Bone Abstracts

How exactly does inflammation early affect bone properties at rheumatoid arthritis (RA) onset? As we have shown, mechanical bone properties are negatively affected by inflammation. This could be viewed as a logic consequence of the reduction BMD that occurs in RA. However, the increased risk of fractures in RA patients is independent from BMD and this has been recognized by the WHO FRAX tool, where RA has been included as one of the risk factors. Thus, RA in itself is independently associated with the occurrence of bone fractures but the underlying mechanisms are not completely understood. In our view, a clue for this problem can be found in our innovative observations using SHG microscopy suggesting that arthritis affects the density and organization of collagen type I. Our hypothesis is that the initial steps towards bone fracture and joint collapse are determined by early changes in collagen type I organization capable of interfering with the intrinsic bone tissue properties. There are a number of arguments for positioning collagen type I fiber damage as an initial event in RA bone disease. Bone mineral phase is stiff and brittle and thus it is responsible for bone’s stiffness, while the collagen matrix is much softer and is the main provider of ductility and the ability to absorb energy. As a corollary, a high ratio of calcium crystals−/−collagen can reduce the ductility and toughness of bone, particularly if the collagen matrix is quantitatively or qualitatively affected. In addition, disturbances in the bone mineralization density distribution can decrease bone strength, without necessarily affecting bone matrix volume and microarchitecture. Finally, mineral particles are strongly oriented in the direction of collagen fibers and may have a distorted distribution if collagen molecules are not adequately organized due to a high turnover rate, affecting toughness and elastic modulus.