• Check Development of face and palate for CLEFT LIP AND PALATE.

I] Diseases Involving teeth:

A. Dental caries
• Streptococcus Viridans (mutans) produces acid (erodes enamel and exposes dentine) via sucrose fermentation.
• Fluoride prevents dental caries.
• Gingivitis - Soft tissue in ammation of the squamous mucosa and soft tissues around teeth, with erythema,
edema, bleeding, and gingival degeneration can also be present.

B. Periodontitis
• In ammation of tooth-supporting structures (e.g., periodontal ligaments, alveolar bone, and cementum)
leading to tooth loss.
• Periodontal infections can also lead to systemic diseases (e.g., infective endocarditis and lung, brain abscesses).
• Actinobacillus is MCC.

II] Inflammatory disorders

A. APHTHOUS ULCER (Canker Sores)
• Painful, super cial ulceration of the oral mucosa.
• Arises in relation to stress and resolves spontaneously, but often recurs.
• Characterized by a grayish base surrounded by erythema.

B. Fibrous Proliferative Lesions

1. Irritation bromas occur along the bite line; nodules of brous tissue are covered by squamous mucosa.
2. Pyogenic granulomas are rapidly growing, highly vascular lesions similar to granulation tissue. Common in
children or during pregnancy, they can regress (particularly after pregnancy).

Irritation
fibroma

Pyogeni Granuloma
C. BEHÇET SYNDROME
• Recurrent triad of aphthous ulcers, genital ulcers, and uveitis.
• Due to immune complex vasculitis involving small vessels.
• Can be seen after viral infection, but etiology is unknown.

III] Infections
A) HERPES SIMPLEX VIRUS INFECTIONS
• Vesicles involving oral mucosa that rupture,
resulting in shallow, painful, red ulcers
• Usually due to HSV-1
• Primary infection occurs in childhood;
lesions heal, but virus remains dormant in ganglia of the trigeminal nerve.
• Stress and sunlight cause reactivation of the virus, leading to vesicles that often arise on the lips (cold sore).
• Cowdry type A intranuclear inclusion bodies seen, with multinucleate polykaryons.

B) Oral Candidiasis (Thrush)

• Candida albicans is part of the normal oral ora in 50% individuals
• MCC of oral fungal infection.
• Present as super cial greyish white in ammatory pseudomembrane, that is easily
scraped away, to reveal a granular, erythematous lesion.
• Fibrinosuppurative exudates with fungus - patient complains of bad taste in mouth.
• It occurs in the setting of broadspectrum antibiotics, diabetes or immunode ciency.

C) Hairy Leukoplakia
• Hairy leukoplakia is seen on tongue lateral borders.
• Caused by Epstein-Barr virus (EBV), and is not premalignant.
• Associated with immunocompromised patients (80% are HIV infected).

Hairy leucoplakia Erytheoplakia

Leucoplakia
IV] PRECANCEROUS AND CANCEROUS LESIONS

A) Leukoplakia and Erythroplakia

Tobacco use is the most common antecedent.
• Leukoplakia is a white plaque on the oral mucosa that cannot be removed by scraping and cannot be classi ed
as another disease entity. It can either be benign epithelial thickenings or highly atypical dysplasia with pre-
malignancy.
• Erythroplakia is a red, velvety, vascularised leukoplakia with a greater risk of malignant transformation.
• Erythroplakia and leukoplakia are often biopsied to rule out carcinoma.

B) SQUAMOUS CELL CARCINOMA

Malignant neoplasm of squamous cells lining the oral mucosa
Importance - Approximately 95% of cancers of the head and neck are SCCs, with the remainder largely consisting of
adenocarcinomas of salivary gland origin.
• Tobacco (chewing & snoking), alcohol, betel nut chewing, paan are major risk factors.
• Floor of mouth is the most common location.
• Oral leukoplakia and erythroplakia are precursor lesions.
• In the oropharynx, as many as 80% of SCCs, particularly those involving the tonsils, the base of the tongue, and
the pharynx, harbor oncogenic variants of HPV, particularly HPV-16.

Plotre