Collagen and Non-Collagenous Protein Content (Osteocalcin, Sialoprotein, Proteoglycan) in the Iliac Crest Bone and Serum Osteocalcin in Women with and without Hand Osteoarthritis

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“…OA bone's hardness is 7% lower than that of osteoporotic bone, indicating that OA bone has a reduced elastic modulus 29 . These results support the view of a more generalized bone metabolic disease in OA [30][31][32] and that alteration of subchondral bone integrity is a key event in OA 33 .…”

“…Indeed, elevated osteocalcin serum levels in women with hand OA and in cortical bone explants 32 , and the observation that insulin-like growth factors (IGF-I and II) and TGF-β levels are higher in samples of iliac crest bone of patients with OA 34 , hence at a site distant from weight-bearing joints, suggest an increased bone anabolism in OA. Moreover, an imbalance between collagen and non-collagen protein synthesis like osteocalcin can lead to an increase in bone volume without a concomitant increase in BMD.…”

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

“…Studies in OA of the knee and the hand reported that the scintigraphic abnormalities correlated with the osteocalcin concentration in the synovial fluid, which is a marker of bone formation, and serum osteopontin, a bone matrix protein, were also elevated [21][22][23]. Gevers and Dequeker also showed elevated serum osteocalcin levels in women with hand OA, and elevated osteocalcin in cortical bone explants [24]. Moreover, levels of growth factors such as insulin-like growth factor (IGF)-1 and -2 and transforming growth factor (TGF)-β1 are also higher in samples of iliac crest bone of patients with OA [25].…”

“…Hence, the apparent increase in bone density in OA may be because of an increase in material density, and not mineral density [31][32][33]. Indications of altered mineralisation and abnormal metabolic subchondral bone can be inferred from the increased osteoid matrix in this OA bone tissue [24,32,34,35]. As the osteoid matrix is primarily composed of an abundant collagen type I matrix, it was therefore of no surprise that this collagen type in the trabecular bone of the femoral heads of OA patients was found to be increased [31,32], along with abnormal collagen type I fibres, as evidenced by an increased ratio of α1 to α2 chains in OA compared to normal trabecular subchondral bone [33].…”

“…Together with the reduced number of cross-links in OA bone tissue [32], this could explain the reduction in bone mineralisation. Moreover, data also showed an increase in osteocalcin and alkaline phosphatase in human OA subchondral bone both in vivo [24] and in vitro [37,38]. Hence, the early marker (alkaline phosphatase), terminal differentiation marker (osteocalcin) and the mineralisation of OA subchondral bone osteoblasts are altered.…”