Tongue

بِسْمِ اللهِ الرَّحْمنِ الرَّحِيم

Surgery of the TongueLECTURE (1)


The oral cavity Extends from the skin–vermilion border of the lips ant. to the junction of the soft palate sup. & the line of circumvallate papillae on the junction of the post. 1/3 and ant. 2/3of tongue posteriorly


AGLOSSIA= absence. Frequent with other congenital or developmental defects (limb and other cranio-facial defects). CLEFT or BIFID TONGUE failure of fusion of 2 lingual processes

DEVELOPMENTAL ANOMALIES OF TONGUE

TONGUE TIE(ANKYLOGLOSSIA): short thick lingual frenum . Presentations 1. Impairment of tongue movements 2.Malocclusion, swallowing & speech defects. Treatment by division of frenum near floor of mouth (LA,GA) best at 3 years age

Congenital syphilis

CONGENITAL FISSURED TONGUE (FURROWING): The surface of the tongue furrowed with a deep median fissure & many shorter fissures run transversely from a median groove unlike syphilis which are longitudinal. This sometimes get infected by candida albicans resulting in median rhomboid glossitis. 
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GEOGRAPHIC TONGUE or benign migratory glossitis : It is a benign condition common in patients with cong. heart dis or acute GIT problems as alternating red & yellowish-white areas due to alternating hypertrophy / atrophy of filiform papillae of unknown etiology Treatment : proper tongue hygiene. Black hairy tongue (or lingua villosa nigra) is a painless benign disorder of unclear etiology


LINGUAL THYROID It is a red lobulated mass behind F.C Treatment : excision after mTC99 scan to confirm presence of normal thyroid gland.

Median rhomboid glossitis smooth, oval- or diamond-shaped nodule on the dorsum of the tongue just ant.to the circumvallate papillae. Treatment antifungals or surgical removal of the hyperplastic tissue.

TONGUE INJURIES

CAUSES: 1.Tongue biting (commonest) e.g. epileptics. 2. Associated with jaw # following road traffic accidents. Bleeding occurs due to lingual vessels injury Why serious especially in unconscious? Tongue hematoma can cause airway obstruction If laceration serious or delayed bleeding. Treatment: 1.Arrest bleeding using pressure by hooking the tongue forwards with a finger & compressing it against mandible. 2. Laceration can be sutured in operating room under GA to estimate its depth & avoid the risk of dehiscence. 3. Big tongue Hematoma if obstructs airways may require tracheotomy. .

TONGUE ULCERS: (commonest lesions )

1-TRAUMATIC ULCERS: DENTAL ULCER Etiology repeated trauma by carious ,broken or ill-fitted denture. Site At tongue side near the site of irritation. Clinically Acute :Painful oval-round ulcers with granulating floor , soft base & sloping margin +/- enlargement of draining LN Chronic : ulcer edge is raised & indurated base + LN enlargement so biopsy is indicated to rule out ca. Treatment: Removal of cause & antiseptic mouth wash.


2-INFLAMMATORY ULCERS: A. IDIOPATHIC APHTHOUS ULCERS (dyspeptic) -Most common lesion . -Recurrent, very painful ulceration / healing -Etiology: ??, nutritional deficiencies, stress, viral TYPES 1)Minor 2)Major 3)Herpetiform B. Oral LICHEN PLANUS Dermatologic disorder ?? due to autoimmune /HIV Ulcers + hyperkeratotic whitish tongue lesions C. HERPETIC ULCERS( herpes simplex type 1). Recurrent painless self limiting multiple small ulcers in children preceded by blisters at tip of tongue D.TUBERCULOUS E. SYPHILITIC (snail track / gummatous ulcers) F. CHRONIC SUPERFICIAL GLOSSITIS 3-NEOPLASTIC ULCERS: A- S.C.C (most common)B-Lymphoma



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Pre-malignant lesions ( not present in majority of cases) High-risk lesions Erythroplakia Speckled erythroplakia Chronic hyperplastic candidiasisMedium-risk lesions Oral submucous fibrosis Syphilitic glossitis Sideropenic dysphagia (Paterson–Kelly syndrome)Low-risk/equivocal-risk lesions Oral lichen planus Discoid lupus erythematosus Discoid keratosis congenita Oral cancer


Potential for malignant change:• With age usually >60 years; & age of the lesion;• With chronic irritation 7 S (Smoking or tobacco chewing, Sharp tooth, chronic dental Sepsis, Syphilis, Spirits, Spices & Snuffing) . • anatomical site of the pre-malignant lesion like leukoplakia is risky on the floor of the mouth &ventral surface of tongue in younger women, even in the absence of associated risk factors.

FIELD CHANGE AND SECOND PRIMARY TUMOURS

Diffuse exposure to irritation leads to a separate tumors at different sites. Presentations eitherSimultaneously or within 6 months (synchronous 25%. ) where patients that develop first tumour in the oral cavity & oropharynx are likely to develop a 2nd primary tumour in the upper oesophagus. OrMay be delayed within the first 2 years of initial presentation (metachronous 75% ). i.e field change or ‘cancerisation’.

Premalignant conditions CLINICAL FEATURES

Leucoplakia White hyperkeratotic patches or plaque that cannot be characterized clinically or pathologically. Size variable small, well-circumscribed, homogenous white plaque to an extensive large surface areas . May be smooth or wrinkled, fissured and vary in colour depending on the thickness giving appearance of white paint coated tongue that can not be rubbed off Speckled leucoplakia Variation of leucoplakia on erythematous base Has a highest rate of malignant transformation Erythroplakia Bright red plaque which cannot be characterized clinically or pathologically Are irregular in outline and separated from nearby normal mucosa The surfaces may be nodular. They occasionally coexist with leucoplakia.

Sideropenia (iron deficiency without anaemia) predisposes to ca. due to epith. Atrophy so oral mucosa exposed to irritation . Management treat sideropenia with iron to reduce epithelial atrophy and risk of ca.
Sideropenic dysphagia (Plummer–Vincent/Paterson–Kelly syndrome) Oral submucous fibrosis Associated with smoking , use of spicy nuts or alcohol. (only Asians) A progressive epithelial fibrosis , atrophy + epithelial hyperplasia / dysplasia with fibrous bands beneath the oral mucosa scarring , contracture, limited mouth opening & restricted tongue movement. Treatment of restricted mouth opening by either intralesional steroids or excision and skin grafts.

Chronic hyperplastic candidiasis

Dense plaques of leucoplakia, around commissures of mouth. May extend on to the vermilion or facial skin Have high incidence of malignant transformation, due to invasion by C. Candida in immune deficient Management :prolonged (6 weeks) topical or systemic anti-fungal (2 weeks). If the lesions persist surgical excision or laser


PATHOLOGY of oral cancer: Main sites : the floor of the mouth, the lateral border of the anterior tongue and the retromolar trigone: GROSS TYPES: 1-Malignant ulcer: deep irregular necrotic floor, raised everted or rolled edge& hard red indurated base. 2-Raised oval white plaque that fungates as cauliflower-like mass +central necrosis .(commonest) 3-Hard sub mucous nodule (less common) 4-Deep indurated chronic fissure that does not heal. 5-Diffuse infiltrative wooden base i.e frozen tongue (rare) MICROSCOPIC TYPES: 1-Ant. 2/3 well differentiated squamous cell ca. > 95%. 2-Post 1/3 ca are less differentiated 3-Basal cell ca & adenoca of minor salivary glands (rare)

SPREAD: CA in situ=no invasion to BM + no spread. 1- Direct (local) spread : Ca ant 2/3 invades lat. then to floor of mouth then to mandible. Post 1/3 ca invades tonsils, pharynx & larynx.. Fascial planes& periosteum act as barriers to direct spread 2-Lymphatic spread: occurs early with 30% clinical / subclinical *Ca. tip of tongue drains bilaterally to submental LN. *Ca. ant.2/3 to ipsilateral SMD& then to DCLN.. * Ca. post 1/3 drains bilaterally to upper DCLN. 3-Blood spread: very rare& occurs in post 1/3 ca & correlates with distant metastases (bad prognosis) 4-Perineural invasion (bad prognosis)


Main clinical features of oral cancer■ Elderly, males +/- risk factors .■ Persistent oral swelling or mouth ulceration for > 4 weeks■ Painless unless deeply invasive (sore tongue)■ Difficulty swallowing■ Jaw or facial swelling■ Painless palpable submandibular or jugular L. nodes . ■ Unexplained tooth mobility■ Trismus ■ Fixation of tongue (Ankyloglossia)

Complications 1-Inhalation of necrotic tissues bronchpneumonia. 2-Combined cancer cachexia & starvation due to pain & dysphagia. 3-Bleeding due to erosion of lingual vessels& erosion of ICA in post 1/3 tumors. 4-Asphyxia due to enlarged fixed LN or due to glottic edema.