Ulf H Lerner1,2, Elin Kindstedt2, Pernilla Lundberg2. 1. Centre for Bone and Arthritis Research at Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. 2. Department of Odontology, Division of Molecular Periodontology, Umeå University, Umeå, Sweden.
Abstract
AIM: In this article, the interplay between bone resorbing and bone forming cells is reviewed. METHOD: This review examines the comprehensive literature on the interaction between bone resorption and bone formation. RESULTS: Coupling between bone resorption and bone formation refers to the process within basic multicellular units, in which osteoclastic bone resorption is met by the differentiation of osteoblasts and their bone forming activity. There are many possible signalling molecules that contribute to coupling at the asynchronously working remodelling sites throughout our skeleton. These include growth factors released from the bone matrix during bone resorption, soluble and membrane products of the osteoclasts and their precursors and signals from osteocytes. CONCLUSIONS: In this review, we describe the potential roles of a number of these factors, whose interactions are essential for a tight control of coupling within individual remodelling units, in order to control skeletal mass. Both pre-clinical evidence and clinical evidence pinpoint that molecules in the WNT signalling pathway could be promising bone augmentation therapeutic targets. Regarding oral implications, there is support, from preclinical studies in rats, that anti-sclerostin antibodies can restore alveolar bone mass.
AIM: In this article, the interplay between bone resorbing and bone forming cells is reviewed. METHOD: This review examines the comprehensive literature on the interaction between bone resorption and bone formation. RESULTS: Coupling between bone resorption and bone formation refers to the process within basic multicellular units, in which osteoclastic bone resorption is met by the differentiation of osteoblasts and their bone forming activity. There are many possible signalling molecules that contribute to coupling at the asynchronously working remodelling sites throughout our skeleton. These include growth factors released from the bone matrix during bone resorption, soluble and membrane products of the osteoclasts and their precursors and signals from osteocytes. CONCLUSIONS: In this review, we describe the potential roles of a number of these factors, whose interactions are essential for a tight control of coupling within individual remodelling units, in order to control skeletal mass. Both pre-clinical evidence and clinical evidence pinpoint that molecules in the WNT signalling pathway could be promising bone augmentation therapeutic targets. Regarding oral implications, there is support, from preclinical studies in rats, that anti-sclerostin antibodies can restore alveolar bone mass.
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