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Abstract
Patients with the classical Philadelphia chromosome-negative chronic myeloproliferative neoplasms including essential thrombocythemia, polycythemia vera and primary myelofibrosis often suffer from comorbidities, in particular, cardiovascular diseases and thrombotic events. Apparently, there is also an increased risk of osteoporotic fractures among these patients. However, the true prevalence, mechanisms involved and therapeutic implications are not well described. In this review, we summarize what is currently known about possible associations between bone disease and chronic myeloproliferative neoplasms. Chronic inflammation has been suggested to explain the initiation of clonal development and progression in chronic myeloproliferative neoplasms. Decreased bone mineral density and enhanced fracture risk are well-known manifestations of many chronic systemic inflammatory diseases. As opposed to systemic mastocytosis (SM) where pathogenic mechanisms for bone manifestations probably involve effects of mast cell mediators on bone metabolism, the mechanisms responsible for increased fracture risk in other chronic myeloproliferative neoplasms are not known.
Acknowledgement
The authors thank Johan Wallin (JW) and Mette Brandt Eriksen (MBE) for their help and guidance with the literature search strategy. The authors thank Sanne Grindsted for the radiographs of osteoporotic fractures.
Financial and competing interests disclosure
This work is supported by grants from Danish Cancer Society (R90-A6062–14S2) and the Region of Southern Denmark (Record no. 11/28457). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Bone disease in chronic myeloproliferative neoplasms (MPNs) other than systemic mastocytosis is not well described.
Apparently, there is an increased risk of osteoporotic fractures among patients with essential thrombocythemia, polycythemia vera and chronic myeloid leukemia.
Whereas pathogenic mechanisms for osteoporosis in mastocytosis involve effects of mast cell mediators on bone metabolism, the mechanisms responsible for increased fracture risk in other MPNs are not known.
Because chronic inflammation has been suggested to initiate the clonal development and progression in MPNs and because enhanced fracture risk is well-known manifestations of many chronic systemic inflammatory diseases, chronic inflammation may also play a role in the pathogenesis of bone disease in MPN.