Abstract
Mast cells (MCs) are important sensor and effector cells of the immune system that are involved in many physiological and pathological conditions. Increasing evidence suggests that they also play an important role in bone metabolism and bone disorders. MCs are located in the bone marrow and secrete a wide spectrum of mediators, which can be rapidly released upon activation of mature MCs following their differentiation in mucosal or connective tissues. Many of these mediators can exert osteocatabolic effects by promoting osteoclast formation [e.g., histamine, tumor necrosis factor (TNF), interleukin-6 (IL-6)] and/or by inhibiting osteoblast activity (e.g., IL-1, TNF). By contrast, MCs could potentially act in an osteoprotective manner by stimulating osteoblasts (e.g., transforming growth factor-β) or reducing osteoclastogenesis (e.g., IL-12, interferon-γ). Experimental studies investigating MC functions in physiological bone turnover using MC-deficient mouse lines give contradictory results, reporting delayed or increased bone turnover or no influence depending on the mouse model used. By contrast, the involvement of MCs in various pathological conditions affecting bone is evident. MCs may contribute to the pathogenesis of primary and secondary osteoporosis as well as inflammatory disorders, including rheumatoid arthritis and osteoarthritis, because increased numbers of MCs were found in patients suffering from these diseases. The clinical observations could be largely confirmed in experimental studies using MC-deficient mouse models, which also provide mechanistic insights. MCs also regulate bone healing after fracture by influencing the inflammatory response toward the fracture, vascularization, bone formation, and callus remodeling by osteoclasts. This review summarizes the current view and understanding of the role of MCs on bone in both physiological and pathological conditions.
Highlights
Mast cells (MCs) are tissue-resident immune cells and are best known for promoting allergic reactions [1]
The scope of this review is to provide an overview of the physiological role of MCs in bone homeostasis based on the current state of knowledge
Bone mass decreased with aging, in the trabecular compartment, both in MCcompetent and -deficient mice. These results suggest that MCs might be redundant for physiological bone turnover as well as in age-induced bone loss (Figure 1A) [10]
Summary
Mast cells (MCs) are tissue-resident immune cells and are best known for promoting allergic reactions [1]. Several groups using MC-deficient mouse models discovered that MCs play an important role in the process of bone fracture healing and might be involved in the regulation of osteoclastogenesis [10, 11]. Our group showed that Mcpt-5 Cre R-DTA mice, which lack CTMCs, were protected from OVX-induced bone loss and no increase in osteoclast numbers or activity occurred after OVX [10].
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