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Peripheral giant cell granuloma is, for all practical purposes, a site-specific variant of pyogenic granuloma embedded with osteoclast-like multinucleated giant cells and arising exclusively from the periodontal ligament enclosing the root of a tooth. This unique origin, of course, means that such a lesion can only be found within or upon the gingiva or alveolar ridge, no other site is acceptable. Called variously giant cell reparative granuloma, osteoclastoma, giant cell epulis, and myeloid epulis, this lesion was first reported as fungus flesh in 1848. Almost half of all cases have lesional cells containing surface receptors for estrogen and this has led to speculation that some peripheral giant cell granulomas are responsive to hormonal influences.
The usual age at diagnosis is the fourth through sixth decades, but there is no marked age predilection. More than 60% of cases occur in females and this female predilection is more pronounced in the older age groups.
Individual lesions are nodular and
pedunculated, frequently with an ulcerated surface, and frequently with a
red, brown or bluish hue (Figures 1 & 2). Generally larger than pyogenic granuloma,
the lesion may exceed 4 cm. in size, but most lesions remain less than 2
cm. in diameter. Any alveolar region may be affected and
radiographs may show either a saucerization of underlying bone, periodontitis
of underlying tissues, or an isthmus of soft tissue connecting to an intraosseous
central giant cell granuloma.
Pathology and Differential Diagnosis
The peripheral giant cell granuloma is comprised of an unencapsulated aggregation of rather primitive but uniform mesenchymal cells with oval, pale nuclei and with a moderate amount of eosinophilic cytoplasm. Mitotic activity is not unusual in the lesion and may even be pronounced in lesions developing in children and adolescents. Mitotic activity within the giant cells is, however, not seen and if present should be considered to be a sign of sarcomatous change.
Stromal cells may be spindled with a background of collagenic fibers, or may be rounded with a less fibrotic background. There may be occasional chronic inflammatory cells admixed with the mesenchymal cells or within surrounding fibrovascular tissues. A thin band of routine fibrovascular tissue separates the lesion from the overlying epithelium, often with dilated veins and capillaries. When surface ulceration is present, the ulcer bed consists of routine fibrinoid necrotic debris over granulation tissue.
Admixed throughout the stroma are numerous osteoclast-like multinucleated giant cells containing varying numbers of pale vesicular nuclei similar to those within the surrounding stromal cells (Figures 3-5). These cells have eosinophilic cytoplasm, which electron microscopy has shown to contain large numbers of mitochondria. Immunohistochemistry has shown the giant cells to be only slightly different from true osteoclasts. The origin of the multinucleated cells is still unknown, but they are assumed to arise from syncytial fusion of mononuclear preosteoclasts of bone marrow origin.
Blood vessels within the lesional stroma show plump endothelial cell nuclei and scattered extravasation of erythrocytes is commonly seen. Hemosiderin deposition may be seen in areas of old hemorrhage. Metaplastic or osteoblastic new bone formation may be seen, usually in the lower third of the lesion. Dystrophic calcification may be present as well.
Occasional lesions show an admixture of tissue types compatible with peripheral giant cell granuloma, peripheral ossifying fibroma and pyogenic granuloma, presumably because of the common pathoetiology of these lesions. Such lesions are traditionally diagnosed according to the dominant tissue type.
Peripheral giant cell granuloma can be differentiated from osteoblastic
osteosarcoma by the uniformity of the stromal cells and by the lack
of dysplasia in these cells. In young persons, however, numerous mitotic
figures and active proliferation of stromal cells may make this distinction
difficult. Peripheral giant cell granuloma may be indistinguishable from
the rare extraosseous brown tumor of hyperparathyroidism.
Treatment and Prognosis
Peripheral giant cell granuloma
is treated by conservative surgical excision followed by curettage of any
underlying bony defect and careful scaling and root planing of associated
teeth. A recurrence rate of 10% or more has been reported,
hence, re-excision may be necessary. Very large or recurring lesions may
represent brown tumors of hyperparathyroidism and will require treatment
of the underlying endocrine dysfunction prior to surgical
References (Chronologic Order)
Note: General references can be found by clicking on that topic to the left.
Tomes J. A course of lectures on dental physiology and surgery (lectures I-XV). Am J Dent Sc 1846-48; 7:1-68, 121-134; 8:33-54, 120-147, 313-350.
Giansanti JS, Waldron CA. Peripheral giant cell granuloma: review of 720 cases. J Oral Surg 1969; 17:787-791.
Sapp JP. Ultrastructure and histogenesis of peripheral giant cell reparative granuloma of the jaws. Cancer 1972; 30:119-129.
Katsikeris N, Kakarantza-Angelopoulou E, Angelopoulos AP. Peripheral giant cell granuloma: clinicopathologic study of 224 new cases and review of 959 reported cases. Int J Oral Maxillofac Surg 1988; 17:94-99.
Smith BR, Fowler CB, Svane TJ. Primary hyperparathyroidism presenting as a "peripheral" giant cell granuloma. J Oral Maxillofac Surg 1988; 46:65-69.
Whitaker SB, Bouquot JE. Identification and semi-quantification of estrogen and progesterone receptors in peripheral giant cell lesions of the jaws. J Perio 1994; 65:280-283.
Bodner L, Peist M, Gatot A, Fliss DM. Growth potential of peripheral
giant cell granuloma. Oral Surg Oral Med Oral Pathol Oral Radiol Endodont 1997; 83:548-551.
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