Giant cell granuloma occurs either as a peripheral exophytic lesion on the gingiva (giant cell epulis, osteoclastoma, peripheral giant cell reparative granuloma) or as a centrally located lesion within the jaw,skull, or facial bones(Figures 7-5, A, and 7-6). It was first described (by Jaffe) as central giant cell reparative granuloma.Both peripheral and central lesions are histologically similar and are considered to be examples of benign inflammatory hyperplasia in which cells with fibroblastic, osteoblastic, and osteoclastic potentials predominate. The
Peripheral giant cell granulomas are five times as common as the central lesions. Central lesions occur preferentially in the mandible, anterior to the first molar, and often cross the midline. Several large series of both peripheral and central giant cell granulomas have been reported in the literature.
The histologic structure of these lesions has been studied in detail,as have their radiographic and computed tomo-
graphic appearances(Figures 7-8 and 7-9; see also Figure 7-5, B and C, and Figures 7-6 and 7-7).
An important consideration in the management of these lesions is the necessity to search for evidence of hyperparathyroidism in all patients with histologically confirmed giant cell lesions of the jaw. There are documented examples of parathyroid lesions having been discovered as a result of blood and urine chemistry studies requested by a dentist following diagnosis of a giant cell lesion.The frequency with which this is likely to happen is probably quite low since in most series of hyperparathyroidism,lesions of the jaw have been among the last clinical manifestations of the disease to appear. Fewer than 10% of patients with hyperparathyroidism have radiographically visible cystic jaw lesions (see Figure 7-8) or even “loss of the lamina dura” (another effect of hyperparathyroidism, often used clinically to screen for the disease). Serum calcium, phosphorus, and alkaline phosphatase determinations should be requested prior to surgical removal of a jaw bone lesion that is radiographically compatible with a giant cell granuloma and immediately following the histologic diagnosis of central giant cell granuloma. Hyperparathyroidism may be primary, in which case there is a functional adenoma of the parathyroid glands, or secondary to renal disease, in which case renal osteodystrophy evolves as a consequence of tubular electrolyte retention abnormalities. In both cases, serum calcium is elevated, and phosphate is decreased. Parathormone levels are elevated.
In large lesions of the jaw bone, the chance that a biopsy specimen is not representative of the entire lesion is high, particularly since the pathologist is usually supplied with multiple small fragments curetted from the bony cavity rather than a solid specimen. In the interpretation of the results of the biopsy specimen analysis, consideration should always be given to the possibility that granulomatous giant cell–containing tissue may represent either a normal reparative response to some other bone lesion or an inflammatory hyperplasia.
The recurrence rate of central giant cell granulomas after initial conservative surgical therapy (curettage) is reported as 12 to 37%; repeat curettage usually prevents further recurrence.
On rare occasions, some giant cell lesions of the jaws behave more aggressively and may eventually require segmental jaw resection with a margin of normal tissue. Debate continues as to the validity of the histologic criteria that have been proposed to distinguish these more aggressive tumors,and curettage with cryosurgery of the walls of the bony cavity is advised by some authors for any recurrent giant cell lesion. There is some evidence that the intralesional injection of steroids will cause the resolution of giant cell lesions of the jaws; however, a large controlled clinical series has yet to be reported.
An important consideration in the management of these lesions is the necessity to search for evidence of hyperparathyroidism in all patients with histologically confirmed giant cell lesions of the jaw. There are documented examples of parathyroid lesions having been discovered as a result of blood and urine chemistry studies requested by a dentist following diagnosis of a giant cell lesion.The frequency with which this is likely to happen is probably quite low since in most series of hyperparathyroidism,lesions of the jaw have been among the last clinical manifestations of the disease to appear. Fewer than 10% of patients with hyperparathyroidism have radiographically visible cystic jaw lesions (see Figure 7-8) or even “loss of the lamina dura” (another effect of hyperparathyroidism, often used clinically to screen for the disease). Serum calcium, phosphorus, and alkaline phosphatase determinations should be requested prior to surgical removal of a jaw bone lesion that is radiographically compatible with a giant cell granuloma and immediately following the histologic diagnosis of central giant cell granuloma. Hyperparathyroidism may be primary, in which case there is a functional adenoma of the parathyroid glands, or secondary to renal disease, in which case renal osteodystrophy evolves as a consequence of tubular electrolyte retention abnormalities. In both cases, serum calcium is elevated, and phosphate is decreased. Parathormone levels are elevated.
In large lesions of the jaw bone, the chance that a biopsy specimen is not representative of the entire lesion is high, particularly since the pathologist is usually supplied with multiple small fragments curetted from the bony cavity rather than a solid specimen. In the interpretation of the results of the biopsy specimen analysis, consideration should always be given to the possibility that granulomatous giant cell–containing tissue may represent either a normal reparative response to some other bone lesion or an inflammatory hyperplasia.
The recurrence rate of central giant cell granulomas after initial conservative surgical therapy (curettage) is reported as 12 to 37%; repeat curettage usually prevents further recurrence.
On rare occasions, some giant cell lesions of the jaws behave more aggressively and may eventually require segmental jaw resection with a margin of normal tissue. Debate continues as to the validity of the histologic criteria that have been proposed to distinguish these more aggressive tumors,and curettage with cryosurgery of the walls of the bony cavity is advised by some authors for any recurrent giant cell lesion. There is some evidence that the intralesional injection of steroids will cause the resolution of giant cell lesions of the jaws; however, a large controlled clinical series has yet to be reported.