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108

Syphilitic Ulcers

During the rst stage of syphilis, a chancre may occur at the tip of the tongue together with enlarged submental and submandibular LNs. During the second stage, mucous patches and snail track ulcers are present on the tongue (multiple and yellowish white) associated with Hutchinson’s warts or condylomata. A gummatous ulcer develops during the third stage of syphilis, at the midline of the dorsum of the tongue. It is painless and single, with clear-cut edges and a wash-leather oor. Leukoplakia of diffuse brosis may also be present.

Chronic Supercial Glossitis

Chronic supercial glossitis may be associated with chronic repeated nonspecic ulcers, usually on the dorsum of the tongue. Ulcers are supercial, small, and painful. They are associated with ssures or vesicles and have a unilateral distribution. Untreated chronic supercial glossitis may lead to leukoplakia, erythroplakia, or overt squamous cell carcinoma (SCC). Treatment includes avoiding the predisposing factors, mouth gargles, close follow-up, and biopsy of any developing lesions.

5.3.1.3 Dyspeptic (Aphthous) Ulcers

A dyspeptic or aphthous ulcer represents the commonest type of ulcer of the oral cavity. They occur in patients with dyspepsia and are characterized by their short history and painful erosions at the tip (Fig.5.1) and sides of the tongue and inner sides of the lips (Fig. 5.2) and cheeks (Fig.5.3). Ulcers are small, multiple, with a whitish oor, hyperemic margins, a sloping edge, and a soft base. The regional LNs are not enlarged.

A. Eweida

Fig. 5.1 An aphthous ulcer at the tip of the tongue

Fig. 5.2 Multiple aphthous ulcers at the inner side of the

lower lip

5.3.1.4 Malignant Ulcers

Malignant ulcers of the oral cavity are most commonly SCCs (epitheliomas) but may be lymphoepitheliomas (in the posterior one-third of the tongue), salivary adenocarcinoma (from minor salivary glands), or, rarely, basal cell car-

t.me/Dr_Mouayyad_AlbtousH

Fig. 5.3 An aphthous ulcer at the inner aspect of the left cheek

5 Surgery oftheOral Cavity

Fig. 5.4 A neglected epitheliomatous ulcer at the side of the anterior two-thirds of the tongue in a 73-year-old gentleman. The large size and everted edge of the ulcer should be noted

cinoma (BCC) or melanoma. An epitheliomatous ulcer usually affects the tongue (Fig.5.4) and lips (Fig.5.5). It is characterized by a raised nodular everted edge, a necrotic oor that bleeds easily on touch, and a hard indurated base. The commonest site is the anterior two-thirds of the tongue. Regional LNs are usually enlarged and hard and are either mobile or xed according to the stage of the disease. There may also be inltration of deeper tissues, including the bone, in neglected cases.

For more details, look below “Neoplastic Lesions of the Oral Cavity.” The differential diagnosis of tongue ulcers is summarized in Table5.3.

109

Fig. 5.5 A neglected epitheliomatous ulcer at the side of the lower lip (reaching the corner of the mouth) in a 62-year-old gentleman. The large size, everted edge, and necrotic oor of the ulcer should be noted

Table 5.3 Differential diagnosis of ulcers of the tongue

Point of difference

Site Side of the

Number Single Multiple Single Single Single or

Pain ++ +++ + ++ +

Teeth Sepsis ± ± Ragged ± Edges Everted Sloping Sloping Sloping Undermined Punched

Base Indurated Soft Firm,

Floor Tumor Whitish Yellowish Wash-

Enlarged LNs

LNs lymph nodes

Malignant ulcer

tongue

Dyspeptic (aphthous)

Dorsal and undersurface

− − −

Frenular (pertussis)

Undersurface and frenulum

Dental (traumatic) Tuberculosis Syphilitic

Side of the anterior two-thirds

granulation tissue

Tip or back of the tongue

multiple

Soft ± brotic

+ +

Midline of the dorsum

Single

−

out

leather

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110

A. Eweida

5.4 Neoplastic Lesions

oftheOral Cavity

5.4.1 Classication

Neoplastic lesions affecting the oral cavity are summarized according to their tissue of origin in Table5.4.

5.4.1.1 Benign Tumors

Fibroepithelial Polyps

A broepithelial polyp presents as a rm swelling (brous tissue) on the inside of the cheek. It results from repeated biting or trauma.

Papilloma oftheOral Cavity

A papilloma of the oral cavity or tongue (Fig.5.6) presents as a sessile or pedunculated, pale or pink, soft and eshy swelling. It should be removed with an adequate margin of tissue and biopsied for histological diagnosis.

Mixed Salivary Tumors oftheMinor Salivary Glands

A mixed tumor of the minor salivary glands usually presents as a submucous, rounded, rm, mobile lobulated mass that increases in size with eating. It is treated by simple excision.

Lingual Thyroid

Lingual thyroid tissue presents as a mass at the dorsum of the tongue. It may cause respiratory obstruction and hemorrhage.

Hemangioma

Pathology

An infantile hemangioma is the most common tumor in infancy and occurs in approximately 10% of the population. Risk factors include female gender, prematurity, low birth weight, and fair skin [21]. Unlike vascular malformations, hemangiomas are real tumors arising from the rapidly dividing endothelial cells. The two main types of hemangiomas are “infantile” and “congenital”. The rare “congenital” hemangioma is less understood and presents at birth. Infantile hemangiomas present shortly after birth most often as a welldemarcated, at, and erythematous red patch. At this stage, hemangiomas may be confused with other red lesions of birth, but rapid proliferation and vertical growth trigger diagnosis.

Hemangiomas grow in three phases: proliferation, quiescence, and involution. About 80% of proliferation occurs by 3months of life. Relative ischemia of the tumors due to rapid growth at this phase can lead to necrosis, ulceration, and eventual bleeding [22]. Involution of 50%, 70%, and 90% of hemangiomas occurs by 5, 7, and 9years of age, respectively [23].

Clinical Presentation

Head and neck hemangiomas frequently coincide with the distribution of the trigeminal nerve. Hemangioma of the oral cavity or the tongue is rather uncommon; however, a beard-like facial distribution is usually associated with a subglottic hemangioma [24]. A child presenting with

Table 5.4 Classication of the tongue and oor of mouth neoplasms according to their origin

Origin Benign tumors (BTs) Malignant tumors (MTs) Epithelial Papilloma – Epithelioma (SSC)

– Lymphoepithelioma – Adenocarcinoma – Basal cell carcinoma (BCC)

Mesenchymal – Hemangioma

– Neurobroma – Fibroma

– Lipoma (extremely rare) Salivary gland Mixed salivary gland tumor Malignant salivary gland tumors Thyroid origin Lingual thyroid Malignancy in remnants of thyroid tissue

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– Hemangioendothelioma – Fibrosarcoma – Lymphoma – Rhabdomyosarcoma

5 Surgery oftheOral Cavity

Fig. 5.6 Papilloma of the tongue in an 18-year-old young gentleman. The pale color and sessile nature of the lesion should be noted

stridor and facial hemangioma should be considered to have subglottic disease until proven otherwise [12].

The diagnosis of a hemangioma mainly depends on the history and clinical examination. When in doubt, a Doppler ultrasound (US) and/or an MRI will dene the diagnosis. Watchful expectancy is usually considered in asymptomatic lesions to differentiate from other vascular malformations and reach maximum involution.

Treatment

Treatment options for symptomatic hemangiomas include systemic propranolol administration, local corticosteroid injections, laser therapy, and surgical excision with various combination protocols.

111

Fig. 5.7 Leukoplakia of the middle of the lower lip in a 67-year-old gentleman (arrow)

being the next common sites. These lesions are usually asymptomatic, but problematic lesions could be treated conservatively through avoiding local irritating factors or through conservative surgical excision. Latest techniques like laser, cryosurgery, and electrodissection cause less bleeding and are well-tolerated by patients with no adverse effects [25].

5.4.1.2 Malignant Tumors oftheOral Cavity

An estimated 263,900 new cases and 128,000 deaths from oral cavity cancer (including lip cancer) occurred in 2008 worldwide. Generally, the highest oral cavity cancer rates are found in Melanesia, South-Central Asia, and Central and Eastern Europe and the lowest in Africa, Central America, and Eastern Asia for both males and females [26].

Pyogenic Granuloma

The term is a misnomer, as the lesion has nothing to do with pyogenic infections. According to the recent ISSVA classication, pyogenic granuloma belongs to “hemangiomas” as the endothelium shows evident hyperplasia [8]. It is commonly seen on the oral mucosa as a smooth or lobulated, exophytic hemorrhagic and compressible papule. The lesion may grow rapidly in size from a few millimeters to centimeters. Due to its hyperplastic nature, it is usually friable and commonly ulcerates. Gingiva is the commonest site for occurrence of pyogenic granulomas with lateral borders of the tongue, buccal mucosa, and lips

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Predisposing Factors

1. Premalignant lesions [27]

(a) The important premalignant disease of

the tongue and oral cavity is chronic supercial glossitis, caused by the chronic irritation of syphilis, smoking, sharp tooth, spirits, spices, and sepsis (6S).

(b) Leukoplakia: This is a homogeneous,

thick, predominantly white or gray patch, which cannot be wiped away (Fig.5.7). It is a not a denite histopathological diagnosis. It is only a clinical diagnostic term of exclusion where it cannot be characterized as any other denable lesion [28].

112

A. Eweida

1978 WHO denition, it is dened as “any lesion of the oral mucosa that presents as bright red velvety plaques which cannot be characterized clinically or pathologically as any other recognizable condition.” It could occur together with leukoplakia (erythroleukoplakia). It has the highest risk among the oral potentially malignant disorders (44.9% of cases will turn malignant) [29].

(d) Lichen planus: This is a chronic inamma-

tory lesion characterized by remission and recurrences and commonly presents bilaterally as reticular plaques. Asymptomatic patients do not require treatment but

should be followed up regularly [30]. (e) Submucous brosis. (f) Benign tumors, e.g., tongue papilloma.

2. Plummer–Vinson syndrome.

3. Human papilloma virus (HPV) infection,

which is usually related to oral sexual behavior [31, 32].

4. Smoking and other smokeless tobacco

products.

5. Alcohol consumption, where smoking and

alcohol have synergistic effects [33].

Sites ontheTongue

Anterior Two-Thirds (80%)

Malignant tongue ulcers are most commonly distributed as follows: Sides of the tongue (50%), mid-dorsum (10%), tip (10%), and undersurface of the tongue (10%).

Posterior Third (20%)

Lesions at this site are usually linked to HPV infection with an increasing trend in the United States and some European countries due to change in the oral sexual behavior [34–36].

Pathology

Macroscopic Picture

– Ulcer: This has everted edges, a necrotic oor,

and a hard indurated base.

– Nodule: This is a nodule with an indurated

base.

– Cauliower-like mass: This has a bad

prognosis.

– Fissure: This is a deep often infected ssure

with surrounding induration.

– Diffuse (Woody) type: This has the worst

prognosis.

Microscopic Picture

1. Primary tumor – Squamous cell carcinoma (SCC): This is

the main variant and occurs mainly in the anterior two-thirds.

– Lymphoepithelioma: This occurs mainly

in the posterior third, owing to the intermingling of undifferentiated carcinoma cells with a prominent lymphoid stroma.

– Adenocarcinoma: This arises from the

minor glands of the tongue. – Basal cell carcinoma (BCC). – Melanoma (extremely rare). – Hemangioendothelioma. – Rhabdomyosarcoma. – Lymphoma.

2. Secondary tumor: This is rare and the primary is usually a breast cancer.

Spread

1. Direct spread: This affects the gums, mandi- ble, fauces, and glottis in addition to the soft palate and pharynx if it lies in the posterior third of the tongue.

2. Lymphatic spread: Occurs early within few weeks or months because of the rich blood and lymphatic supply of the region. Metastasis occurs mostly in order through the rst station nodes (levels I and II) and second station nodes, including levels III, IV, and V, where the central lesions are bilaterally drained [37].

3. Blood spread: This is quite rare (8–17%) and affects the lungs, liver, and bone where the probability of distant metastasis increases with respect to the stage of the disease.

Clinical Presentation

A malignant ulcer usually occurs in individuals older than 50 or 60years but may be as early as 20 or as late as 70years. Males are more affected than are females (2.2:1) [36]. A typical presentation would be:

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5 Surgery oftheOral Cavity

113

– An ulcer, a ssure, a nodule, a mass, etc. – Pain: Local or referred to the ear. The referred

otalgia could be explained according to the convergence projection theory. The signals are falsely interpreted to be emerging either from the auriculotemporal nerve of the mandibular nerve (V3) (rather than the lingual nerve) or from the tympanic branch (Jacobson’s nerve) of the glossopharyngeal nerve (IX) rather than the lingual branch of IX [38].

– Increased salivation, which may be

blood-stained.

– Fetor oris (foul oral odor) due to necrosis and

infection.

– Ankyloglossia: Limited movement with xa-

tion (no protrusion or deviation). – Severe hemorrhage. – Dysarthria (diminished articulation) due to

pain, salivation, and ankylosis. – Difculty in chewing, swallowing, or

speaking. – Lump in the neck: Cervical lymphadenopathy

may be the rst symptom, especially in poste-

rior lesions (occult primary).

Primary Tumor (T )

TX: Primary tumor cannot be assessed T0: No evidence of primary tumor Tis: Carcinoma in situ T1: Tumor ≤2cm in greatest dimension T2: Tumor >2 cm but not >4 cm in greatest

dimension

T3: Tumor >4cm in greatest dimension T4:

– T4a: Moderately advanced local disease.

The tumor invades adjacent structures (e.g., through the cortical bone [mandible or maxilla] into the deep [extrinsic] muscle of the tongue [genioglossus, hyoglossus, palatoglossus, and styloglossus], maxillary sinus, and skin of the face).

– T4b: Extremely advanced local dis-

ease. The tumor invades the masticator space, pterygoid plates, or skull base and/or encases the internal carotid artery. Note: Superficial erosion alone of the bone/tooth socket by primary gingival is not sufficient to classify a tumor as T4.

Thorough clinical examination of the oral cav-

ity for detection of the lesion and examination of the neck for LNs is mandatory. Other benign lesions should be ruled out, and suspicious lesions should be biopsied.

Complications (Terminal Events)

Neglected cases of tongue cancer may be complicated with secondary infection, aspiration pneumonia, asphyxia (due to edema of the glottis or compression of the air passages by LNs), hemorrhage (from the primary tumor or LN due to erosion of a blood vessel such as the lingual artery), starvation and cancer cachexia, and, nally, spread (local, lymphatic, hematogenous).

Staging

Oral cavity cancer is classied according to the American Joint Committee on Cancer (AJCC) TNM (tumor, node, and metastasis) system (2010) [39].

Regional Lymph Nodes (N)

NX: Regional LNs cannot be assessed N0: No regional LN metastasis N1: Metastasis in a single ipsilateral LN, ≤3cm

in greatest dimension

N2: Metastasis in a single ipsilateral LN, 3–6cm

in greatest dimension; or in multiple ipsilateral LNs, none >6cm; or in bilateral or contralateral LNs, none >6cm

– N2a: Metastasis in a single ipsilateral

LN, >3 cm but not >6 cm in greatest dimension

– N2b: Metastasis in multiple ipsilateral

LNs, none >6cm in greatest dimension

– N2c: Metastasis in bilateral or contralateral

LNs, none >6cm in greatest dimension

N3: Metastasis in an LN >6 cm in greatest

dimension

Distant Metastasis (M)

M0: No distant metastasis M1: Distant metastasis

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114

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Stage grouping of malignant tumors in the

oral cavity is listed in Table5.5.

Histological Grade (G)

GX: Grade cannot be assessed G1: Well-differentiated G2: Moderately differentiated G3: Poorly differentiated G4: Undifferentiated

Investigations

1. General laboratory tests: Complete blood picture, serum urea and creatinine, coagulation prole, blood glucose level, etc.

2. Imaging:

(a) Plain X-ray: Mandible, skull, and chest. (b) For the primary: MRI is superior to CT in

tumor staging and in dening the extrinsic and intrinsic tongue muscles.

sensitive in detecting the involved LNs but neck US is more specic in diagnosing suspicious nodes, especially if combined with US-guided ne-needle aspiration biopsy (FNAB).

3. Evaluation under anesthesia (EUA) is benecial in dening the involvement of the tumor surroundings by brosis or tumefaction. This helps in planning for the extent of surgical excision and reconstruction.

Table 5.5 Stage grouping of malignant tumors

Stage T N M 0 Tis N0 M0 I T1 N0 M0 II T2 N0 M0 III T3 N0 M0

T1 N1 M0 T2 N1 M0 T3 N1 M0

IV-A T4a N0 M0

T4a N1 M0 T4a N2 M0 T1 N2 M0 T2 N2 M0 T3 N2 M0

IV-B T4b Any N M0

Any T N3 M0

IV-C Any T Any N M1

4. Pharyngolaryngoscopy for SCC to exclude synchronous primary tumors where the incidence of synchronous second malignant tumors in the thorax is 4% [40].

5. Biopsy (excisional or incisional).

6. Metastatic workup, including a positron emission tomography (PET)/CT scan in stage III and IV disease.

Treatment

A patient with oral cancer gets the best management plan through a multidisciplinary tumor board, consisting of a head and neck surgeon, a reconstructive surgeon, a radiologist, a pathologist, a radio/chemotherapist, a prosthodontist, a phonetician, and a psychiatrist.

Surgical Treatment

This is the mainstay treatment of operable cases aiming at local disease control and in some selected inoperable (but resectable) cases as a palliative modality.

1. The primary tumor

For T1–T4a (resectable) tumors, it entails en bloc wide local excision of the tumor with an adequate safety margin of 1.5–2cm of the palpable normal mucosa (preferably through an intraoperative frozen section) with reconstruction. The extent of resection depends on tumor stage (T) and varies from wedge resection up to subtotal glossectomy in advanced tongue cancer. Partial or segmental mandibular resection may be necessary to achieve adequate tumor-free margins. The primary tumor should be marked adequately for the surgical pathologist. Reconstruction varies accordingly from simple closure or splitthickness skin grafts up to free tissue transfer (workhorse is a free radial forearm fasciocutaneous ap).

2. Neck nodes Due to the early metastatic behavior of the

tumor, a prophylactic selective supraomohyoid neck dissection (levels I–III) is recommended for clinically N0 necks. N-positive necks should be managed by ipsilateral or bilateral comprehensive neck dissection

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5 Surgery oftheOral Cavity

115

(either radical or modied radical according to the extent of invasion) [37].

Radiotherapy (RT)

1. As a denitive modality Curative treatment can be achieved for

small tumors T1–2 with N0 neck by external beam irradiation applied to the primary tumor (total dose of 66–74 Gy in fractions along 7 weeks) and to the uninvolved neck (44–64 Gy in fractions). Palliative treatment is indicated in unresectable disease and in patients unt for surgery. It is usually combined with systemic chemotherapy.

2. As adjuvant therapy Following surgical resection to the primary

site (a total dose of 60–66Gy in fractions to be started within 6weeks after surgical resection) and to the neck (60–66Gy to the involved levels and 44–64Gy to the uninvolved levels).

Note: Brachytherapy could be used instead of external beam irradiation but should be resorted to in selected cases and in specialized centers [41, 42].

Chemotherapy

1. As a denitive modality: For inoperable

patients, usually combined with RT

2. An adjuvant therapy: Usually as a single agent

+ RT in selected advanced tumors

Management ofRecurrences

Recurrences should be reevaluated and treated with curative intent if feasible. Neck disease in an untreated neck should be addressed by formal neck dissection or modication depending on the clinical situation.

Follow-Up

All patients should have regular follow-up visits to assess possible tumor recurrence, nutrition, dental health, speech, and swallowing function.

Prognosis

For many head and neck cancer sites, survival of patients with stage I disease exceeds 80%. For patients with locally advanced disease at the time

of diagnosis (i.e., stages III and IV disease), survival drops to below 40% [43].

A prognosis of oral cancer, however, is multifactorial and does not only depend on the TNM staging system, which is purely a clinical staging system. From a demographic viewpoint, prognosis of oral SCC was found to be poor for females, for patients above 40years of age, for those with comorbidities, for those of a Southeast Asian origin, for consumers of tobacco and alcohol, and for those consuming a predominantly nonvegetarian diet.

A combination of RT and surgical therapy provides a better prognosis. Patients with a tumor on the oor of the mouth, soft palate, and posterior tongue, with tumor diameter>2cm, tumor thickness>5mm, and total tumor volume>6cm3 would have poor outcome. Histologically, patients with high-grade tumors, with positive resection margins have a bad prognosis. Regarding the neck nodes, development of nodal metastases reduces survival of a patient with a small primary tumor by about 50%. The involvement of more than two cervical groups of LNs with extracapsular invasion would have a poor survival rate. Some molecular markers could also adjunct the assessment of prognosis [44]. Some studies with multivariate analyses revealed that those who were single, were a widow/widower, or were divorced/separated had a poorer prognosis than did those who were married (P=0.008). It also showed that those without religious beliefs tended to have a higher probability of death than those who held religious beliefs (P<0.001) [45].

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