Search

During life, bone extracellular matrix (ECM) undergoes a continuous remodeling process that determines the proper preservation of bone mass and architecture. An increase in bone remodeling level, as well as the imbalance in the osteoblasts-osteoclasts coupling, leads to an altered bone tissue microarchitecture, enhancing bone fragility and fracture risk, features of osteoporosis (OP) [1,2]. Dysregulation in bone ECM proteins is considered a key marker of OP [3,4] and an accurate analysis of their distribution, expression and mutual relationship in the onset or maintenance of OP is far from being elucidated. In the present study we correlated the microarchitectural changes observed in osteoporotic femoral heads with the expression of Collagen Type I (COL1A1, COL1A2) and non-collagenous proteins (NCPs) like Transforming Growth Factor beta (TGF-beta), Decorin, Osteopontin, Bone Sialoprotein 2 (BSP-2), Osteonectin and Osteocalcin. Sirius Red staining, immunohistochemistry, Western Blotting analysis, and histomorphometry were used. Our analyses confirmed the alterations of bone area fraction, cortical and trabecular thickness in OP bone tissue. Moreover, we detected opposing correlation between the changes in Type I Collagen distribution and the expression of Decorin, Osteocalcin, Osteopontin, and BSP-2. These NCPs exert a central role in bone ECM structure and function (e.g., cell-matrix interaction, OB and OC recruitment and maturation, and HA nucleation) with agonist or antagonist effect in tissue maturity, bone formation and resorption and mineralization. An unbalance in their crosstalk supports the increase of tissue immaturity, also possibly caused by a high resorption rate, observed in OP tissue. These heterogeneous ECM network-dependent effects need to be taken as a whole for targeted therapeutic strategies aimed at preserving bone mass. [ABSTRACT FROM AUTHOR]