Tumour spread and staging

Staging is carried out according to the TNM classification {947,2418}. Recent additions to the coding have been provided for micrometatses, isolated tumour cells, findings in sentinel nodes and tumour detection by molecular methods. Some of these are discussed in the following sections.

Local spread of oral SCC, in the early stages, is relatively predictable in tissues that have not been previously irradiated. It is influenced by local anatomical features. Lip SCC spreads superficially and then into deeper tissues. Floor of mouth SCC spreads superficially rather than in depth, being unlikely to invade into the mylohyoid muscle or the sublingual gland until a late stage. Tumour involving the lateral margin of tongue, whether arising there directly or by superficial spread from the floor of mouth, tends to spread in depth. The intrinsic muscles of tongue run in small bundles in all directions such that invading tumour encounters some muscle running at right angles to the surface. The line of least resistance to tumour spread is therefore along these muscle bundles and into the tongue. Tumours of palate spread superficially rather than in depth and this is also true for more posterior tumours of the oropharynx.

For most oral SCC other than tongue, the extent of spread in an area can be predicted from the extent of surface involvement. Tongue and tonsil tumours can spread beneath intact normal appearing surface, giving a larger area of tumour involvement. Spread of oral SCC into bone is a frequent problem. The mandible is involved much more frequently than the maxilla. In dentate jaws the usual route of entry into mandible is along the periodontal ligament. In edentulous areas of mandible the tumour spread is through the crest of the alveolus directly into the marrow spaces between trabeculae of cancellous bone {1682}. This occurs because of failure of formation of an intact cortex of alveolar bone as resorption of edentulous alveolus progresses. Tumours in the mandible can involve the inferior alveolar nerve {1683} with a particular likelihood of spread posteriorly along the nerve, sometimes extending well beyond the mandibular foramen. Cancers arising in gingiva or alveolus and those involving these sites by extension from adjacent sites are unlikely to invade into the mandible other than by periodontal ligament or the crest of edentulous alveolus. Extension into the mandible through foramina, for example the mental foramen from lip cancer, does occur, but is uncommon.

Spread in previously irradiated tissues

Tumour spread in previously irradiated soft tissues tends to be more extensive and less predictable than in normal tissues and as a consequence requires more extensive surgery if excision is attempted. Tumour invasion into irradiated mandible tends to occur wherever the tumour approaches bone, often at multiple sites {l682}.

Lymphatic spread

Spread to local lymph nodes worsens the prognosis in oral and oropharyngeal cancer. The mechanism of spread from the primary site to lymph nodes is almost always by embolism. Permeation in lymphatics adjacent to tumours is uncommon and it is debatable if this spread extends as far as lymph nodes. Once tumour is present in the neck, however, spread between nodes may be embolic or by permeation. The lymph nodes in the neck are divided into levels. The lymphatic dra-ianage from different head and neck sites is realtively predictable {1789}. Levels at high risk for metastasis from oral cavity SCC are Levels I, II and III, and to a lesser extent Level IV. Although Level II is the most frequently involved, some tumours spread to Level III or IV, with or without involvement of Level I. This has given rise to the concept of skip metastsasis. In reality the lymphatic drainage is complex and does not follow a regular sequence of lev els of involvement in many patients {2817}. Bilateral spread to the neck is likely to occur from tumours involving the midline, especially tumours of posterior tongue or soft palate. Extracapsular spread of tumour involving lymph nodes is associated with a poor prognosis {2819}.

There have been many studies attempting to predict the presence of lymphatic spread from features of the primary tumour {872,2820}. Tumour size and site are relevant. Tumour differentiation is not a reliable predictor. The pattern of the invasive front is a useful predictor in that a non-cohesive front is associated with increased likelihood of metastasis. Other factors associated with increased risk of metastasis are perineural spread at the invasive front, lymphovascualr invasion and tumour thickness. The tumour thickness is measured from the deepest tumour invasion to the presumed original surface level, that is, ignoring exophytic growth or assessing the original surface level in ulcerated tumours. For diagnostic purposes a thickness of 5mm or greater is used as indicating increased risk of nodal spread {395}.

Haematogenous spread

Until relatively recently, haematogenous spread of oral and oropharyngeal cancer has been regarded as less important than local and lymphatic spread. However, its importance is increasing as loco-regional control improves. Blood borne spread most often involves lung {754,1958}. The best predictor of the likelihood of this spread is involvement of the neck at multiple levels. This suggests that the route of entry of tumours into the circulation is most often via the large veins in the neck and that haematogenous spread is in effect tertiary spread following extracap-sular spread from neck nodes.

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