Insight into the pathogenesis and nature of Central giant cell lesions of the jaws

Abstract

Central giant cell lesions of the jaws are not uncommon. While the majority of these represent single, sporadic lesions, histologically identical lesions are seen in association with a number of other bone lesions, as well as in certain syndromes. This manuscript offers a brief update on recent developments in this area that provide new insight into the pathogenesis and nature of Central Giant Cell Lesions of the Jaws. Key words:Central giant cell lesion, RASopathy

“Central giant cell granuloma” – An update

“…In fact, there is evidence in plenty that indicated local factors generated in the microenvironment of bone-resorbing cells are much more powerful regulators of osteoclast function than by the hormones like parathyroid hormone, calcitonin secreted and sent in the blood circulation. [ 6 ]…”

Immunoexpression of calcitonin and glucocorticoid receptors in central giant cell lesions of the jaws

“…However, in contrast to other studies, evaluation of CTR and GR expression prior treatment did not affect the response to corticosteroid therapy in the present sample. The CGCLs are considered a heterogeneous group of lesions, and it is possible that many environmental and intrinsic factors can influence the variable response to clinical treatment …”

“…The CGCLs are considered a heterogeneous group of lesions, and it is possible that many environmental and intrinsic factors can influence the variable response to clinical treatment. 27 Among these factors, several studies have tried to find a good indicator for CGCL aggressiveness, such as angiogenic index, 26,28 mitotic activity, 2 number or size of giant cells, 29 and presence of myofibroblasts. 30 Our findings demonstrated that CTR staining and GR staining in MGCs and MSCs are not useful to distinguish aggressive from non-aggressive CGCLs, in accordance with previous studies, 8,9,14 suggesting that nonsurgical treatment with glucocorticoids and calcitonin may represent a good therapeutic choice for CGCLs regardless of their aggressiveness.…”

Paraspinal neurofibromas and hypertrophic neuropathy in Noonan syndrome with multiple lentigines

“…As a role of PTPN11 mutations is suggested in cardiac morphogenesis and hypertrophic cardiomyopathy,11 a similar mechanism may be responsible for the nerve overgrowth and formation of neurofibromas in NSML. There might also be an analogy with multiple giant cell lesions in RASopathies where extensive multilocular tumour development has been observed in a few cases with no strict correlation to the underlying germline mutation 17. Further studies are necessary to elucidate the molecular basis of tumorigenesis and nerve hypertrophy in this disorder.…”