Benign fibro-osseous lesions of the maxillofacial skeleton constitute a heterogeneous group of disorders that includes developmental, reactive (dysplastic) and neoplastic lesions. Although their classification has been reviewed multiple times in the past, the most common benign fibro-osseous lesions are fibrous dysplasia, osseous dysplasia and ossifying fibroma. For the dental clinician, the challenges involve diagnosis and treatment (or lack thereof). A careful correlation of all clinical, radiologic and microscopic features is essential to establish a proper diagnosis and a clear treatment plan. This article aimed to review the clinical, radiologic and histopathologic characteristics of benign fibro-osseous lesions of the jaws, with emphasis on their differential diagnoses. With a deeper understanding of benign fibro-osseous lesions, clinicians will be better prepared to manage these lesions in their practice.

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Cyclin D1 protein overexpression may be involved in the formation of the giant cells and the pathogenesis of central giant cell granuloma. As the distribution of immunostaining is identical to that observed in giant cell tumor of bone, our results support the possibility that central giant cell granuloma of the jaws and giant cell tumor of bone represent a similar disease process that clinically and histologically may have somewhat different features because of differences in the anatomical site of involvement.

Cyclins play an important role in regulating the passage of dividing cells through critical checkpoints in the cell cycle. Because alterations of several cyclins, especially cyclin D1, have been implicated in the development of many human neoplasms, we examined 32 cases of giant cell tumor of long bones for cyclin D1 gene amplification and protein overexpression using differential polymerase chain reaction and immunohistochemistry, respectively. In addition, the expression of cyclin D3, cyclin B1, and the proliferation-associated antigen Ki-67 (MIB-1) was assessed immunohistochemically. Low-level cyclin D1 gene amplification was detected in 61% of giant cell tumor cases. All tumors showed cyclin D1, cyclin D3, cyclin B1, and Ki-67 (MIB-1) staining; however, the distribution was very characteristic. Cyclin D1 protein expression was seen predominantly in the nuclei of the giant cells, with occasional mononuclear cells staining. There was no correlation between cyclin D1 gene amplification and protein overexpression. Cyclin D3 staining showed a similar distribution, with 88% of cases showing protein overexpression. Cyclin D1 and/or D3 staining in the giant cells was never associated with staining for either cyclin B1 or Ki-67 (MIB-1), as the expression of the latter two proteins was restricted to the mononuclear cells. Cyclin B1 overexpression was seen in 44% of cases. Ki-67 (MIB-1) staining was present in all cases, and between 10 to 50% of the mononuclear cells were positive. These results suggest that alterations in cyclin D1 and/or D3 might play a role in the pathogenesis of giant cell tumor of bone. Alterations of several cell cycle regulatory proteins, especially those involved in the G1-to-S transition, such as D-type cyclins, are detected in many human tumors. Genes encoding D-type cyclins (D1, D2, and D3) are induced by mitogenic stimuli (1) and, together with their catalytic partners CDK4 and CDK6, phosphorylate the retinoblastoma protein (pRb) (2) and allow cells to cross the G1/S restriction point. The cells then become committed to DNA replication and completion of the cell cycle (3). Because D-type cyclins provide the link between mitogenic signals and activation of the cell cycle (1, 4) and because of their regulatory function in the G1-to-S transition (5), constitutive activation of the D-cyclin pathway can reduce or overcome certain mitogen requirements for cell proliferation (6) and thereby contribute to oncogenic transformation (7-9). Although studies suggest that overexpression of cyclin D1 appears to be insufficient on its own to transform primary cells, it may cooperate with other oncogenes to induce transformation (10 -13). Amplification of the cyclin D1 gene and/or overexpression of the protein are observed in a number of human malignancies, such as certain types of epithelial cancers, lymphomas, and some central nervous system tumors (14). Benign and premalignant lesions of the breast (15) and epithelial dysplasias of the oral and laryngeal mucosa (16, 17) also show cyclin D1 alterations, s...