Orofacial Granulomatosis

erable intercellular oedema and infiltration of the spongiform spaces by neutrophils, especially in the presence of gross dental plaque and calculus deposits. Many lymphocytes and plasma cells are present in the inflammatory infiltrate and dense, basophilic, granular deposits of extracellular immunoglobulin are common. Russell bodies may be a conspicuous feature. There is variable loss of collagen in areas of severe inflammation. However, in younger patients especially, there may be a prolif-erative response with extensive formation of new fibrous tissue leading to localised areas of fibrous hyperplasia. The enlarged gingiva may prevent effective cleaning of the related tooth, predisposing to further plaque accumulation and progressive inflammation. This type of localised inflammatory gingival hyperplasia is seen much more frequently on the buccal or labial aspects of the gingiva than in the palatal or lingual areas. Such overgrowths, although frequently removed as part of a gin-givectomy procedure are not commonly sent for histo-logical examination.

no bearing on the likely behaviour. Osseous metaplasia and dystrophic calcification may be present, usually in the middle or deeper aspects of the lesion.

Giant cell epulis is indistinguishable microscopically from central giant cell granuloma and the brown tumour of hyperparathyroidism. Radiographs should be taken to exclude the possibility of a central bone lesion. If such a lesion is detected, hyperparathyroidism is excluded by assessing serum calcium, phosphate and alkaline phosphatase and measuring parathormone levels if necessary.

Treatment is usually by conservative surgical excision with curettage of the underlying bone, but about 10% of cases recur. Some cases in children have been treated by daily administration of calcitonin, delivered either by subcutaneous injections or nasal spray for up to 1 year. Although the treatment is protracted it appears to be effective [96].

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