The role of mast cells in osteoporosis.
Publication/Presentation Date
8-1-2006
Abstract
OBJECTIVES: The notion that mast cells and their secreted products play a potentially pathogenic role in osteoporosis bone loss is novel, but gaining substantial support. We reviewed the literature from 1950 to present to demonstrate an association between mast cells and bone turnover. The effect of primary increase in mast cells, deficiency in mast cells, and effect of mast cells during high remodeling states is discussed in this review.
METHODS: A retrospective review of the literature was performed using Medline and MD Consult databases from 1957 to 2004. The keywords mast cell and osteoporosis revealed 200 abstracts, limited to English and review articles. The references were further selected based on relevance to pathogenesis, research, and histamine's role in osteoporosis.
RESULTS: Using the model of systemic mastocytosis, increased numbers of mast cells led to an acceleration of bone turnover. Activation mutations in tyrosine growth factor receptor, KIT, may be responsible for this occurrence. Mast cell deficiency demonstrates delayed osteoclastic recruitment and a delayed osteoblastic formation phase. Histamine deficiencies lead to a decrease in osteoclast number as reflected by tartrate-resistant acid phosphatase staining. Osteoblasts stimulated by parathyroid hormone synthesize abundant stem cell factor, which contributes to enhanced osteoclastogenesis.
CONCLUSIONS: Mast cells appear to be relevant in the pathogenesis of bone turnover. Their deficiency has been associated with low remodeling states, while their excess is associated with accelerated bone loss. Even their byproducts are responsible for increased bone resorption. Inhibiting mast cells and/or their products many be a novel therapy for treating osteoporosis in the future.
Volume
36
Issue
1
First Page
32
Last Page
36
ISSN
0049-0172
Published In/Presented At
Chiappetta, N., & Gruber, B. (2006). The role of mast cells in osteoporosis. Seminars in arthritis and rheumatism, 36(1), 32–36. https://doi.org/10.1016/j.semarthrit.2006.03.004
Disciplines
Medicine and Health Sciences
PubMedID
16887466
Department(s)
Department of Medicine
Document Type
Article