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World J Orthop. Jul 18, 2014; 5(3): 242-246
Published online Jul 18, 2014. doi: 10.5312/wjo.v5.i3.242
Osteoporosis and obesity: Role of Wnt pathway in human and murine models
Graziana Colaianni, Giacomina Brunetti, Maria Felicia Faienza, Silvia Colucci, Maria Grano
Graziana Colaianni, Giacomina Brunetti, Silvia Colucci, Maria Grano, Department of Basic Medical Science, Neuroscience and Sense Organs, Section of Human Anatomy and Histology, University of Bari, 70124 Bari, Italy
Maria Felicia Faienza, Department of Biomedical Sciences and Human Oncology, University of Bari, 70124 Bari, Italy
Author contributions: Colaianni G, Brunetti G, Faienza MF, Colucci S and Grano M wrote the paper.
Correspondence to: Graziana Colaianni, PhD, Department of Basic Medical Science, Neuroscience and Sense Organs, Section of Human Anatomy and Histology, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, Italy. graziana.colaianni@libero.it
Telephone: +39-080-5478306 Fax: +39-080-5478308
Received: December 29, 2013
Revised: March 4, 2014
Accepted: April 17, 2014
Published online: July 18, 2014
Abstract

Studies concerning the pathophysiological connection between obesity and osteoporosis are currently an intriguing area of research. Although the onset of these two diseases can occur in a different way, recent studies have shown that obesity and osteoporosis share common genetic and environmental factors. Despite being a risk factor for health, obesity has traditionally been considered positive to bone because of beneficial effect of mechanical loading, exerted by high body mass, on bone formation. However, contrasting studies have not achieved a clear consensus, suggesting instead that excessive fat mass derived from obesity condition may not protect against osteoporosis or, even worse, could be rather detrimental to bone. On the other hand, it is hitherto better established that, since adipocytes and osteoblasts are derived from a common mesenchymal stem cell precursor, molecules that lead to osteoblastogenesis inhibit adipogenesis and vice versa. Here we will discuss the role of the key molecules regulating adipocytes and osteoblasts differentiation, which are peroxisome proliferators activated receptor-γ and Wnts, respectively. In particular, we will focus on the role of both canonical and non-canonical Wnt signalling, involved in mesenchymal cell fate regulation. Moreover, at present there are no experimental data that relate any influence of the Wnt inhibitor Sclerostin to adipogenesis, although it is well known its role on bone metabolism. In addition, the most common pathological condition in which there is a simultaneous increase of adiposity and decrease of bone mass is menopause. Given that postmenopausal women have high Sclerostin level inversely associated with circulating estradiol level and since the sex hormone replacement therapy has proved to be effective in attenuating bone loss and reversing menopause-related obesity, we hypothesize that Sclerostin contribution in adipogenesis could be an active focus of research in the coming years.

Keywords: Osteoporosis, Obesity, Bone, Fat, Wnt, Peroxisome proliferators activated receptor-γ, Dickkopf, Sclerostin

Core tip: Here we will discuss the role of the key molecules influencing adipocytes and osteoblasts differentiation, which are peroxisome proliferators activated receptor-γ and Wnts, respectively. Besides these proteins, the Wnt inhibitor molecules are also necessary to control the Wnt signalling balance from active to inactive state, in favour of osteogenesis or adipogenesis. It seems remarkably important a deepen analysis of these molecules, not only for their involvement in the regulation of the differentiation processes but also in coordinating the switch toward osteo- or adipo-genesis fate within bone marrow.