Dental Caries and Gingivitis

• Diseases of the teeth and supporting structures include caries, gingivitis, and periodontitis.

Caries (Tooth Decay)

• Dental caries is caused by demineralization of tooth structure by acidic products of bacterial sugar fermentation.
• Caries is the main cause of tooth loss before age 35.
• Caries rates have decreased in industrialized countries due to better oral hygiene and water fluoridation.
• Fluoroapatite in tooth enamel is more resistant to acid degradation than hydroxylapatite.
• Increased processed food consumption leads to higher caries rates in developing countries.

Gingivitis

• Gingivitis is inflammation of the oral mucosa around the teeth, caused by dental plaque and calculus accumulation.
• Dental plaque is a biofilm containing bacteria, salivary proteins, and epithelial cells.
• Plaque mineralizes into calculus (tartar) if not removed.
• Gingivitis symptoms include erythema, edema, bleeding, contour changes, and loss of tissue adaptation.
• Gingivitis is reversible through plaque and calculus reduction via oral hygiene.

Periodontitis

• Periodontitis is an inflammatory process affecting the supporting structures of the teeth, including periodontal ligaments, alveolar bone, and cementum.
• Periodontitis can cause destruction of the periodontal ligament, leading to tooth loosening and loss.
• Periodontitis is associated with poor oral hygiene and changes in the oral microbiome composition.
• Healthy gingival sites predominantly host facultative gram-positive organisms.
• Active periodontitis sites have anaerobic and microaerophilic gram-negative flora.
• Bacteria associated with adult periodontitis include Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia.
• Periodontal disease can be localized or a component of systemic diseases like AIDS, leukemia, Crohn's disease, diabetes, Down syndrome, sarcoidosis, and neutrophil defects.
• Periodontal infections can lead to infective endocarditis and abscesses in the lungs and brain.

Aphthous Ulcers (Canker Sores)

• Aphthous ulcers are common, recurrent, and painful.
• Up to 40% of the population is affected, mostly during the first two decades of life.
• Immunologic disorders such as celiac disease, inflammatory bowel disease, and Behçet's disease can be associated with aphthous ulcers.
• Lesions appear as single or multiple, shallow, hyperemic mucosal ulcerations with a thin exudate and erythematous rim.
• The inflammatory infiltrate is initially mononuclear, becoming neutrophil-rich with secondary infection.
• Lesions typically resolve in 7 to 10 days but may persist longer in immunocompromised patients.

Fibrous Proliferative Lesions

• Irritation fibroma (traumatic fibroma, focal fibrous hyperplasia) is a submucosal nodule of fibrous connective tissue, usually on the buccal mucosa or gingiva.
• It is a reactive process caused by repetitive trauma.
• Treatment involves complete surgical excision.
• Pyogenic granuloma occurs on the gingiva of children, young adults, and pregnant women (pregnancy tumor).
• This exophytic inflammatory lesion is red to purple and often ulcerated.
• It is a highly vascularized proliferation of granulation tissue.
• Pyogenic granulomas can regress, mature into fibrous masses, or develop into peripheral ossifying fibroma.
• Treatment involves complete surgical excision.
• Peripheral ossifying fibroma is a common gingival growth, likely reactive rather than neoplastic.
• It can arise from pyogenic granulomas or de novo from periodontal ligament cells.
• Lesions appear as red, ulcerated, nodular growths on the gingiva.
• Peak incidence is in young females.
• Surgical excision down to the periosteum is required due to a 15% to 20% recurrence rate.
• Peripheral giant cell granuloma is an uncommon oral cavity lesion representing a reactive inflammatory process.
• Lesions may be covered by intact gingival mucosa or ulcerated.
• Histologically, they contain multinucleate giant cells in a fibroangiomatous stroma.
• Lesions are usually well delimited and easily excised.
• They need to be differentiated from central giant-cell tumors and brown tumors seen in hyperparathyroidism.

Herpes Simplex Virus Infections

• Oral herpes presents as gingivostomatitis in children, pharyngitis in adults, and chronic mucocutaneous infection in immunocompromised patients.
• Most orofacial herpetic infections are caused by herpes simplex virus type 1 (HSV-1).
• Primary infections in children (2-4 years old) may present as acute herpetic gingivostomatitis with vesicles and ulcerations of the oral mucosa, lymphadenopathy, fever, and anorexia.
• Acute herpes pharyngitis is common and may recur in adults.
• Herpes vesicles rupture to become painful, red-rimmed, shallow ulcerations.
• Intracellular edema and acantholysis create vesicles.
• Microscopic examination shows eosinophilic intranuclear viral inclusions or multinucleate giant cells (Tzanck test).
• Vesicles and ulcers clear in 3 to 4 weeks, but the virus becomes latent in local ganglia (e.g., trigeminal ganglion).
• Reactivation of latent HSV causes recurrent herpetic stomatitis, associated with trauma, allergies, UV light, upper respiratory infection, pregnancy, menstruation, immunosuppression, and temperature extremes.
• Recurrent herpetic stomatitis appears as small vesicles on the lips (herpes labialis), nasal orifices, buccal mucosa, gingiva, and hard palate.
• Lesions resolve in 7 to 10 days but may persist in immunocompromised patients, requiring antiviral therapy.
• Other viral infections in the oral cavity include herpes zoster, Epstein-Barr virus (EBV), cytomegalovirus, enterovirus, and rubeola (measles).

Oral Candidiasis (Thrush)

• Candida albicans is a normal component of the oral flora in about 50% of the population and is the most common fungal infection of the oral cavity.
• Factors influencing infection include the strain of C. albicans, oral microbiome composition, and immune status.
• Oral candidiasis can be pseudomembranous, erythematous, or hyperplastic.
• Pseudomembranous form (thrush) is characterized by a superficial, gray to white inflammatory membrane that can be scraped off, revealing an erythematous base.
• Infection remains superficial except in immunosuppressed individuals (organ transplants, neutropenia, chemotherapy, AIDS, or diabetes).
• Broad-spectrum antibiotics can promote thrush by altering normal bacterial flora.

Deep Fungal Infections

• Deep fungal infections, like histoplasmosis, blastomycosis, coccidioidomycosis, cryptococcosis, zygomycosis, and aspergillosis, can affect the oral cavity, head, and neck.
• The incidence of oral fungal infections has increased with the growing number of immunocompromised patients (AIDS, cancer therapies, organ transplantation).

Hairy Leukoplakia

• Hairy leukoplakia is an oral lesion on the lateral border of the tongue caused by EBV, usually in immunocompromised patients.
• In HIV-infected patients, it may indicate the development of AIDS.
• Lesions are white, confluent patches of fluffy, hyperkeratotic thickenings on the lateral tongue.
• The lesion cannot be scraped off, unlike thrush.
• Microscopic appearance includes hyperparakeratosis and acanthosis with "balloon cells" in the upper spinous layer.
• EBV RNA transcripts and proteins are detectable in the lesional cells.
• Superimposed candidal infection can add to the "hairiness."

Leukoplakia and Erythroplakia

• Leukoplakia is a white patch or plaque that cannot be scraped off and cannot be characterized as any other disease.
• Approximately 3% of the world's population have leukoplakia; 5% to 25% of these lesions are premalignant.
• All leukoplakias should be considered precancerous until proven otherwise.
• Erythroplakia is a red, velvety, possibly eroded area within the oral cavity.
• The risk of malignant transformation is much higher than with leukoplakia.
• Speckled leukoerythroplakia are intermediate forms with characteristics of both leukoplakia and erythroplakia.
• Leukoplakia and erythroplakia are usually found in persons 40 to 70 years of age, with a 2:1 male preponderance.
• Tobacco use is a common factor.
• Leukoplakia may occur anywhere in the oral cavity (favored locations are buccal mucosa, floor of the mouth, ventral surface of the tongue, palate, and gingiva).
• Leukoplakia appears as solitary or multiple white patches or plaques, often with sharply demarcated borders.
• Histologic examination shows epithelial changes ranging from hyperkeratosis to markedly dysplastic changes.
• Histologic changes in erythroplakia rarely demonstrate orderly epidermal maturation; most display severe dysplasia, carcinoma in situ, or minimally invasive carcinoma.
• An intense subepithelial inflammatory reaction with vascular dilation contributes to the reddish appearance.