The oral cavity
It’s lined by mucous membrane which is pink in colour non-keratinizing stratified squamous epithelia contain taste buds and minor salivary glands.
Anatomy
Posteriorly: separated from the oropharynx by the ant. Pillar of the tonsil laterally, the junction of the hard and soft palate above, and the line of the circumvalate papillae bellow.
anteriorly:  the junction of the mucosa & vermillion border with the skin of the lips.
Retromolar trigone: is the mucosal area covering the ascending ramus of the mandible, its triangular in shape the base is the posterior surface of the last lower molar tooth and the apex is the maxillary tuberosity.
Inferiorly: the junction of the ant. 2/3 and the posterior 1/3 of the tongue.
Superiorly: the junction of the hard palate and soft palate.
Sensory nerve supply:                                                       
ant.2/3 tongue:
Gen. sensation: V (V3) via lingual nerve. Taste VII via chorda tympani.
Post. 1/3: IX (gen. sensation +taste).
Roof: gen. sensation V (V2)

I. Congenital conditions of the oral cavity:
A.	Cleft lip and palate.
B.	Congenital abnormalities of the jaws e.g./Pierre Robin syndrome.
C.	Mucosal abnormalities:
1.	Dyskeratosis congenita: it’s a rare congenital abnormality resulting in dyskeratotic white patches in the mouth also associated with abnormalities of the skin, nails, cornea, and hairs (which may be absent).
2.	Fodyces spots: it’s an atopic sebaceous glands in the buccal and labial mucosa which is small yellowish lesions of no significance.
3.	White sponge naevus: it’s an autosomal dominant disease , the lesion is a raised whitish lesion of no significance.
4.	Hereditary hemorrhagic telangeiectasia(Osler-Weber disease): it’s an autosomal dominant disease present in the lip and oral mucosa.
D.	Congenital lesions of the tongue: 
1.	Macroglossia: occurs in : -congenital diseases e.g./Down syndrome, Cretinism, Beckwith’s syndrome.  –non congenital e.g./lymphangioma, amyloidosis, acromegaly.
2.	Ankylossia (tongue tie): it occurs due to short lingual frenulum and is rarely severe enough to affect suckling or later speech, treated by horizontal incision and vertical repair.
3.	Median rhomboid glossitis: it’s of no significance flat pink area on the dorsum of the tongue anterior to the circumvalate papillae and is devoid of papillae.
4.	Lingual thyroid: part or the whole of the thyroid tissue will stay in the foramen cecum (in the midline of the posterior 1/3 of the tongue) as a soft tissue mass. It’s important to remember that it may be the only thyroid tissue in the body and may be a site of a thyroid neoplasm.

II. stomatitis and oral ulcerations:
A.	 Oral manifestations of systemic diseases:
1.	Hematological diseases:
a.	Agranulocytosis: it may be due to drug hypersensitivity e.g./ sulphonamides, chloramphinicol, carbimazole, isoniazide. Or a normal response to (bleomycin, methotixate). It causes acute ulcers and sloughing in the oral cavity.
b.	Acute leukemia: ulcers and bleeding from the gingiva.
c.	AIDS: causes hairy leukoplakia, oral candidiasis, herpetic stomatitis, and Kaposi sarcoma.
2.	Acute exanthemas:
a.	Chicken pox--------→ vesicles.
b.	Acute streptococcal tonsillitis-----→ strawberry tongue.
c.	Measles -------→ Kopliks spots.
d.	Glandular fever-----→ petechial rash on the hard palate.
3.	Drug reactions: 
a.	Agranulocytosis.
b.	Gingival hyperplasia (phenytoin).
c.	Gingivitis (gold).
d.	Agranulocytosis and erythema multiformi (penicillin, sulphonamides, and barbiturates).
4.	Vitamin deficiency:
a.	Vit-C → gingivitis.
b.	Iron, folate, B12 → glossitis.
c.	B2 (riboflavin) and nicotinic acid → angular Cheilitis and glossitis.
5.	Auto-immune diseases: 
a.	chronic lupus and SLE →vesicular and ulcerative lesions.
b.	Scleroderma and PAN (poly arteritis nodosa) →ulceration.
c.	Sjorgren’s syndrome and rheumatoid arthritis→xerostomia.
d.	Behget’s disease, pemphigus, pemphigoid→ulceration.

B.	Oral pigmentations:
1.	Normal in black people.
2.	Haemochromatosis, Al bright’s disease, Peutz-Jegher syndrome.
3.	Von-Recklinghausen’s disease, Addison’s disease, melanoma.
4.	Mercury, bismuth, and lead poisoning.
C.	Infections:
a.	Viral:
1.	Primary herpetic gingivostomatitis: its caused by herpes simplex  virus frequently affecting children and adults not exposed to the virus before. Clinically the patient had fever, malaise, vesicular lesions 2-4 mm in size which breaks forming ulcers with yellowish base and erythematous halo, it last’s 1-2 weeks. Diagnosis is by identifying the virus in the smear or culture or by exfoliative cytology. Note: recurrent oral herpes is very unusual while herpes labialis (cold sore) is very common. 
2.	Herpes zoster: the virus affect the Vth CN leading to intraoral lesions which are always unilateral often painful may be associated with cervical lymph nodes and sometimes VIIth CN palsy (Ramsey hunt syndrome).
3.	Hand foot mouth disease: caused by group A coxsackie virus mostly occurs in epidemics in children the incubation period is 1 week and it last about 1 week. The patient is feverish with malaise, with vesicles on the hand, feet, buttocks, and mouth and later ulcers.
4.	Herpangina: it occurs mainly in children and caused by different viruses (Coxsackie, ECHO, human orphan viruses). It’s similar to herpes simplex but the lesions are more in the oropharynx than the oral cavity. 

b.	Bacterial infections:  
1.	Acute necrotizing gingivitis: its caused by spirochaete borrellia vincenti and anaerobic bacillus fusiformis, it affect the inter dental papillae in debilitated adults with poor dental hygiene. The patient had pain, foeter, fever, enlarged lymph nodes, ulceration, and necrotic membrane which may spread to the tonsil and nasopharynx. Treatment is by local mouth wash and systemic penicillin and flagyl (IV).
2.	Gangrenous stomatitis (cancrum oris): caused by mixed bacteria and affect debilitated children with rapidly enlarging ulcer and necrosis in the oral cavity and upper and lower jaws. Treatment is by oral hygiene and IV penicillin and flagyl.
3.	Syphilis:  caused by spirochaete treponema pallidum (discussed elsewhere).primary stage→ chancre. Secondary stage→ snail-truck ulcers. Tertiary stage→ gumma. 
4.	TB:  it only affect the oral cavity in sputum +ve pulmonary TB leading to multiple superficial painful ulcers on the tongue and other areas.
c.	Fungal infections: 
1.	Candidiasis: its caused by candida albicans which is a normal commensal in the mouth and become pathogenic in: debilitating disease, long term antibiotic use, anticancer chemotherapy, and steroids (local or systemic). Acute type: clinically the patient had multiple small white patches when wiped off leaving painful erythematous patch. Treatment is by correcting the underlying cause and local nystatin or amphotericine. Chronic type: clinically the patient had white lesion cannot be rubbed off giving the appearance of leukoplakia (candidal leukoplakia) mainly inside the corner of the mouth. Treatment is by local or systemic antifungal (ketokonazole) may be of benefit, but excision is the only way of removing the lesion.
2.	Histoplasmosis: is due to histoplasma capsulatum causing granular looking ulcers usually in wide spread systemic Histoplasmosis. Treatment is by ketokonazole.
d.	Traumatic oral ulceration: caused by:-
1.	Hard food.
2.	Rough denture.
3.	Sharp rough dentition.
4.	Patient biting his tongue or buccal mucosa.
Note: (Quinn’s rule for stomatitis) any ulcer should heal within 2 weeks and if not it should be biopsied.
e.	Miscellaneous conditions:
1.	Aphthus ulceration: it’s a very common ulcers with unknown etiology (suggested causes: hypersensitivity reaction, hormonal, Vit. Deficiency, and stress). The patient had a single or multiple ulcers 2-10 mm in diameter and heal within 10 days (if not should be biopsied). Treatment is by local steroid to decrease inflammation and assist healing.
2.	Behget’s  syndrome: it’s of unknown etiology clinically the patient had relapsing oral and genital ulcerations, associated with uveitis, vasculitis of the skin, synovitis, and meningoencephalitis. Treatment is by oral steroids.
3.	Pemphigus vulgaris: there is bullae in the skin and oral cavity (palate, buccal mucosa, and tongue) it affect late middle age and elderly patients occur due to acantholysis of the epithelia with frequent serious relapses. Nikolisky’s sign is positive (stroke the mucous membrane will lead to vesicle or bullae formation). Treatment is by steroids.
4.	Benign mucous membrane pemphigoid: less serious than  pemphigus vulgaris resulting in chronic scaring of the conjunctiva, it causes sub-epithelial clefts affecting females with vesicles in the mucous membrane (skin lesions are rare) of the oral cavity, pharynx, larynx, and conjunctiva rupture of the vesicles causes less painful ulcers than pemphigoid also there is no acantholysis. No treatment is required sometimes steroids is used.
5.	Erythema multiformi: is of unknown etiology affecting young patients (10-30 yrs) secondary to herpes and mycoplasma infections or drugs e.g./penicillin, sulphonamides, barbiturates. Clinically the patient had nodular lesions with bluish centre, bullae, vesicles in the skin, and oral lesions more common in the major form of the disease i.e./Steven Johnson syndrome (1/4 have lesions only in the oral cavity). The disease lasts 2-3 weeks the lips are covered with hemorrhagic crusts and in Steven Johnson syndrome the patient is ill with pyrexia. Treatment is by steroids.
6.	Necrotizing sialometaplasia: uncommon ulceration of the hard palate or oropharynx. its differentiated from CA by biopsy and self limiting disease heal within few weeks.
7.	Lichen planus: there is  keratosis, parakeratosis, pointed or saw toothed rete pegs, and accumulation of fluid along the basement membrane. It’s an uncommon disease with 2-types: Reticular: slightly raised lesion with white bluish tinge and reticular pattern of striae. Erosive: erythematous painful ulcerated lesion. Biopsy done to differentiate it from CA, leukoplakia, erythroplakia. Treatment is by local steroids and observation.
8.	Leukoplakia: important precancerous white lesion with histological changes like: keratosis (accumulation of keratin), hyperkeratosis (thickening of stratum cornium). Parakeratosis (increase nucleated cells). Acanthosis (elongation of the rete pegs of stratum granulosum). The most important factor is the degree of abnormality or dyskeratosis with nuclear hyperchromatisim, nuclear pleomorphism, mitosis, and loss of the normal maturation of the cells i.e./ loss of the polarity and intercellular adherence. It vary from mild atypia to frank CA.
9.	Erythroplakia: mucosal abnormality which is erythematous due to dysplasia without keratosis. The dysplasia is severe with high malignant potential.
10.	Geographical tongue: also called migratory glossitis or erythema migrans it’s a benign condition of unknown etiology. Clinically the patient is asymptomatic with map like appearance tongue due to loss of papillae which may regress or increase. No treatment is required.
11.	Hairy tongue: coated tongue due to elongation and accumulation of keratin associated with the filiform papillae, it usually appear white in color and become black in smokers, it’s of unknown etiology. Treatment is by scraping off the keratin with a brush.
III. Benign swellings of the oral cavity: 
A.	Cysts in the mouth: 
1.	Developmental cysts: they may be midline or lateral where the maxillary and premaxillary elements fuse.
2.	Cyst associated with the teeth.
3.	Nasopalatine cyst.
4.	Cyst and tumers of the jaws.
5.	 Dermoid cyst: it may be submental or in the floor of the mouth and tongue.
6.	Retention cyst or ranula: its uni. or multilocular mucous filled cyst in the floor of the mouth and classified into 2-types: 1-simple ranula which an epithelial lining and confined to the floor of the mouth.2-plunging ranula which is lined by connective tissue and it can be confined to the floor of the mouth or may extend through the mylohyoid muscle into the neck. It may arise from damaged and obstructed sublingual salivary gland and sometimes submandibular salivary gland, another theories of origin are; develop from embryonic epithelial rests, submucosal bursa, or from Dermoid cyst. 
      Clinically there is no age limit, but generally seen in children and young adults, it’s a bluish translucent cyst in the floor of the mouth on one side of the frenulum causing the frog belly appearance. Sometimes may reach large size or burst and recur. 
       Treatment by marsupialization is effective for the simple type and sometimes failed in plunging ranula because the remaining salivary tissue continue to secret mucous so is treated by marsupialization and excision of the sublingual salivary gland.

	

Saif AlDeen Adil