Bone remodeling in W/Wv mast cell deficient mice

• Published in: Bone (New York, N.Y.) Vol. 12; no. 4; pp. 227 - 236
• Main Authors: SILBERSTEIN, R, MELNICK, M, GREENBERG, G, MINKIN, C
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Science 1991
• Subjects: Animals; Biological and medical sciences; Bone Remodeling - physiology; Bone Resorption - pathology; Bone Resorption - physiopathology; Cell Count; Fundamental and applied biological sciences. Psychology; Male; Mast Cells - physiology; Mice; Mice, Mutant Strains; Minerals - metabolism; Skeleton and joints; Space life sciences; Vertebrates: osteoarticular system, musculoskeletal system; Animal model; Vertebrata; Mammalia; Mouse; Morphology; Rodentia; Histology; Mast cell; Mutation; Bone; Osteogenesis
• ISSN: 8756-3282; 1873-2763
• DOI: 10.1016/8756-3282(91)90068-T

Strong experimental evidence exists for a relationship between mast cells and bone disease, but the role of mast cells in the regulation of bone remodeling is unknown. In order to address this question, mast cell deficient mice (W/Wv) were paired with their mast cell sufficient (+/+) littermates and evaluated for differences in response to an induced cycle of bone remodeling. This was achieved using a tooth egression protocol, in which a synchronous cycle of bone remodeling was induced in the mandibular buccal alveolar periosteum by extraction of the opposing dentition. Quantitative histomorphometric changes during the activation, resorption, reversal, and formation phases of bone remodeling were documented using standard techniques. Most cell deficient mutants exhibited the following defects in response to an induced cycle of bone remodeling: (a) the onset of the remodeling cycle was delayed by a prolonged activation phase, (b) the duration and extent of the active formation phase was decreased, and (c) the amount of new bone matrix synthesized was diminished while mineralization rates were found to be normal. These results suggest that mast cells and their mediators provide a paracrine mechanism which influences the recruitment of osteoclast and osteoblast progenitors and their participation in bone remodeling. Nonetheless, since bone remodeling occurs in mast cell deficient mice, albeit less efficiently, this mechanism is most likely one of several redundant mechanisms that provide for adequate skeletal homeostasis.