Microarchitectural adaptations in aging and osteoarthrotic subchondral bone issues.

Abstract

The human skeleton optimizes its microarchitecture by elaborate adaptations to mechanical loading during development and growth. The mechanisms for adaptation involve a multistep process of cellular mechanotransduction stimulating bone modelling, and remodeling resulting in either bone formation or resorption. This process causes appropriate microarchitectural changes tending to adjust and improve the bone structure to its prevailing mechanical environment. Normal individual reaches peak bone mass at age between 25 and 30 years, and thereafter bone mass declines with age in both genders. The bone loss is accompanied by microarchitectural deterioration resulting in reduced mechanical strength likely leading to fragility fractures. With aging, inevitable bone loss occurs, which is frequently the cause of osteoporosis; and inevitable bone and joint degeneration happens, which often results in osteoarthrosis. These diseases are among the major health care problems in terms of socio-economic costs. The overall goals of the current series of studies were to investigate the age-related and osteoarthrosis (OA) related changes in the 3-D microarchitectural properties, mechanical properties, collagen and mineral quality of subchondral cancellous and cortical bone tissues. The studies included mainly two parts. For human subjects: aging- (I–IV) and early OArelated (V–VI) changes in cancellous bone properties were assessed. For OA guinea pig models (VII–IX), three topics were studied: firstly, the spontaneous, age-related development of guinea pig OA; secondly, the potential effects of hyaluronan on OA subchondral bone tissues; and thirdly, the effects on OA progression of an increase in subchondral bone density by inhibition of bone remodeling with a bisphosphonate. These investigations aimed to obtain more insight into the age-related and OA-related subchondral bone adaptations.