diseases, medications, malnutrition) contributing to that.

SOLELY PLAQUE INDUCED GINGIVAL DISEASES

Gingivitis caused by plaque accumulation. There is a correlation between the aetiological factor and the clinical appearance. Symptoms are swollen gingival margins, reddish/purplish discolouration, bleeding (in the beginning to mechanical irritation, in severe cases spontaneously). Changes start at the papilla and proceed to the gingival margin. The orange skin texture of the attached gingiva can be still present. If the inflammation persists, papillae become rounded, the gingival margin and papillae can get fibrotic, pseudopockets can develop. The bacterial flora changes, but no specific strain grows its proportion.

Plaque induced gingivitis - result in gingival enlargement

Gingival inflammation cannot only attack intact periodontium. After periodontal attachment loss or recession, inflammation free soft tissues can get re-infected. This is called reduced periodontium gingivitis. It differs from the re-establishment of periodontitis by not resulting in further attachment loss.

In case of re-established oral hygiene, usually even fibrotic gingival margins can go through complete healing.

Reduced periodontium gingivits

Solely plaque induced gingivitis, combined with local irritative factors

In this case, local factors stimulate plaque formation, or inhibit adequate oral hygiene. Local factors can be natural or artificial. Artificial factors are restorations with improper marginal closure, micro-mechanical elements of removable partial dentures, or orthodontic appliances. Natural factors are tooth with malformations (enamel pearl, prolonged fissures) or malpositioned, crowded teeth.

A special condition is found in mouth breathers, which restricts to surfaces not covered by the lips while breathing, like incisor buccal surfaces.

Treatment in these situations is the same, with the difference of the need to eliminate local irritative factors.

Patient with gingivitis due to mouth breathing

Gingivitis due to mouth breathing - typical signs

GUM DISEASES WITH SYSTEMIC BACKGROUND

This group gathers gum diseases influenced by endocrine and haematological conditions. Most of the time, endocrine modifying factors restrict to sexual hormones and diabetes mellitus, but parathyroid and adrenal cortex hormones can also influence these diseases.

Plaque induced gingivitis modified by sexual hormones

The most common modifying factors are oestrogen and progesterone hormone level changes in women. These changes occur in puberty, during menstruation and pregnancy, and after menopause. It is important to emphasise that these changes do not develop gum diseases, they just amplify the symptoms.

Sexual hormones cannot only affect the mucosa of the uterus, but all other mucosa, including the oral mucosa. By increasing vascular permeability, the tendency for oedema and bleeding increases as well. Through biologic mediators, they can alter immune reactions, and secreting in the sulcular fluid, some specific periodonto-pathogen strains use them as growth factors, this way changing bacterial composition of the plaque. Aetiologic consequences of sexual hormones will be discussed in detail in Chapter 5.13.2.

Puberty gingivitis

During puberty, hormonal changes are dramatic. This explains gingival inflammation on the papillae, even in case of relatively good oral hygiene. The gingival margin can get oedematous, and the tendency for bleeding increases. The consistency of the gums is rather tender, due to accumulated fluids. After settlement of the menstruation cycle, symptoms moderate. Incidence is very high, close to 100%, according to some authors. By re-establishing proper oral hygiene, the inflammation goes through complete remission. Interdental cleaning is of great importance with the help of dental floss, or interdental brushes (Chapter 4.1).

Puberty gingivitis

Menstruation gingivitis

It is most commonly accompanied by the ovulation cycle. In more than 2/3 of women, sulcular fluid increases by 1/5 during ovulation. In rare cases, inflammatory symptoms come with the menstruation cycle, even under non-compromised oral hygiene.

Symptoms are not pronounced, rather restricted to increased tendency to bleed. The condition can be eliminated by good oral hygiene.

Pregnancy gingivitis

It was discovered in the late 1800s that during pregnancy, pre-existing minor gingivitis gets more and more severe till the end of the 8th month of gestation. The changes are periodical. In the first trimester, the changes of gonadotrope hormones, at the end of the third trimester, oestrogen and progesterone hormone changes facilitate the symptoms.

Vascular changes are even more pronounced than in other hormone influenced gingivitis. Therefore, gingival swelling is more severe, bleeding tendency is greater, discolouration of the gums leads to vivid reddish/purplish colour. Papillae can even have berry-like surface.

Symptoms become minor after delivery, but will still be present until the end of nursing. Complete remission can only be achieved by re-establishing appropriate oral hygiene, and eliminating all plaque retentive factors.

Pregnancy gingivitis

Vascular changes during pregnancy can get to a level, where localised, or even generalised tumour-like gingival growth can develop. This is called pregnancy granuloma, or pregnancy epulis. Other synonyms in the literature are pyogenic granuloma, granuloma gravidarum, epulis angimatosa, nodular gingival hyperplasia, lobular capillary hemangioma, etc. Surgical intervention during pregnancy is contraindicated due to the high recidivation. After delivery, it can heal even spontaneously, or after non-surgical therapy entirely.

Pregnancy epulis

Mucosal changes in menopause

With lowering oestrogen levels, the mucosa becomes thinner, layers of stratum basocellulare and stratum spinocellulare become atrophic. This causes subjective symptoms on the mucosa, sometimes on the gingiva, which are more pronounced. Clinical signs are burning sensation on the mucosa, dry mouth with tingling sensation, taste dysfunction. Symptoms react well to hormonal treatment.

Diabetes mellitus

Diabetes mellitus – especially in adults – can enhance symptoms of periodontitis. In type I diabetes mellitus, with an insufficient metabolic control, children can develop severe gingivitis, which cannot be explained by local irritative factors.

Haematological diseases manifesting on the gums

All cellular components of the blood are important to maintain gingival health. White blood cells are responsible for both specific and non-specific immune reactions. Red blood cells are responsible for oxygen supply of the tissues, and platelets are responsible for clotting. Most common and most severe diseases are related to leukocytes, but in myelo-proliferative diseases (leukaemia), generally all three types of blood cells become defected in production and function.

Leukaemia

As we mentioned before, in leukaemia besides leukocytes, erythrocytes and thrombocytes also suffer disturbances in production. This makes insufficiently oxygenised tissues more vulnerable to infections, which develops more easily due to deficient leukocytes, and tendency for bleeding also increases as a result of thrombocytopenia and coagulopathy.

Typical symptoms: gingival swelling, ulcerations (orally), severe bleeding, petechiae on the skin and mucosa. Symptoms resemble gingivitis ulcerosa.

For differential diagnosis, localisation and spreading of the ulceration, existence of an inflammatory margin can be helpful.

  1. Localisation of the ulceration: gingivitis ulcerosa affects the front teeth and wisdom teeth, ulcerations can be found on the buccal aspect. In leukaemia, ulcerations can be found at every tooth, more pronounced orally.

  2. Spreading of the ulcerations: Leukaemia related ulcerations spread into deeper layers, while gingivitis ulcerosa stays superficial in the tissues.

  3. In gingivitis ulcerosa, ulcerations are surrounded by an inflammatory margin, but in leukaemia, this margin cannot be found.

Chronic myeloid leukaemia (from Prof. I. Gorzó)

Chronic myeloid leukaemia with deep ulceration in the oral side (from Prof. I. Gorzó)

Agranulocytosis

Agranulocytosis is the complete disappearance of neutrophil granulocytes from the blood, while neutropenia is the reduced number of them. Aetiological factors can be the following:

  • •bone marrow diseases

    1. aplastic anaemia isolated leukocyte aplasia

    2. congenital - rare

    3. cyclical neutropenia

    4. medications (antibiotics, procainamide, phenytoin, chlorpromazine, methimazol, etc.)

    5. chronic benign

  • peripheral diseases

    1. hypersplenia

    2. sepsis - immune

    3. Felty syndrome

Diseases accompanied by decrease in leukocytes result in severe destructive periodontitis with large ulcerations not only on the gingiva, but on other areas of the mucosa, and even the tonsils.

Ulcers due to agranulocytosis

The rest of the haematological diseases can be found detailed in Chapter 5.13.13.

GUM DISEASES RELATED TO MEDICATIONS

Medications taken for systemic conditions/diseases, can modify gingival inflammation, or in most cases, cause gingival overgrowth. Many of the medications used today, can cause gingival overgrowth. The major uncommon aetiological factor though is dento-gingival plaque. Gingival growth begins with the papillae, but in extreme cases, can cover the whole tooth. The three most common medications causing gingival overgrowth are hydantoine, Cyclosporine A, and Calcium-channel blockers. Uncommon properties among these are immunosuppressive and Calcium-antagonist effects. There are differences in effect mechanisms, but all provoke gingival fibroblast activity, and prevent connective tissue break down (collagenase activity, phagocytosis).

Typical histological changes are present in hyperplasia. The ”rete peg”, the wave-like run of the oral epithelium becomes long and deep. Acanthosis can be observed in the epithelium. The amount of collagen increases, the run of fibres becomes irregular. Vascularisation increases, new vessels develop. The amount of fibroblasts increase as well, plasma cell, or lymphocyte infiltration is detectable. The relative amount of collagen type III increases, while type I decreases. Other, non-collagen protein proportions also increase. Proteoglycane, hexose-amine, glucose-amino-glycane amounts increase in the connective tissues. The amount of glucocorticotoid receptors and activity of certain cytokines (TGF-β, bFGF) increase. Collagenase activity decreases.

Hydantoin is no more used in epilepsy therapy, therefore, hydantoine induced hyperplasia is rarely observed. Cyclosporine was used following organ transplantations for immunosuppression to prevent organ rejection. It is also used to treat several autoimmune diseases (Crohn-disease, ulcerative colitis). Calcium-channel blockers are the most common drugs, which are used in anti-arrhythmia and anti-ischaemia therapy. In some rare instances, erythromycin (antibiotic) and bleomycin (cytostatic drug) can also lead to gum hyperplasia.

Clinical symptoms are typical: hard consistency, discoloured swollen gums ranging from pink to red colour. Connective tissue fibres, and matrix are both overproduced, and even the epithelium becomes thicker. Sometimes tissue growth is so advanced that only diathermical knife or high power lasers can remove the excess.

Gingival enlargement due to calcium-channel blocker medication

Post op. 6 weeks after gingivectomy by electrosurgery

Taking of contraceptive drugs (early generation, high hormone dose) can also cause gingival inflammation accompanied by hyperplasia. Symptoms are really similar to pregnancy gingivitis, since the hormone levels are relatively the same. When taking modern, low hormone dose pills, these side-effects are no longer present.

Contraceptive induced gingiva hyperplasia

MALNUTRITION RELATED GINGIVAL DISEASES

Nowadays, severe Vitamin-C malnutrition (scurvy) is rather historical. Malnutrition of Vitamin-C is not the direct cause of the disease, but the disturbance of collagen metabolism, which enlarges the symptoms of plaque related gingivitis. No other vitamin malnutrition results in periodontal symptoms, because these diseases are not present today. Vitamin-B malnutrition can cause typical mucosal and skin lesions (see Chapter 2.6). Malnutrition of folic acid is related to systemic diseases with gingival symptoms. Protein malnutrition can only lead to ulcerative gingival lesions in developing countries.

NON-PLAQUE RELATED GINGIVAL DISEASES

These diseases have no relationship with dento-gingival plaque, they can develop irrespective of the oral hygiene level.

Gingival diseases of specific origin

Bacteria, as well as viruses and fungi can lead to specific infections on the gums and oral mucosa.

Specific bacterial infections are caused by neisseria gonorrhoea, which resembles the clinical appearance of gingivitis ulcerosa. The TB ulceration (caused by Mycobacterium tuberculosis) has an irregular shape, is not painful, has a red surface, and is covered by a greyish-yellowish membrane. The symptom of syphilis (Treponema pallidum) is a regular, round shaped, painless lesion with a hardened base.

Most common specific viral infections are primary and secondary gingivostomatitis herpetica. The disease is discussed in details with acute periodontal diseases. Varicella zoster infection appears more infrequently. Symptoms of primary infection resemble gingivostomatitis herpetica. In secondary infection, reactivating viruses released from the ganglions induce one sided vesicular lesions on the gums and mucosa with a neuralgiform pain. Tearing and joining of the vesicles end up in painful, ulcerative lesions.

Candida albicans related diseases were mentioned in Chapter 2.6. Manifestation in gingival lesions only occurs in severe immunodeficient conditions, like AIDS. Xerostomia, smoking, steroid treatment, antibiotic therapy, chemotherapy, and radiotherapy can facilitate pseudo-membranous fungal infections.

GUM DISEASES WITH GENETIC BACKGROUND

Hereditary fibromatosis gingivae is an autosomal dominant hereditary deficiency, which manifests in regular overgrowth of the papillae, and marginal gingiva. Its localised form is called tuberal fibrosis.

Hereditary fibromatosis gingivae

GINGIVAL DISEASES RELATED TO SYSTEMIC CONDITIONS

These conditions gather mucosal diseases, which affect the gingiva causing desquamative gingivitis. Diseases together called desquamative gingivitis are characterised by bullous formation, erosions, atrophical spots, which in severe cases, peel off the underlying connective tissue, leaving a greyish-bluish unepithelialised area behind. They create major subjective complaints, especially in connection with irritative food and drink consumption (spicy foods, carbonated drinks, acidic foods, etc). This is the oral manifestation of Pemphigus vulgaris, Pemphigoid, Lichen planus, Erythema multiforme, Lupus erythematosus.

Erosive (desquamatic) lesions on the gingiva

TRAUMATIC LESIONS, FOREIGN BODY REACTIONS

Gingival trauma can be caused by chemical irritation (iatrogenic: chemicals, medications, bleaching agents, acids, bases applied in dental treatment), mechanical irritation (improper oral hygiene, food particles), and thermal irritation (hot foods, drinks, dental instruments).

Foreign body reactions can be caused by dental materials, like piece of amalgam, or metal crown margin, etc.

OTHER, NON-PLAQUE RELATED GINGIVITIS

These are mainly tumours of the gingiva, and heavy metal intoxication related gingival lesions (bismuth, lead, mercury)

Melanosis gingivae is a physiological dark spot on the gingiva in some dark ethnical groups, which are the result of high amount of melanocytes in the gingiva. A demonstrative image can be found in Chapter 1.6.

DIFFERENCIAL DIAGNOSIS OF GINGIVAL OVERGROWTH

Gingival overgrowth can be due to inflammation related to oedematous swelling, or hyperplasia caused by overproduction of connective tissue fibres and matrix, together with thickening of the epithelium. In chronic infections, besides oedema, connective tissue producing processes can also affect the gingiva.

Gingival overgrowth

  1. infection related

  2. medication related (Ca-antagonist, hydantoine, Cyclosporine-A, Erythromycin, Bleomycin)

  3. modified by systemic conditions (pregnancy, puberty, Vitamin-C malnutrition plasma cell infiltration, non-specific pyogenic granuloma)

  4. provoked by systemic conditions (leukaemia, granulomatosus diseases, sarcoidosis)

  5. tumours (malignant, benign)

  6. hereditary fibromatosis gingivae

  7. idiopathic

Acute periodontal diseases

Acute periodontal diseases are usually accompanied by pain, which brings many, previously untreated patients to the dental practice. The most common acute diseases of the periodontal structures are the following:

NECROTIZING PERIODONTAL DISEASES

Acute necrotising ulcerative gingivitis (ANUG)

During the world wars, it was an endemic disease, also called „trench disease”. This was the first disease linking a specific pathogen to a periodontal disease. Fortunately today, the prevalence of this disease is really low, due to disposing factors being less and less common.

Disposing factors are categorised as local and systemic ones. Systemic factors are the sympato-mimetic effect of nicotine in smokers, stress, seasonality: the disease had higher occurrence in autumn and winter due to nutritional factors. It is most common among young adults with poor general health (e.g. HIV), or on the ground of malnutrition. Local predisposing factors are poor oral hygiene and the presence of plaque retentive factors. The plaque is dominated by Fusobacterium species. Tar present in cigarettes also facilitates the development of the disease.

The onset of symptoms is typically sudden. It comes with severe pain, necrosis of the papillae: blunt papillae besides the incisors and wisdom teeth, which are covered with a greyish pseudo-membrane. Necrotic ulcerations are present beside them. Ulcerations are typically present on the labial side. Bad breath is also a typical characteristic of the disease. Bleeding starts on mechanical irritation, in later stages even spontaneously. Systemic symptoms are rare, sub-febrility can occur in rare cases. More severe cases involve swelling of the regional lymph nodes.

Necrotizing gingivitis

In adverse cases, contact ulcerations may be present on the pharyngeal mucosa, tongue, lips (Vincent angina), and in the most severe cases, on the buccal tissues, which can lead to perforations (cancrum oris or noma). In severe cases, systemic symptoms can develop. The disease may involve the attached gingiva and alveolar bone (Acute Necrotizing Ulcerative Periodontitis).

It is important to differentiate it from leukaemic ulcerations: this can be done by determining the spreading, location of the ulcerations, and whether the inflammatory margin is present or not (see also Chapter 2.19.!). The differential diagnosis distinguishes the disease from gingival carcinoma and gingivostomatitis herpetica.

GINGIVAL DISEASES OF SPECIFIC ORIGIN

Herpetic gingivostomatitis

It is a form of gingival inflammation caused by specific pathogens. This is Herpes Simplex virus 1. Primarily it develops in 2–6 year old infants. From 10,000 acute diseases, 1.6 cases are identified as this disease. It is foregone by a prodromal phase: 1 week before the development of the actual disease, an upper-respiratory catarrhal disease precedes it. In parallel with oral symptoms, systemic symptoms develop: weakness, high fever, and painfully swollen lymph nodes. Small coloured blisters develop in the oral cavity with reddish surrounding, which are soaked within 24 hours. By the time patients visit their doctor, round ulcerations are present, covered by yellowish-whitish fibrin pseudo-membrane. The marginal gingiva is scalloped. The ulcerations can later converge. It is accompanied by bad breath.

Herpetic gingivostomatitis

Typical signs of herpetic lesions on marginal gingiva: scalloped formation

Healing is spontaneous in 10–14 days. Immunity does not develop against is, the viruses survive in ganglia, and can be reactivated by external or internal changes. Secondary disease develops in young adults, and the symptoms are similar to that of the primary disease. Later on, labial herpes is more likely to develop.

It has to be differentiated from ANUG and aphtha (more likely on the mucosa), herpes zoster (typically unilateral), perhaps erythema exudativa multiform, based on the typical symptoms.

Coccal gingivitis

It is also caused by specific pathogens, but instead of viruses, Streptococcus bacteria are the triggers. It is most likely to develop in immunocompromised patients with poor oral health, typically on the ground of chronic periodontitis.

Besides systemic symptoms (sub-febriltiy, fever, swelling of regional lymph nodes), it is likely to be accompanied by reddish swollen gingiva with ulcerations on the papillae and marginal gingiva. Pus forms in the pockets, which can be drained by pressure. The teeth and gums are tender and painful.

PERIODONTAL ABSCESSES

Based on the classification by AAP in 1990, they form a separate group. They are divided into three main categories: gingival, periodontal, and pericoronal abscesses. The most common form of these is the periodontal abscess, which needs to be distinguished from similar diseases (periapical abscess, infected ateral cyst), to have the opportunity to provide the adequate therapy.

Gingival abscess

It develops typically on attached the gingiva due to mechanical trauma (e.g. food remnant, oral hygiene instrument, or braces). After 1–2 days of reddish shiny deformity, spontaneous melding occurs. Pus develops on the border between the connective tissue and the epithelium, or within the connective tissue. Fluctuation can be observed. It opens without treatment spontaneously.

Periodontal abscess

It is the third most common acute periodontal disease (8–14% of all cases). Its significance is shown by the fact that it is present in 60% of untreated periodontal patients. Many patients first get in contact with the specialist because of this disease. Periodontal abscess is the purulent inflammation of the periodontal connective tissue. Pathogens need to infiltrate the connective tissue of the periodontium directly or indirectly. This happens if inflammatory products cannot be drained from the pocket: either the virulence of bacteria increases the amount of inflammatory infiltrates under open orifice pockets, or obstruction of the pocket occurs, possibly related to treatment (post-therapy abscess).

Based on the aetiology, we distinguish between periodontal infection related and non-related abscesses. The latter can be caused by a foreign body (food remnant, oral hygiene instrument, or dental material) incorporation into the gingival sulcus, or anatomical or pathological (resorption, perforation, or fracture) alteration of the root. In connection with periodontal infection: chronic infection exacerbation or post-treatment forms (after scaling, antibiotic therapy, or as a result of surgery) may develop.

Thorough history and clinical examination is required to set up a diagnosis. There is no sign on radiograms, only general signs of a periodontal infection can be visualised. A radiogram with a Guttapercha point leading into the fistula can help us in the differential diagnosis.

The nature of the pain is an important feature of the history, as well as the presence of facial swelling, and information regarding aetiology (previous treatments, incorporation of food remnant, etc.).

The first steps of clinical examination are localisation of the swelling, probing of the tooth, palpation of the tooth, evaluation of sensibility and occlusal discrepancies. Based on the above mentioned symptoms, a periodontal abscess may result in:

  • dull pain

  • lateral palpation tenderness

  • swelling of marginal gingiva, reddish, shiny gingiva above

  • no face deformity in most cases

  • pocket on probing, pus formation

  • teeth are generally intact, sensible

  • teeth often become supra-occlusal, resulting in early contacts

  • no radiological sign (besides general periodontal infection)

  • systemic symptoms are unusual

Periodontal abscess

As differential diagnosis, pulpal originated subperiostal abscess is relevant. This comes with vertical palpation tenderness, sharp pain, and often facial deformity. The tooth is not vital. The crown is usually severely decayed or restored in some way. Systemic symptoms can be pronounced (sub-febrility and swollen lymph nodes). The swelling is localised to the root apex, there is no pocket on probing, or if it drains through the pocket, the base is always wider than the orifice. This is the sign of primary endodontal origin endo-periodontal lesions. The radiogram shows signs of a periapical infection.

Periapical abscess - fistula with opening

A lateral periodontal cyst can also show the signs of a periodontal abscess. In case of infection, there is shiny, reddish swelling besides the root, and a fistula may often develop. This disease has its typical radiographic appearance: sharp edged, radiolucent picture, wide periodontal space around the root.

Lateral periodontal cyst

Pericoronal abscess

It develops around partially erupted wisdom teeth, infiltrating the coronal part of the covering gingiva, on the ground of pericoronitis. It comes with pain, swelling of the gums, partial trismus, an it is often accompanied by systemic symptoms (fever and swelling of the regional lymph nodes). The real danger is that the inflammation can spread to the neighbouring connective tissue spaces (spatium), which can lead to even life-threatening conditions.

Periodontal diseases (Vályi P.)

The irreversible, destructive inflammatory disease of the structures supporting the teeth is called periodontitis. The obligatory symptoms are inflammation and destruction of the supporting tissues, which leads to attachment loss and pocket formation. Periodontal diseases also have secondary symptoms, which are not present at every stage of the disease. Such symptoms are: pathologic mobility, furcation involvement, abscess formation, bad breath, changes in position and angle, hypereruption, pus formation, gingival recession, masticatory dysfunction.

CLASSIFICATION OF PERIODONTAL DISEASES

Before the introduction of the classification described in chapter 2.15.2., periodontal diseases were classified according to the age of disease development. Early onset periodontitis is considered to be fast progressing, while adult periodontitis (starting around the age of 35-40), is considered to be of slow progression. The drawback of the classification is that early onset periodontitis can also be of slow progression with its typical appearance, and adult periodontitis may progress fast with its typical clinical appearance. On the other hand, determining the time of disease development is difficult or sometimes impossible even with a precise history.

According to the classification approved by AAP, chronic and aggressive periodontitis are separate disease entities, just like the periodontal manifestation of systemic diseases. Acute ulcerative gingivitis is also classified separately. It can progress to acute ulcerative periodontitis and spread to the supporting structures. If periodontal lesions develop together with endodontic lesions, they are classified as endo-periodontal lesions.

Identifying different forms of periodontitis is not pointless; however, the outcome of the disease is quite similar: destruction of periodontal supporting tissues. When setting up a diagnosis, it is important to identify the aetiological factors which influence therapeutic methods, as well as the genetic and environmental factors which determine the prognosis.

Chronic periodontitis (ChP)

Chronic periodontitis (earlier known as adult periodontitis) is most common among middle aged and elderly people, but it can develop at any age. Typical clinical symptoms are shown in the next image:

Typical symptoms of chronic periodontitis

During the evaluation of periodontal parameters and clinical symptoms, it can be stated that aetiological factors (plaque, calculus, plaque retentive factors, smoking, stress, systemic factors) are directly proportional to the severity of the disease. A mixed subgingival flora, which varies from tooth to tooth, surface to surface is typical. Subgingival calculus is present in all cases.

Patient with chronic periodontitis

Radiological signs of chronic periodontitis

Progression is typically slow. While Socransky believed in alternating active and passive stages, others consider it as a continuous destructive process. Recent publications have led to a consensus among researchers: the constant destructive process is interrupted by stages of fast progression and severe destruction. Among patients undergoing treatment, untreated or poorly treated areas (individual or professional oral hygiene) are at risk of further attachment loss.

Classification can also be based on severity or location. Mild (1-2 mm), moderate (3-4 mm) and severe (5‹ mm) forms are distinguished based on attachment loss. Localised forms are confined to 30% of the dentition at most. If affected tooth surface exceeds 30%, the disease is generalized.

Chronic periodontitis has a high prevalence in developing and developed countries as well. The prevalence of the moderate form (WHO standards, large study sample) among 35-44 year-old patients is 42% (Denmark), 61% (Finland) and 73.6 % (Canada). Some countries have extreme low1.5-21.4 %- (India, France) or extreme high 91% (Chile) prevalence. The severe form is present in 5-21% of the same age group. Prevalence is higher in high-risk groups (smokers, Afro-Americans, Hispanic population, low social status and education) and elderly people.

Chronic periodontitis is more likely to develop in people with one or more risk factors present: persistent gingivitis (due to poor oral hygiene, constant “bacterial load” of periodonto-pathogenic strains), elderly age, smoking, systemic diseases (diabetes mellitus, PMN disorders, leukaemia, medications associated with gum hyperplasia), stress. Although there is no sound evidence for genetic background, some twin studies support that genetic factors play a role in half of the cases. Research on gene polymorphism suggests that in the chronic form of the disease IL-1 polymorphism (forced cytokine production) is an aetiological factor: patients with IL-1 beta polymorphism are very likely to develop the disease.

Aggressive periodontitis (AgP)

Aggressive periodontitis usually develops at a young age, it is typically present in the family history and has a fast progression. Lang et al defined primary and secondary characteristics, which can be found in the figure below:

Characteristics of aggressive form of periodontitis

Aggressive periodontitis is a term including Local Juvenile Periodontitis and General Juvenile Periodontitis, also known as Early Onset Periodontitis (EOP).

It is important to rule out the presence of systemic diseases, because periodontitis as a symptom of certain systemic diseases can lead to similarly fast-progressing, destructive periodontal diseases by compromising the immune system. Typical features are fast progression and vertical bone resorption starting proximally, resulting in intra-osseal periodontal pockets. Due to the fast progression and destructive manner, secondary symptoms (hypermobility, pocket formation, abscess formation, changes in position and angulation, hypereruption) develop quickly. After thorough questioning, the presence of the disease in the family is often revealed.

Secondary signs of AgP: tipping, movement, diasthema forming between central incisors, deep bite

The aggressive form is a heterogenic disease, which can be divided into localised and generalised forms. The generalised disease itself has a variable manifestation. Characteristic features of the two forms are shown in the following image:

Characteristics of forms of AgP

Patient with AgP

Radiological signs of AgP

Aggressive periodontitis affects about 1-5% of the population. Tinoco and Albandar published an article on racial distribution in 2002:

  • Caucasian:0.1-0.2%

  • African, African-American:1.0-3.0%

  • Hispanic, South-American:0.5-1.0%

  • Asian:0.4-1.0%

The prevalence of the localised form in puberty and youth age is 0.1-0.2% among Caucasian people and 2.6% in the African-American population. Screening is important and increasingly easy to perform as a result of more widespread orthodontic treatment and x-ray facilities. The distance between the CEJ and the marginal bone is considered pathological if it exceeds 2 mm. The following results were published based on these measurements:

  • Deciduous teeth showed destruction on one or more surfaces in 2% at the age of 7, in 3.1% at the age of 8 and in 4.5% at the age of 9 (Sjödin, 1994)

  • In retrospective studies patients with Juvenile Periodontitis who had more than 2 teeth affected, had detectable radiographic resorption in 52% of the cases already around deciduous teeth. This percentage was 20% in patients who had destruction around one tooth only, and 5% in the control group, who had no radiographic bone loss around permanent teeth (Sjödin 1993)

  • Patients with Juvenile Periodontitis had bony defects around deciduous teeth in 71.4% of the cases and in 85.7% of the cases in mixed dentition according to a retrospective analysis. (Cogen, 1992)

The simple analysis described above can help identify patients at high risk for periodontal infections. This way an individualised oral hygiene program can prevent or at least postpone the development of destructive diseases in these patients.

Radiological signs of localized form of AgP

Specific bacterial flora plays a major role in the destructive, fast–progressing, aggressive form of periodontitis. Host responses are generally compromised, mostly due to genetic abnormalities. Bacteria produce virulence factors and they also have special properties: leukotoxins damage PMN cells and macrophages of the immune system, the production of endotoxins stimulates the production of catabolic cytokines, bacteriocins prevent the growth of normal bacterial flora, immunosuppressive factors inhibit the production of IgG and IgM, collagenase production damages connective tissue fibres and inhibits the chemotactic migration of neutrophils preventing them from reaching the defence line.

Changes in host immune response (local, systemic) play a major role in the development of destructive diseases. A certain degree of PMN function disorder is noticeable, which prevents them from migrating and performing antibacterial functions, but it only manifests in periodontal diseases, not in any other disease. A similar dysfunction is lower mixed lymphocyte response with increased B-cell response, increased pro-inflammatory cytokine production of PMN-s and macrophages. While systemic antibody response is pronounced in the localised form, antibody levels in the blood are relatively low in generalised aggressive periodontitis.

Periodontitis as a manifestation of systemic diseases

Several (rare) systemic diseases show symptoms similar to aggressive periodontitis. These are mostly parts of syndromes. The table below gives a list of these diseases:

Periodontitis as a manifestation of systemic diseases

The necrotising form was mentioned in the previous chapter, the form linked to endodontic disease will be mentioned in the following chapter.

Non-bacterial lesions of the periodontal tissues and peri-implant lesions (Vályi P.)

PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS

Aetiology

Since periodontal tissues are connected to the pulpal tissues through the apical foramen, a pulpal disease can influence the periodontium and vice versa: periodontal diseases can affect the health of the pulp. Endo-periodontal lesions can develop in different ways. Lateral root canals, which can be found in the apical and middle third of the root, are on average 4-250 micrometres in diameter. Most of the time they have capillaries inside them. Through these, periodontal vessels can carry nutrients into the pulp chamber. Pulpal and periodontal processes can communicate through these connections. The other form of connection is the dentine tubules. Excessive root planing is not proven to cause pulp necrosis, but it is a possibility. Iatrogenic harm is much more common: when a false way is created during root canal treatment, it enables irrigating solutions to pass through to the periodontal space, thus creating an infection. Root fracture can be another cause of problems. Root perforation can also occur as a result of internal resorption. Trauma can disrupt the neurovascular connection of the pulp chamber, which can also lead to endo-periodontal lesions, sometimes even without infection.

Inflammation of the vital pulp does not result in periodontal lesions. Most bacteria causing pulpal infections are also periodontal pathogenic bacteria, although the bacterial composition of the necrotic pulp is much less complex than that of periodontal pockets. Necrotic pulp is a good substrate for these Gram negative bacteria.

From the pulp chamber there are two ways for the infection to proceed to the periodontal space: the apical foramen and the lateral root canals. In most cases, it is diagnosed as periapical periodontitis and damages the periodontal tissues around the apex. Infections exiting lateral root canals lead to lateral periodontitis. Infections exiting at the furcation level imitate the clinical picture of true furcation lesions.

There are three ways in which the infection can proceed: through the periodontal space and bone, under the periosteum reaching the marginal periodontium and passing through both the bone and the periosteum (and mucosa) into the vestibule through a fistula.

The degree of damage depends on the amount of bacteria, their virulence factor and host defense system. Inflammation can go two ways, depending on host defense reactions. Acute periapical inflammation (purulent, serous) will develop, if host defense is insufficient. If the immune system functions properly, granulation tissue containing inflammatory cells can embed the inflammation, which can be present asymptomatically for years. If the inflamed area is surrounded by a fibrocellular connective tissue cover, bacteria from the pulp chamber rarely get to the surrounding tissues.

When acute inflammation is present, the excessive amount of inflammatory products spreads fast. When reaching the periodontal pocket, it is hard to differentiate from a periodontal abscess.

For differential diagnosis patient records, evaluation of clinical symptoms (location of swelling, configuration of pocket, direction of percussion tenderness, nature of pain, vitality test, degree of tooth destruction) and radiological examination can be of help. Previous chapters discussed the difference between a periodontal and a pulpal abscess. The morphology of the pocket can be helpful when probing: an apically narrowing pocket indicates a periodontal lesion, while an apically widening pocket is a sign of pulpal disease.

Continuous resorptive and rebuilding processes of the bone are separated from the dental hard tissues by periodontal ligaments and cementoblasts. If this barrier is injured and the root cementum gets in direct contact with the active bone cells, a resorptive process begins on the root. It only shows clinical signs when it is accompanied by an infectious or inflammatory process. Minimal surface resorption is present in case of occlusial trauma or smaller injuries on the cementum, caused by orthodontic treatment. The damage caused by osteoclasts in these cases is quickly repaired by cementoblasts. Replacement resorption can take place when periodontal ligaments get injured following tooth trauma or if autografts (containing vital bone cells) are used to fill periodontal pockets. This resorption ends with large resorption lacunas, which cannot be repaired by cementoblasts, therefore, osteoblasts gradually replace the defect by creating bone. This is most commonly recognised on radiographs without any clinical signs.

External inflammatory resorption is caused by granulation tissue developing around the root. This can happen after major trauma, accompanied by pulpal infection and necrosis. This scenario is associated with continuous irritation caused by the infection, as well as replacement resorption. The same process takes place after periodontal therapy, when treated root surfaces are populated by epithelial cells instead of fibroblasts.

Classification of endo-periodontal lesions

Several classifications are present, but the most recognised one is the Guldener and Langeland classification:

  1. primary endodontal lesionThe necrotised pulp is causing the periapical or lateral periodontal lesion. The inflammatory products can deflect into the gingival sulcus and to the vestibule through a fistula.

  2. primary periodontal lesionPeriodontal inflammation and consequent attachment loss can lead to the opening of accessory root canals. Pulp can get infected through these canals.

  3. combined endo-periodontal lesion Pulp necrosis and periodontal lesion caused by persisting severe periodontitis develop at the same time.

DEVELOPMENTAL AND ACQUIRED PERIODONTAL DEFECTS AND CONDITIONS

Periodontal conditions or mucogingival deformities which influence the development and progression of periodontal inflammatory diseases, but can also occur independently of dento-gingival plaque.

Localised periodontal conditions, modified by tooth- related predisposing factors

Anatomical factors of the tooth

Changes in the shape of the tooth can modify interdental spaces and shapes of the papillae or lead to their absence. Interdental spaces might be too narrow (crowded teeth) or too wide (pronounced curvature of clinical crowns). These deformations can be the result of rare anatomical structures, fissures engaging the root or enamel pearls.

Effects of restorations

Incorrect marginal closures of crowns, fillings, micro-mechanical retentive structures can irritate the gums. Besides facilitating plaque accumulation, their direct traumatising effect can harm the periodontal tissues.

Root fracture

Infections caused by traumatic root injuries

Cervical root resorption

Root resorption was mentioned above

Mucogingival deformities

Gingival recession

In case of alveolar dehiscence or fenestration, the lack of bony support makes the gums more susceptible to infections and mechanical trauma, which may lead to gingival recession.

Lack of keratinised gingiva

Periodontal health can be maintained in the lack of keratinised gingiva with good oral hygiene. However, lack of keratinised gingiva may inhibit appropriate oral hygiene, which can lead to inflammation. When performing restorations with crowns, a minimum of 3 mm keratinised gingiva is necessary to preserve periodontal health, especially in thin biotype.

Shallow vestibule

Shallow vestibule may prevent proper oral hygiene

Pronounced frenule

Pronounced frenule can prohibit proper oral hygiene. Highly attached frenule can damage the marginal gingiva.

Gingival overgrowth, pseudo-pocket, irregular gingival contour

These conditions make appropriate individual oral hygiene impossible. They support plaque-induced inflammatory diseases and their progression.

Gummy smile

Gummy smile is mostly an aesthetic concern, but gums can be mechanically irritated as a result of mouth breathing.

Gingival overgrowth, pigment disorders

These disorders were mentioned in detail at the beginning of this chapter.

Mucogingival deformities on the edentulous ridge

The edentulous ridge suffers constant involution following teeth loss. If the tooth was affected by periodontal disease, cyst, surgical trauma or developmental disorder, its loss leads to various tissue deficiencies.

The ridge may lose volume horizontally as well as vertically. Seibert, Allen and Wang classified defects into

  • Horizontal (H, Class I, Type A),

  • Vertical (V, Class II, Type B) and

  • Combined (C, Class III, Type C) defects.

Studer determined the severity of the horizontal defect relative to the dentate arch, and that of the vertical defect based on the papilla height of the adjacent tooth: 0-3 mm: moderate, 3-6 mm: advanced, 6 mm severe bone resorption.

According to the studies of Seibert and Allen, defects are combined in more than half of the cases, horizontal only in one-third of the cases, and isolated vertical defects are extremely rare . In less than 1 of 10 there is no deficiency at all.

Correction of the edentulous ridge is inevitable for both fixed partial dentures and implant restorations.

However, not only tissue deficiency, but also shallow vestibule, gingival overgrowth, pronounced, highly attached frenules can cause problems associated with the edentulous ridge.

Occlusal trauma

All adaptive and pathological changes in the periodontium caused by overload of the masticatory function are called occlusal trauma. Unfavourable forces can appear after the adjustment of occlusion, early tooth contact and parafunction. Early contact can be the result of tooth loss, periodontitis, changes in dentition (elongation, tooth malposition or mobility) or poorly designed restorations. In case of primary occlusal trauma, the tooth is periodontally healthy, but is subject to increased loading forces. In secondary occlusal trauma, the force might even be normal, but affected teeth are periodontally compromised.

Occlusal trauma can lead to qualitative and quantitative changes in periodontal tissues, which can regenerate in part or completely if the damaging forces no longer exist. As a result of the pathological process, the periodontal space gets wider, the alveolar bone starts to resorb, vascular changes take place in the ligaments, degenerative changes in the cementum and the amount of collagen decreases in the alveolar bone. The pathological mobility of tooth can be divided into two stages: progressive (increasing) and stabilised (persistent).

Clinical signs of occlusal trauma: high tooth mobility, increasing tooth mobility, tooth wearing, facets on teeth, tooth migration, tooth tilting, failure of restoration, pain. The radiographic image shows extended periodontal space, which is „U”; „V”; or sandglass shaped. Cementiculi can develop within the periodontal space and hypercementosis can occur on the apical portion of the root.

Two types of forces can reach the tooth. One way, or orthodontic type forces are present if resorptive and rebuilding processes induced by orthodontic movement are not evenly distributed, because of over forcing. Jiggling type forces create resorptive forces on both sides of the tooth. Widening of the periodontal space and bone destruction (together with increased mobility) will go on until adaptive measures compensate for high forces.

Occlusal trauma is not responsible for periodontal inflammatory diseases by itself, but forces exceeding adaptive capacity of the periodontium may trigger inflammatory processes. Several human studies proved that occlusal trauma contributes to the severity of plaque induced inflammation, and it even influences the success of the therapy in a negative way.

LESIONS OF PERI-IMPLANT TISSUES

Implant failures can be classified as early and late. Early failures develop around the implants before osseointegration. Late failures can affect implants in function. Implant loss can be due to overloading (improper size, surface characteristics, bone quality) or infection.

Alberktsson and Izidor applied the following definitions on implants, based on definitions related to natural dentition:

Peri-implant mucositis: reversible soft tissue lesion around implants

Peri-implantitis: inflammation affecting osseointegrated implants in function, resulting in supporting bone loss

Incidence

The longest study on periimplantitis was conducted by Roos and Jansaker (implants placed 9-14 years ago). They found that 16% of study subjects and 6.6% of implants were affected. According to Zitzmann and Berglundhs, who refined the criteria, over 56% of patients and 28% of implants revealed a lesion. Periimplantitis had a 2-10% prevalence in a 5-year period. Peri-implant mucositis was present in more than two-thirds of the patients with implants in function for 9-14 years.

Risk factors

Based on available data, peri-implant and periodontal infections have a lot of risk factors in common. Peri-implant diseases are much more likely to occur in patients with a history of periodontitis, smoking, inadequate oral hygiene or local disturbing factors present. Further risk factors are diabetes mellitus and genetic factors (IL-1 gene polymorphism). Overloading does not cause bone resorption by itself but facilitates inflammation.

Characteristics of the lesion

Plaque induced changes in the peri-implant mucosa are similar to gingival inflammation in the first three weeks. Following this, fibroblasts appear in a much higher number in the inflamed gingiva than in the mucosa. Apical and horizontal spread of the lesion is much wider, reparation is much less pronounced. Inflammatory cells are widespread in the mucosa, inflammation is much less contained. (bordered)

A large portion of the soft tissues gets infiltrated. A large number of inflammatory cells (macrophage, plasma cell, lymphocyte) appear in the histological specimens. The biofilm is not separated from the connective tissue by an epithelial barrier. A large number of PMN cells are present in the lesion, even further away from the implant surface, perivascularly. Elastaze-activity and lactoferrin-concentration is higher in the sulcus in periimplantitis compared to the healthy mucosa.

The composition of the biofilm is similar in periodontal and peri-implant lesions.

Symptoms:

Bone resorption on the radiographic image. Inflammatory signs (swelling, reddish peri-implant mucosa, bleeding on probing, suppuration) are noticeable in peri-implant soft tissues. Stability of the implant is maintained for a long time.

Peri-implantitis

Radiological signs of peri-implantitis

Periodontitis and systemic diseases. Focal infection (Péter Vályi DMD - László Párkányi DMD)

It has been suspected since the time of Hippocrates that oral diseases can have an effect on systemic diseases. From the late 19th century till the beginning of the 20th century, „oral sepsis” and „focal infection” were well known terms, but pointless and brutal tooth extractions did not fulfil expectations: systemic conditions did not improve in most patients after the treatment. As a result of modern diagnostic procedures and broader immunological knowledge, in the late 20th century studies confirmed that oral infections can cause damage to distant organs and can influence the development of systemic diseases.

DENTAL FOCUS OF INFECTION

Focal infection is a chronic, isolated, symptomless inflammation, from which bacteria or their toxins and antigens spread to distant organs, where they provoke inflammatory and immune reactions, causing secondary diseases. Focal infections can be categorised based on their relation to the oral cavity (open, closed) or by aetiology (periodontal, endodontic). There are major differences between periodontal and endodontic infections in duration, possibility of spreading (bacteraemia–involved surface area) and incidence (bacteraemia can develop from periodontal pockets during daily oral hygiene or even chewing), as well as in number and types of bacteria. Some bacteria spread directly to specific organs (e.g.: T. forsythensys and P. gingivalis prefer the endothelium); this is called tropism. There are also differences in the frequency of clinical symptoms. The spread of bacterial products can be direct or indirect. Classification of focal infections, ways of spreading and target organs are listed in the table below:

Classification of dental foci, ways of spreading and target organs

The damaging effect of focal infections is also due to the special anatomical conditions: bacteria can get from the oral cavity directly to the heart through veins, and form there directly into the systemic circulation without passing through the liver, which plays a major role in immune responses. Adhesion to Kupffer cells (fixed macrophages) in the liver causes increased adhesion of granulocytes and release of chemotactic substances, cytokines, which activate further components of the immune system. Passing by this mechanism, pathogens can easily get to targeted organs. In the targeted organs they need to attach and reproduce. Previous chapters mentioned the virulence factors of bacteria which can dodge immune responses and secure their survival in targeted tissues.

Focal dental infections trigger destructive procedures not only by the spread of bacteria themselves (metastatic infection) but also by releasing toxins (metastatic damage)). In this case, these toxins can be isolated, and linked to specific bacteria, and their antigens provoke immune response and inflammation in the target organs (metastatic infection). Antigens of these toxins act as super-antigens (toxic shock syndrome), furthermore they can lead to autoimmune diseases by cross-reactions, stimulating the production of autoantibodies.

SECONDARY DISEASES IN TARGET ORGANS

Quite rarely, severe infections can spread from the head and neck region directly between cervical muscles, mediastinum, cranium (cerebral abscess) and sometimes to masticatory muscles. Infection in the sinuses and deeper facial tissues is much more common.

From digestive system diseases, Helicobacter pylori can persist in periodontal pockets maintaining underlying diseases, e.g. duodenal abscess. Periodonto-pathogenic bacteria may be the aetiological factor of autoimmune inflammatory intestinal diseases (P. gingivalis).

Long-term artificial respiration or aspiration among frail elderly patients can lead to respiratory infections, caused by oral pathogens. Relationship between pneumonia, lung abscess, COPD and periodontitis is confirmed by epidemiological studies.

Inflammations originating from the head and neck region can lead to autoimmune diseases of the kidneys through antigen-triggered immune complexes in the target organ. Possible relationship between dental infections and liver abscesses have also been mentioned in some studies.

Ophthalmological (uveitis, endophthalmitis) and dermatological (erythema nodosum, pustulosus palmo-plantaris) diseases have also been linked to dental infections as aetiological factors, with some supporting evidence. Joint diseases have also been related to dental infections, but evidence is lacking to prove this hypothesis. Relationship with cardiovascular, genital diseases and diabetes mellitus will be detailed in Chapter 5.13.

Benign tumours of the oral and maxillofacial region (Péter Novák MD)

Papilloma

Papilloma is a benign epithelial tumour, which frequently appears on the oral mucosa. Local irritation and infection, especially viral infection (human papilloma virus) may play a role in its development.

Symptoms: a pedunculated or sessile, white, or whitish-grey, papillary surfaced tissue growth, which does not cause any symtoms. A slowly proliferating, smaller or larger epithelial tumour may also develop. It occurs mostly in the palates, tongue, gingiva and lips.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Papilloma

Fibroma

Fibromas are benign, slow-growing tumours of the oral cavity composed of connective tissue. Fibroma is the most common tumour of the oral mucosa, which particularly occurs on the buccal mucosa and on the tongue. In the oral cavity, fibromas are reactive proliferative lesions, which develop secondarily to irritation (by sharp tooth edges, artificial teeth or calculus) or low grade infection. The lesion feels solid or soft on palpation. It is sessile or pedunculated, smooth-surfaced, reddish or pale and covered with intact mucosa, but as a result of mechanical irritation it may become whitish leukoplakia due to keratinisation or may become ulcerated. No other clinical sign or pain can be observed.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

epulis, pyogenic granuloma, granuloma fissuratum and neurinoma.

Fibroma

Lipoma

They are rare, painless and benign tumours in the oral cavity, which arise from the fat tissue and grow slowly. Lesions mostly involve the bucca, the tongue and the floor of the mouth. The growth is mainly single, rounded or oval, mobile, pedunculated, soft, yellowish translucent and painless. The surface is vascularised.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

mucocele, ranula, dermoid cyst, lymphangioma and adenoma.

Pleomorphic adenoma

It is also called a “mixed tumour”. The epithelial tumour mainly originates from the small and large salivary glands, it is hard, springy and lobulated, and grows slowly without causing any pain. Extraorally, it mainly arises from the parotid gland. Small and large (giant and weighty) tumours occur alike. In the oral cavity, in addition to other localisations, the tumour predominantly appears on the hard palate, which occasionally interferes with eating and speaking.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

cystadenocarcinoma, epulis.

Papillary cystadenoma lymphomatosum (Warthin’s tumour)

Warthin’s tumour or adenolymphoma is a rare and benign condition, which almost exclusively develops in the parotid glands. It rarely involves the submandibular glands or the intraoral small salivary glands. Usually men are affected.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

lymphoepithelial cyst (branchial cyst) and other benign and malignant tumours.

Capillary haemangioma

The benign tumour develops as a result of vascular proliferation. The congenital form is considered to be rather a congenital disorder (malformation) than a real tumour, since it may regress spontaneously. The capillary form is composed of a capillary network, and is soft, small and bluish-red. Manual compression of the lesions expresses blood, leaving behind an empty sac (vitropression), thus temporarily they fade away.

Cavernous haemangioma

This type of haemangioma is a hamartoma (not a neoplasm), which histopathologically does not have a capsule. It mostly involves the tongue, lips and the bucca, and reaches an extreme size (macrocheilia, macroglossia), thus hindering speech and swallowing. It occurs as a flat or exophytic, painless growth with a raspberry-like appearance. Its colour ranges from red to dark blue.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

haematoma, lymphangioma, pyogenic granuloma, malignant melanoma, mucocele.

Haemangioma

TUMOUR-LIKE LESIONS

Pyogenic granuloma

The tumour-like reactive tissue proliferation may develop in response to trauma or infection, but it may also occur as a result of hormonal changes (pregnancy, menopause, or puberty), the administration of oral contraceptives, steroid drugs and anti-diabetics. Most frequently it develops on the gingiva, bucca, lips and tongue. It is a raised, pedunculated, flat or wart-like lesion with a dark red or pink colour depending on the vascularisation of the affected area. In case of ulceration, it is covered with yellowish fibrin. Its diameter ranges from a few millimetres to a centimetre. It is a painless tumour, which easily bleeds.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

epulis, papilloma, fibroma, haemangioma, granuloma gravidarum and malignant tumours.

Pyogenic granuloma

Granuloma gravidarum

After the first trimester of pregnancy, a single or rarely multiple, dark red, ulcerated tumour-like lesion which is prone to bleeding develops mostly on the gingiva. It mostly involves the vestibular gingiva at the level of the upper premolars, but it may also appear in other areas. During pregnancy, it may recur despite its removal, but after delivery it may spontaneously disappear. The clinical and pathological picture is similar to that of pyogenic granuloma.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

pyogenic granuloma, epulis and haemangioma.

Postextraction granuloma

This reactive, inflammatory tumour-like lesion develops after tooth extraction as a result of retained root, broken pieces of bones, amalgam or other foreign body.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

epulis and gingival tumour.

Postextraction granuloma

Epulis granulomatosa

It is not a real neoplasm, but a reparative tissue proliferation arising from the mucoperiosteum of the tooth socket or from the periodontal membrane. The diagnosis of ”epulis” may be applied only clinically. The growth is a painless, red lesion, which is prone to bleeding and occurs mostly on the vestibular surface of the front and premolar teeth. It is mostly brought about by chronic inflammation (tartar, excess filling, or crown).

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

pyogenic granuloma and granuloma gravidarum.

Epulis granulomatosa

Fibrosus epulis

It is the most common type of epulis. It is a light red or yellowish-white, stiff tissue proliferation, which grows slowly.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

fibroma.

Peripheral giant cell epulis

It is a soft, bluish-red, often ulcerated growth covered with yellowish, fibrinous pseudomembrane, which may reach 2–3 cm in diameter. The teeth may loosen due to the destruction of the surrounding bones. In rare cases, the tumour becomes malignant. It develops less frequently than the granulomatous or the fibromatous forms.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

pyogenic granuloma, granuloma gravidarum, central haemangioma, gingival cancer, malignant melanoma.

Pigmented naevus (intradermalis)

Intradermal naevus is the most common lesion of the skin. It is usually elevated and as a result of fibrous tissue, stiff, brown or brownish-black, in rare cases colourless (amelanotic), occasionally papillary-surfaced or pedunculated develops. Malignant degeneration may result from irritants (collar, bras, or shaving) or insufficient treatment. It appears as a flat or slightly raised, brownish or brownish-black macule on the bucca or lips.

Pigmented naevus

BENIGN ODONTOGENIC AND NON-ODONTOGENIC TUMOURS

Ameloblastoma

It is benign, locally aggressive and grows invasively. It is four times more frequent in the mandible than in the maxilla. Ameloblastoma may present in all ages, however, regarding the average age it is the most common in the fourth decade. The tumour grows slowly, and in 80% of the cases, it does not cause pain. A tumour in the jaw bone may cause facial deformation of various severity.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

follicular cyst, keratocyst.

Odontoma

Odontomas should be considered hamartomas rather than real tumours. This relatively common odontogenic tumour develops in the jaw bones mainly in children and young adults. The tumour has few symptoms and leads to swelling of the jaw bones, sometimes with a diameter of 5–6 centimetres.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

ameloblastoma, fibrous dysplasia.

Osteoma

Osteoid osteoma is a rare, benign, non-odontogenic tumor of the jaw bones. It occurs more frequently in women than in men, and it presents more commonly in the mandible than in the maxilla. It is a slowly-growing, usually painless, hard tumour that is bone-like to the touch and causes facial deformity.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

osteosarcoma, maxillary tumour, exostosis.

Exostosis

The disease should be differentiated from osteoma, which is a real osteogenic tumour. The cause of exostosis is unknown. It is not a real neoplasm but a reactive lesion.

Torus palatinus

It is a developmental malformation of unknown origin, which presents as a slowly growing, bony growth (exostosis) in the middle of the hard palate, covered with intact mucosa. The growth is hard and feels like bone to the touch.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

palatal abscess, nasopalatine cyst.

Torus mandibularis

The disease can be manifested on the lingual surface of the mandible, unilaterally or bilaterally, at the site of the premolars, and may reach various sizes. The bony outgrowth is clearly visible in the radiogram.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

osteoma, mandibular cyst.

Torus mandibularis

Precancerous states and lesions (potentially malignant lesions) (Péter Novák MD)

All morphologically altered tissues that have a greater predisposition to develop cancer than surrounding, apparently normal tissues are considered to be precancerous. The term leukoplakia is merely a clinical designation, which refers to any white lesions of the oral mucosa that cannot be wiped off and cannot be classified as any other well-defined disease.

Leukoplakia simplex (homogeneous)

Causes: the underlying cause for leukoplakia is unknown, however, predisposing factors may include genetic factors, inappropriate oral hygiene, vitamin A or C deficiency, smoking, alcohol, trauma, candida albicans, viral infections (HPV), systemic diseases (syphilis, sideropenia, hepatopathy), galvanism and immunological alterations, but it may also occur idiopathically.

The general prevalence of leukoplakia within the population is 0.1–5%. Carcinoma has already developed at the time of detection in 5% of the cases on average. 3–8% of all leukoplakias develop into malignancies, and most of them occur in mostly men at the ages of 40–60 or over. Malignant transformations are more common among women and non-smoking patients with leukoplakia. Leukoplakias on the tongue and the floor of the mouth are more likely to develop into malignancies. Leukoplakias may occur at any location within the oral cavity, but they are the most common in the retrocommissural triangle, bucca, tongue, palate, lips, gingiva and floor of the mouth.

Leukoplakia simplex (homogeneous)

Non-homogenous leukoplakia

Verrucous leukoplakia

These are greyish-white, white and asymptomatic alterations that protrude from the oral mucosa similarly to verrucae and have a wrinkled or corrugated surface and a ”cobblestone” display. Chronic inflammations and keratinisation of the oral mucosa is irreversible due to its intensity, and reacts only to the proper clinical therapy.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Lichen oris, oral candidiasis, morsicatio buccarum.

Verrucous leukoplakia

Nodular leukoplakia

These alterations occur mostly in the retrocommissures or on the bucca and appear as white nodules on an exophytic, erythematous background. Histologically, results may include epithelial dysplasia or carcinoma in situ or even invasive carcinoma.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Hyperplastic candidiasis.

Erythroleukoplakia

Keratinised mucosal tissues may develop ulcers; clinically, the surface of these alterations may become nodular and speckled with red and white patches. The most common location of these alterations is the oral mucosa behind the commissure of the lips. Most of the patients seek medical help because of the increased tenderness during eating caused by the erosions, or less commonly, because of the pain these alterations may cause. Malignancies evolve from erosive areas without epithelium more easily and more frequently than in case of simple or verrucous alterations.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Erosive lichen, chronic discoid lupus erythematosus, pemphigus vegetans

Proliferative verrucous leukoplakia

This alteration occurs rarely, effects non-smoking women more commonly, and it is clinically similar to verrucous leukoplakia; however, a major difference is that its surface is not homogenous, it resembles “soaked skin”, while its surface is crinite and deeply fissured and it is visibly multifocal and frequently covers a wide area. It is more common on the gingival mucosa, bucca, tongue and lips. This chalk-white, exophytic alteration is free of any clinical symptoms. This condition has a marked tendency to become malignant.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Lichen oris, verrucous carcinoma.

Erythroplakia

Similarly to leukoplakia, erythroplakia is a clinical term, which describes a vivid, velvety, soft, well-circumscribed, flat alteration that is slightly indented or less commonly, slightly elevated from the surrounding tissues, but it does not resemble a plaque. These alterations cause no symptoms for the patient; however, during meals, a slight burning sensation or tenderness may infrequently occur. Erythroplakias develop into malignancies commonly and easily. These rare alterations occur at the ages of 50–70, the most common locations are the soft palate, bucca, tongue and the floor of the mouth. White, hyperkeratotic areas appear in the lateral regions of these alterations. Histology often shows severe epithelial dysplasia, carcinoma in situ and in more than 50% of the cases, squamous cell carcinoma.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Erosive lichen, atrophic candidiasis.

Erythroplakia

Chronic actinic cheilitis

This form of chronic inflammation caused by sunshine (solar cheilitis), wind or agrochemical compounds (sprays) occurs mostly on the lower lip in patients working outdoors (agricultural workers). It is more common among men than among women. The lower lip becomes crusty to some extent, and later, it also becomes swollen and hard due to the accumulation of connective tissue (macrocheilia). It may easily crack, bleed or become painful. Symptoms of this chronic inflammation of the lips become worse during the summer, and they improve in the autumn and winter. After some years, these alterations may evolve into lip cancer, thus, they should be treated as precancerous conditions.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Multiform exudative erythema, Quincke’s oedema, lip cancer, lupus erythematosus.

Lichen planus

Reticular lichen

This condition of unknown origin is a result of chronic inflammation, it reoccurs quite commonly and effects the skin and mucosal tissues. Autoimmune causes and psychological factors are more and more in the foreground nowadays as underlying causes of this disease. Diabetes mellitus, hypertension and hepatic lesions may increase the predisposition to this condition. These conditions occur most commonly in the medial and posterior third of the bucca bilaterally, but they may also appear on the tongue, lips, gingiva; however, they are quite rare on the palate. This is a whitish-grey, slightly protruding, pearlescent, reticular and hyperkeratotic alteration, which appears as a branch-like structure (Wickham’s striae). This is the most common clinical type. The alterations themselves cause no pain, and patients usually feel a slightly uneven spot on their oral mucosa which may be firmer than the surrounding mucosa.

Reticular lichen

Atrophic lichen

Atrophic, lively red, painful spots appear mostly on the bucca and tongue, which are surrounded by reticular alterations (Wickham’s striae). This condition is hard to differentiate from erythroplakia (the latter is not surrounded by a white contour) and discoid lupus erythematosus (which is characterised by dermal symptoms and distinctive histological and immunofluorescent findings).

Ulcerative lichen

In most of the cases, ulcerative alterations are preceded by atrophic lichen. Ulcers lacking epithelium and partially covered by yellowish-white, fibrinous pseudomembranes appear on the mucosa, and these ulcers cause pain spontaneously as well as during meals. Establishing the proper diagnosis is aided by the fact that reticular lichen is observable surrounding the ulcers on both buccal areas. Similarly to atrophic lichen, these alterations have a low risk (1–3%) of developing into malignancies.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

erythroplakia, oral pemphigus, allergic stomatitis.

Actinic keratosis

This is a precancerous condition, which evolves primarily in elderly agricultural workers due to exposure to sunlight; however, it may also accompany immunosuppression, chronic ulcers or human papilloma virus (HPV) infection. According to recent views, solar keratosis is a superficial form of epithelial cancer. These alterations are mostly flat or slightly protruded, multiple, their surface is rough, hyperkeratotic, red or yellowish-brown (and pigmented). These precancerous alterations occur mostly on the face, forehead, nasal crest, ears, neck and back of the hand. After years or even decades, these keratotic lesions may transform into carcinomas in about 25% of the cases.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Basalioma, seborrhoeic verruca, and dermal cancer

Malignant tumors of the head and neck region (Péter Novák MD-Róbert Paczona MD -József Piffkó MD, DMD)

INTRODUCTION

Head and neck cancer describes a range of tumours that arises in the head and neck region, which includes the oral cavity, pharynx, larynx, nasal cavity, paranasal sinuses, thyroid gland, and salivary glands.

INCIDENCE AND PREVALENCE

The worldwide incidence of head and neck cancer exceeds half a million cases annually, ranking it as the fifth most common cancer worldwide. Most commonly “head and neck cancer” refers to epithelial squamous cell carcinomas that arise from the mucosal surfaces of the upper aero-digestive tract. However, the impact of this disease on society is not measured solely by its relatively low absolute mortality, but also by the acute and chronic cosmetic, functional, and psychological morbidities experienced by all patients. Head and neck cancer thus remains a feared disease associated with significant rates of both morbidity and mortality.

RISK FACTORS

Alcohol and tobacco

Alcohol and tobacco containing products remain the most significant risk factors for this disease. All fermented and distilled alcoholic beverages contain carcinogens that promote the development of head and neck cancer. Tobacco-containing products have carcinogenic effects on the upper aero-digestive tract identical to those reported in the lungs. Important to the head and neck region, the local effects of alcohol and tobacco carcinogens are both dose-dependent, and synergistic. Smokeless tobacco abuse results in a local exposure to carcinogens that promotes cancers of the oral cavity and to a lesser extent, the oropharynx. Leukoplakia and erythroplakia are pre-malignant mucosal lesions associated with a risk for transformation to in-situ and invasive cancers. Both lesions are commonly found in the oral cavity and oropharynx, where chronic exposure to alcohol and tobacco carcinogens is most significant.

Nutrition

Dietary factors may also contribute to their development. The incidence of head and neck cancer is highest in people with the lowest consumption of fruits and vegetables. Recognising the latter association, clinical trials of various vitamin and anti-oxidants supplements have been conducted. To date, however, micronutrient supplementation has not led to a reduction in the risk of developing head and neck cancer.

Viruses

Exposure and prolonged local infection by Epstein–Barr virus or the high risk HPV subtypes (16 and 18) are associated with cancers of the epithelial cancers of the nasopharynx and oropharynx, respectively. For both viruses, transient infection without long-term sequaelae is common. Persistence of the viral genome and induction of malignant transformation is a rare event. Nasopharyngeal cancer occurs endemically in some countries of the Mediterranean and Far East.

Irritating factors

Other significant risk factors for this disease include prolonged exposure to asbestos (larynx cancer), textile fibers, nickel refining, and wood dust and leather tanning (nasal cavity and paranasal sinuses, adenocarcinomas).

Genetic predisposition

Perhaps the single greatest risk factor for developing a squamous cancer of the head and neck region is having had one at an earlier time. Similar to the situation with breast, colorectal, bladder, and lung cancer, having one cancer is associated with a significant risk for the development of a second cancer. Indeed, following the curative treatment of a primary head and neck cancer, the annual risk for developing a second unrelated squamous cancer of the upper aero-digestive tract is approximately 2%.

CLINICAL SIGNS AND NATURAL COURSE OF THE DISEASE

Squamous cell cancers of the head and neck region are occasionally discovered during routine dental or ENT (Ear-Nose-Throat) examinations. More commonly, they are discovered after weeks to months of relatively non-specific symptoms arising from the primary site, such as altered speech or swallowing, bleeding, localised pain or referred otalgia. Alternatively, many patients will present with new onset cervical adenopathy of unknown origin. Such patients are often treated empirically for infection, and later discovered to have head and neck cancer after the adenopathy persists or enlarges and the primary physician or a surgical consultant consequently performs a detailed examination of the head and neck region. Distant metastatic disease at presentation is unusual, and symptomatic disease related to such is rarely seen.

Squamous cell cancers of the head and neck region are locally aggressive and carry a moderate risk of spread to regional lymph nodes and a low probability of spread to more distant sites. This common natural history has several site-specific exceptions. For example, certain primary sites are more likely associated with regional disease at presentation (e.g. the nasopharnyx, hypopharynx, base of tongue, and supraglottic larynx). In contrast, other sites have a relatively low risk for regional spread (e.g. paranasal sinuses, small lesions of true glottis).

SITE SPECIFIC CLINICAL SIGNS

Oral cavity, pharyngeal and laryngeal cancer’s typical complaints:

  • odynophagia

  • foreign body sensation

  • hoarseness haemoptisis

  • cough

  • solitary or multiple, painless neck lymph node enlargement

Nasopharyngeal or nasal, paranasal sinus tumours:

  • blocked nose

  • unilateral hearing loss (serous otitis media)

  • epistaxis

  • facial sensory or motility disturbances

  • visual problems

  • solitary or multiple, painless neck lymph node enlargement

Nota Bene: in case of hoarseness or dysphagia lasting for more than two weeks, thorough ENT examination should be performed.

MALIGNANT TUMOURS OF THE ORAL AND MAXILLOFACIAL REGION

MALIGNANT EPITHELIAL TUMOURS

Cancer of the lower lip

Cancer of the lower lip is one of the most frequent malignant epithelial tumours of the orofacial region. It is a mature-cell (well-differentiated) epithelial cancer in 90–95% of the cases. Besides smoking a pipe or cigarettes (heat and mechanical), sunlight (ultraviolet light), wind, viruses (HPV, herpes simplex), candidiasis, syphylis as well as genetic factors, malnutrition, vitamin A or C deficiency, immunosuppressed state (HIV, organ-transplanted patient), agrochemical substances and alcohol are listed among the predisposing factors. It is the disease of elderly men working in the agriculture. The frequency ratio between cancers of the upper and lower lips is 20:1.

Three types can be differentiated clinically: exophytic, ulcerative and verrucous types. The commonest is the exophytic type.

Lower lip cancer forms metastasise rarely and only in advanced stages. The tumour is symptomless for a long time. The development of labial cancer is usually preceded by chronic cheilitis or leukoplakia.

The prognosis of lower lip cancer is good, the recovery rate ranges from 90 to 98%, depending on the stage of the tumour.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

keratoacanthoma, actinic cheilitis, specific (tuberculotic, syphilitic) ulcers.

Cancer of the lower lip

Cancer of the upper lip

While cancers of the lower lip account for 90–95% of oral cavity cancers, upper lip cancers represent 3–10%. Clinical types of upper lip cancer correspond with those of lower lip cancer. The prognosis of the upper lip cancer is worse than that of the lower lip cancer, and it metastasises earlier and more frequently.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

pyogenic granuloma, keratoacanthoma.

Tongue cancer

The frequency of tongue cancer follows that of the lip cancer, but its prognosis is worse. It is the most frequent site within the mouth; 35–45% of malignant oral tumours affect the tongue.

The predilection site is the middle third of the lateral border of the tongue, and the ventral surface and base of the tongue (pharyngeal tongue).

Primarily, alcohol (liver damage – cirrhosis) and smoking have a role in triggering the disease, but chronic irritating factors, poor oral hygiene, sideropenic and syphilitic atrophic glossitis, Candida albicans, viruses (HSV, HPV) and hot and spicy food may also contribute to its development.

The tumour is symptom-free at the beginning, thus patients present late, when the diameter of the thick-feeling tumour is more than 2 centimetres (endophytic type). At this time, regional metastases may also be palpated in 60–70% of the cases. Tumours in the posterior third of the tongue (pharyngeal tongue), and the ulcerated form cause pain (‘sore throat’), bleeding and difficulty swallowing, eating and speaking more frequently and earlier than other forms. Tongue cancers are mainly squamous cell carcinomas (90%).

Only 24–51% of patients with tongue cancer survive for more than five years following the diagnosis, and the prognosis is even worse in case of tumours in the posterior third of the organ.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

decubital ulcer, specific (tuberculosis, syphilis) and non-specific ulcers.

Tongue cancer

Cancer of the floor of the mouth

The frequency of the disease follows those of lip and tongue carcinomas (20–25%). Usually it affects elderly, alcohol consuming (liver cirrhosis), and smoking men.

The tumour develops in the anterior third of the floor of the mouth more frequently than in the posterior third. Pain appears only in a late stage, when the tumour becomes thick and ulcerated and infiltrates its surroundings (bone).

The prognosis of early-stage tumours is better than that of tongue cancer and it metastasises later and less frequently. However, in case of tumours developing from the middle and posterior sublingual region and infiltrating the periosteum of the mandible, the bone and the tongue (anaesthesia, trismus), the prognosis is also poor.

The tumour metastasises primarily into the submandibular lymph nodes, unilaterally or bilaterally.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

leukoplakia, ranula.

Cancer of the floor of the mouth

Buccal cancer

Buccal cancer accounts for 10% of carcinomas of the oral cavity. Cancers situated closer to the angle of mouth have a better prognosis than those in the middle third of the bucca, and especially than those located in the posterior third.

Among triggering factors, smoking and traumas play crucial roles. Buccal carcinoma frequently develops from leukoplakia or erythroleukoplakia that has persisted for a longer time.

Lymph node metastases occur in the submandibular and jugulodigastric lymph nodes.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

verrucous carcinoma, specific (tuberculotic, syphilitic) ulcers, large thrush.

Gingival cancer

The disease develops mostly on toothless alveolar ridges, where it spreads from the gingiva to the alveolar mucosa and to the surrounding oral structures. Gingival cancer accounts for 8–12% of oral cavity tumours.

Beside smoking and alcohol, mainly chronic irritating factors (odontolith, prosthesis, etc.) may play a role in triggering gingival cancer.

The disease destroys the periosteum and the bone if it reaches them, and loosens the teeth. Gingival cancer is more frequent on the mandibular gingiva than on the maxillary, and mandibular gingival cancer metastasises regionally more frequently. Metastases occur mainly in the submandibular region. Similarly to oral cavity cancers located elsewhere, it is mainly the disease of the elderly (50–70-year-old) men, and histologically most of the cases are squamous epithelial cancers. Incisional biopsy is necessary.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

epulis, pyogenic granulomas.

Gingival cancer

Palate cancer

Palate cancer is rare among cancers of the oral cavity. It is more frequent on the soft palate (15–20%) than on the hard palate (5%).

The prognosis of hard palate cancer is better than that of soft palate cancer, which metastasises regionally more frequently. On the soft palate, squamous cell carcinomas, while on the hard palate, adenocarcinomas are more common. Clinical differentiation is supported by the fact that while squamous cell palate carcinomas are almost always ulcerated, adenocarcinomas rarely show ulceration. Ulcerated palate cancers may penetrate into the paranasal sinus, then to the orbit, due to destruction of the palatine bone. Incisional biopsy is necessary.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

specific ulcers, abscess, cylindroma.

Basal cell carcinoma

Basal cell carcinoma is the most common skin cancer on the skin of the head and neck (80%). The ratio between basal cell carcinomas and squamous cell carcinomas is 5:1. Basal cell carcinomas usually appear in the periorificial region, and only exceptionally occur in the oral cavity, on the oral mucosa and on the lips. The disease is more common in elderly patients, especially among those working in the agriculture (sunlight). The tumour grows slowly and invasively, however, if it reaches the cartilage or the bone, it destroys them. Metastasising is extremely rare, it occurs mainly if the basal cell carcinoma is transformed into a keratinising squamous cell carcinoma.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

seborrheic verruca, squamous cell carcinoma.

MALIGNANT TUMOUR OF THE SALIVARY GLAND

Adenoid cystic carcinoma (cylindroma)

Among malignant salivary gland tumours of the oral cavity, the infiltratively growing adenoid cystic carcinoma (cylindroma) is the most frequent one. It may develop from the small accessory salivary glands of the hard or soft palate, or it may appear in the parotid gland and in the submandibular salivary glands as well. Cylindromas originating from the submandibular salivary glands almost always affect women and, besides rapid progression, they have a poor prognosis.

It is a tumour with a firm and elastic touch, sometimes leading to facial paresis (parotid gland) accompanied by pain and ulceration. Usually it is regarded as a slowly growing tumour; however, rapidly infiltrating tumours should also be counted on. Regional metastases develop rarely and in late stages. It is a malignancy prone to recurrence. The prognosis of cylindromas is unfavourable.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

pleomorphic adenoma, palate cancer, malignant lymphoma, palatal abscess.

Mucoepidermoid carcinoma

It is the most frequent malignant tumour of the salivary glands. It develops mainly in the parotid gland (89%), but it may also appear in the submandibular and small salivary glands (palate, tongue, bucca, etc.). In children, it is the most common malignancy originating from the salivary glands. Its low-grade malignity form grows slowly and painlessly, feels like a fluctuating cyst on palpation and rarely becomes large. It develops on the palate, tongue and bucca and lips. Its high-grade malignant form shows rapid, painful and infiltrative growth and may cause facial paralysis (parotid gland), reach large sizes and ulcerate.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

malignant lymphoma, pleomorphic adenoma, mucocele, cysts of the jaw bones.

PIGMENTED MALIGNANCIES OF THE SKIN AND THE ORAL MUCOSA

Malignant melanoma

Malignant melanomas are life-threatening malignancies with a poor prognosis, originating from the melanocyte precursors and naevus cells of the skin and arising as a result of solar radiation; however, genetic factors may also play an important role. They are most commonly located on the skin, there are only a few rare cases originating from the oral cavity, however, in these cases the prognosis is even worse than in case of melanomas of the skin.

The most common locations: the palate, (maxillary) gingiva, bucca, and the lips.

Alterations preceding melanoblastomas (pigmented naevus, dysplastic naevus, juvenile melanoma, blue naevus, circumscribed preblastomatous melanosis) or lentigo maligna may become malignant. Therefore, any trauma or insolation of these alterations as well as hormonal changes caused by age may pose a threat.

If any pigmented lesion on the skin or oral mucosa shows signs of accelerated growth, becomes ulcerative, and crusty or it is surrounded by an inflamed halo, becomes indurated, asymmetric with an irregular border, darker in colour, itchy, or it bleeds, one should inevitably think of a malignant transformation (starting symptoms). The deeper these malignancies invade the surrounding connective tissues (the thicker they are), the worse the prognosis will be. These tumours may metastasise into regional and remote lymph nodes (lungs, liver) via lymphatic and blood vessels easily and at an early stage.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

haemangioma, pyogenic granuloma, epulis, haematoma.

MALIGNANT ORAL TUMOURS OF MESENCHIMAL ORIGIN (SARCOMA)

Kaposi’s sarcoma

This is a vascular, relatively rare malignancy dominantly effecting male patients. Since the appearance of AIDS, it has become the most common type of sarcoma of the oral cavity. In most of the cases, dermal symptoms are followed by rare symptoms in the oral cavity; however, the earliest manifestations of the disease may evolve directly within the oral cavity. It is more common in patients suffering from AIDS, lymphomas or leukaemia, and Kaposi’s sarcoma may develop following an immunosuppressive treatment as well. Multiple, pink or dark blue maculae, plaques, nodules and tumours occur on the skin. The most common localisations within the oral cavity are the palate, tongue, lips and bucca.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

haemangioma, malignant melanoma, pyogenic granuloma

ORAL MALIGNANCIES OF THE LYMPHORETICULAR AND HAEMOPOIETIC SYSTEM

Hodgkin’s lymphoma

The aetiology of Hodgkin’s disease and non-Hodgkin’s lymphoma is still unclear. Hodgkin’s lymphoma is less common than non-Hodgkin’s lymphoma. Painless, swollen lymph nodes within the neck region may be the first warning signs, while another characteristic sign is that these lymph nodes become painful after alcohol consumption.

Oral symptoms rarely occur; however, they may precede and thus indicate the systemic disease itself. Oral symptoms occur as the swelling of soft tissue in the beginning, and then painful ulcers may develop, which may actually cause bone destruction beneath them.

Lymphomas may transform into leukaemias if they continue to exist for a long period of time.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

non-Hodgkin’s lymphoma, cylindroma, tuberculosis

Non-Hodgkin’s lymphoma

It develops from the proliferation of the lymphocytes of the immune system. Non-Hodgkin’s lymphomas usually evolve in lymph nodes accompanied by painless swelling. Tumorous infiltration occurs mainly in the lymph nodes of the neck region; however, the alterations may develop in the lymph nodes of other regions or even in extranodal regions (skin, mucosa, gastrointestinal tract, kidneys, bones, or parotid gland).

This disease is quite uncommon within the oral cavity, however, when it does occur there, the extranodal type is more common, and in these cases, the most common locations are the Waldeyer’s lymphatic ring, the palate, gingiva, tonsils and root of the tongue.

The tumours themselves are usually painless, soft to the touch and may become ulcerative at an early stage. Apart from the soft tissues, these alterations may erode surrounding osseous structures (teeth may become loose). The prognosis is worse than in case of Hodgkin’s lymphoma.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

Hodgkin’s disease, eosinophil granulomas, epithelial cancer.

Acute myeloblastic leukaemia

Leukaemia is actually the appearance of young, immature white blood cell formations showing signs of atypical signs. Currently, this condition is considered to be an oncogenic bone marrow disease. The disease itself can be divided into acute and chronic forms according to differentiations between groups of leukaemias arising from the pluripotential marrow stem cells.

The aetiology is unknown, however, there is a number of factors held responsible for causing this disease (genetic causes, exposure to radiation, chemical substances, pharmaceutical products, etc.). Apart from pathologic leukocytosis, anaemia and thrombocytopenia may also accompany this disease. Oral symptoms are more common in the acute form, but may occur in chronic cases as well.

Symptoms: initially they resemble infectious diseases (fever, tonsillitis, pharyngitis, malaise, fatigue, etc.). Generalised swelling of the lymph nodes is quite rare; however, the swelling of lymph nodes in the neck and submandibular regions may be important concomitant signs. One particular sign of this disease is the increase in the number of immature white blood cells. It is particularly common among adult patients.

Extensive, profound ulcers develop in the oral cavity and commissure of the lips of leukaemic patients due to fusospirochetal infections, candidiasis or other infectious causes. The most common oral symptom is gingival bleeding, however, purpuras, petechiae and ecchymoses due to thrombocytopenia may develop in other mucosal regions as well.

Due to the risk of haemorrhagic diathesis, no tooth extractions or any other types of oral surgeries are recommended.

Oral symptoms may be the primary signs of this disease, thus, dentists should be quite aware of this condition. Gingival and mucosal ulcers are profound; the resorption of parodontium may cause the teeth to become loose. Gingival hyperplasia may accompany oral symptoms.

When establishing the correct diagnosis, laboratory examinations are quite decisive. The prognosis is quite poor.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

ulcerative gingivitis, ulcero-gangrenous stomatitis, infectious mononucleosis, haemorrhagic diathesis, agranulocytosis, Hodgkin’s disease

Acute lymphoblastic leukaemia

Acute lymphoid leukaemia is particularly more common in childhood (80%) than myeloid or monocytic leukaemia, however, the lymphoid type is the least common to cause any oral symptoms. The prognosis is better than it is for myeloid leukaemias (60% of these cases result in full recovery).

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

the same as in myeloid leukaemia

Chronic myeloid leukaemia

After the manifestation of the clinical symptoms, the disease will prospectively progress for another 3–6 years. The disease usually starts with a latent period. Myeloid leukaemia is more common among middle-aged men, while lymphoid leukaemia particularly affects elderly male patients.

Symptoms: general symptoms causing complaints usually include stabbing or painful swelling of the spleen; however, hepatomegaly may also occur. Headaches, fatigue and occasional high temperature may develop. Patients usually seek medical care due to gingival bleeding. Lymph node swelling is quite uncommon in myeloid leukaemia, while it is common in the lymphoid type of the disease. Oral symptoms are rarely primary, and these manifestations are not pathognomic, however, gingival hyperplasia and haemorrhage may persist and even profound, persistent ulcers or the loosening of the teeth may occur. Parotid swelling is more common than it is in patients suffering from acute leukaemia. Concomitant herpes zoster, pemphigus and candidiasis may also occur. The prognosis of chronic lymphoid leukaemia is better than that of the myeloid types of the disease.

Differential diagnosis: verruca vulgaris, condyloma acuminatum and verrucous carcinoma.

epulis, ulcerative gingivostomatitis, hydantoin hyperplasia, or agranulocytosis

Chronic lymphocytic leukaemia

This is the type of leukaemia, which shows the slowest rate of progression (with an overall survival of 6–10 years). A characteristic sign of chronic lymphocytic leukaemia is lymph node swelling at an early stage of the disease. Generalised lymphadenopathy is commonly accompanied by splenomegaly. This disease usually occurs at an elderly age. Apart from these symptoms, other, non-specific dermal symptoms may occur as well, such as papulous eczema and the formation of vesicles and bullae. Skin infections, advanced periodontitis, ulcers and bleeding may occur within the oral cavity.