A decreased subchondral trabecular bone tissue elastic modulus is associated with pre‐arthritic cartilage damage

Abstract

In osteoarthritis, one postulate is that changes in the mechanical properties of the subchondral bone layer result in cartilage damage. The goal of this study was to examine changes in subchondral trabecular bone properties at the calcified tissue level in the early stages of cartilage damage. Finite element models were constructed from microCT scans of trabecular bone from the proximal tibia of donors with mild cartilage damage and from normal donors. In the donors with cartilage damage, macroscopic damage was present only in the medial compartment. The effective tissue elastic moduli were determined using a combination of finite element models and mechanical testing. The bone tissue modulus was reduced by 60% in the medial condyle of the cases with cartilage damage compared to the control specimens. Neither the presence of cartilage damage nor the anatomic site (medial vs. lateral) affected the elastic modulus at the apparent level. The volume fraction of trabecular bone was higher in the medial compartment compared to the lateral compartment of tibiae with cartilage damage (but not the controls), suggesting that mechanical properties were preserved in part at the apparent level by an increase in the bone volume fraction. It seems likely that the normal equilibrium between cartilage properties, bone tissue properties and bone volume fraction is disrupted early in the development of osteoarthritis. © 2001 Orthopaedic Research Society. Punlished by Elsevier Science Ltd. All rights reserved.

Analysis of bone architecture sensitivity for changes in mechanical loading, cellular activity, mechanotransduction, and tissue properties

“…In contrast, variations in the bone matrix stiffness did have a marked effect on bone architecture and may play a role in both osteoarthritis and osteogenesis imperfecta. Bone matrix stiffness is decreased in osteoarthritic joints (Day et al 2001), and similar to our simulations, bone fraction and trabecular thickness are increased, while trabecular number and trabecular separation are decreased in osteoarthritic joints (Bobinac et al 2003;Grynpas et al 1991;Fazzalari and Parkinson 1998). In analogy with this, the changes in bone structure observed in osteogenesis imperfecta might be caused by an increase in bone matrix stiffness as a result of increased mineralization.…”

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

“…Moreover, the data indicate that fragile subchondral bone might be an etiologic lesion in OA (15,17). Data from previous studies of human hip and knee OA have supported the notion that abnormalities in the subchondral bone may play a role in OA, although the nature of the bone changes as well as whether they are etiologic or secondary to cartilage degeneration remains to be determined (16,32,33).…”

“…Surgical injury to either the subchondral bone or articular cartilage can lead to OA (13,46). Alterations in the subchondral bone can compromise the mechanical properties of the bone and change the distribution of force experienced by the cartilage (15,47). In this manner, abnormal impact loading and sheer forces may alter the capacity of chondrocytes to maintain cartilage integrity or may even induce chondrocyte apoptosis (13).…”

“…It has also been suggested that alterations in the subchondral bone can lead to OA (9)(10)(11)(12)(13). However, the nature and quality of the bone in OA have not been determined (14,15). Epidemiologic studies have indicated an inverse correlation between osteoporosis and OA of the knee (16), suggesting that increased subchondral bone density may contribute to OA.…”

Osteoarthritis and bone mineral density: are strong bones bad for joints?

“…In the 1970s, Radin and Rose 63 proposed that increased stiffness of subchondral bone might lead to articular cartilage degeneration through the mechanical effects of increased shear stress. However, subsequent studies using a variety of techniques at different stages of OA progression have revealed complex and opposing changes in apparent density, material density, and stiffness in osteoarthritic subchondral bone, [64][65][66] suggesting that this explanation is too simplistic. 40,67 Thinning of the articular cartilage from below, owing to reactivation of endochondral ossification at the bone-cartilage interface in OA joints resulting in tidemark duplication and advancement, may represent another important mechanism by which increased bone formation could drive the OA process.…”