Limits...
Subchondral bone in osteoarthritis: insight into risk factors and microstructural changes.

Li G, Yin J, Gao J, Cheng TS, Pavlos NJ, Zhang C, Zheng MH - Arthritis Res. Ther. (2013)

Bottom Line: Importantly, we discuss risk factors influencing subchondral bone integrity.We also focus on the microarchitectural and histopathological changes of subchondral bone in OA, and provide an overview of their potential contribution to the progression of OA.A hypothetical model for the pathogenesis of OA is proposed.

View Article: PubMed Central - HTML - PubMed

ABSTRACT
Osteoarthritis (OA) is a major cause of disability in the adult population. As a progressive degenerative joint disorder, OA is characterized by cartilage damage, changes in the subchondral bone, osteophyte formation, muscle weakness, and inflammation of the synovium tissue and tendon. Although OA has long been viewed as a primary disorder of articular cartilage, subchondral bone is attracting increasing attention. It is commonly reported to play a vital role in the pathogenesis of OA. Subchondral bone sclerosis, together with progressive cartilage degradation, is widely considered as a hallmark of OA. Despite the increase in bone volume fraction, subchondral bone is hypomineralized, due to abnormal bone remodeling. Some histopathological changes in the subchondral bone have also been detected, including microdamage, bone marrow edema-like lesions and bone cysts. This review summarizes basic features of the osteochondral junction, which comprises subchondral bone and articular cartilage. Importantly, we discuss risk factors influencing subchondral bone integrity. We also focus on the microarchitectural and histopathological changes of subchondral bone in OA, and provide an overview of their potential contribution to the progression of OA. A hypothetical model for the pathogenesis of OA is proposed.

Show MeSH

Related in: MedlinePlus

Hypothetical model of osteoarthritis (OA) pathogenesis. Normal subchondralbone suffering from a non-physiological strain (induced by risk factors) starts apathological cascade reaction, leading to osteoarthritic changes in differenttissues. In early-stage OA, subchondral plate becomes thinner and more porous,together with initial cartilage degeneration. Subchondral trabecular bone alsodeteriorates, with increased separation and thinner trabeculae. At the same time,microdamage begins to appear in both calcified cartilage and subchondral bone,which will persist throughout the whole pathological process. In late-stage OA,calcified cartilage and subchondral plate become thicker, with reduplicatedtidemarks and progressive non-calcified cartilage damage. Subchondral trabecularbone becomes sclerotic. The sclerosis of periarticular mineralized tissues may bea biomechanical compensational adaptation to the widespread cysts and microdamagein subchondral bone, which render subchondral bone structure more fragile.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4061721&req=5

Figure 5: Hypothetical model of osteoarthritis (OA) pathogenesis. Normal subchondralbone suffering from a non-physiological strain (induced by risk factors) starts apathological cascade reaction, leading to osteoarthritic changes in differenttissues. In early-stage OA, subchondral plate becomes thinner and more porous,together with initial cartilage degeneration. Subchondral trabecular bone alsodeteriorates, with increased separation and thinner trabeculae. At the same time,microdamage begins to appear in both calcified cartilage and subchondral bone,which will persist throughout the whole pathological process. In late-stage OA,calcified cartilage and subchondral plate become thicker, with reduplicatedtidemarks and progressive non-calcified cartilage damage. Subchondral trabecularbone becomes sclerotic. The sclerosis of periarticular mineralized tissues may bea biomechanical compensational adaptation to the widespread cysts and microdamagein subchondral bone, which render subchondral bone structure more fragile.

Mentions: Despite the numerous pathophysiological alterations detected in subchondral bone withOA, we still lack a clear understanding of the mechanisms underpinning these phenomenaand how these different aspects are interrelated to each other. Based on the currentstate of knowledge, one hypothesis for the pathogenesis of OA emerges (FigureĀ 5). Subchondral bone plays an important role in the pathogenesis ofOA, manifesting both microarchitectural and histopathological changes (BMELs, SBCs andmicrodamage). These histopathological changes not only have intimate interactions witheach other, but also have a close relationship with bone remodeling that wouldsubsequently lead to microarchitectural changes in the subchondral bone and theoverlying cartilage.


Subchondral bone in osteoarthritis: insight into risk factors and microstructural changes.

Li G, Yin J, Gao J, Cheng TS, Pavlos NJ, Zhang C, Zheng MH - Arthritis Res. Ther. (2013)

Hypothetical model of osteoarthritis (OA) pathogenesis. Normal subchondralbone suffering from a non-physiological strain (induced by risk factors) starts apathological cascade reaction, leading to osteoarthritic changes in differenttissues. In early-stage OA, subchondral plate becomes thinner and more porous,together with initial cartilage degeneration. Subchondral trabecular bone alsodeteriorates, with increased separation and thinner trabeculae. At the same time,microdamage begins to appear in both calcified cartilage and subchondral bone,which will persist throughout the whole pathological process. In late-stage OA,calcified cartilage and subchondral plate become thicker, with reduplicatedtidemarks and progressive non-calcified cartilage damage. Subchondral trabecularbone becomes sclerotic. The sclerosis of periarticular mineralized tissues may bea biomechanical compensational adaptation to the widespread cysts and microdamagein subchondral bone, which render subchondral bone structure more fragile.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4061721&req=5

Figure 5: Hypothetical model of osteoarthritis (OA) pathogenesis. Normal subchondralbone suffering from a non-physiological strain (induced by risk factors) starts apathological cascade reaction, leading to osteoarthritic changes in differenttissues. In early-stage OA, subchondral plate becomes thinner and more porous,together with initial cartilage degeneration. Subchondral trabecular bone alsodeteriorates, with increased separation and thinner trabeculae. At the same time,microdamage begins to appear in both calcified cartilage and subchondral bone,which will persist throughout the whole pathological process. In late-stage OA,calcified cartilage and subchondral plate become thicker, with reduplicatedtidemarks and progressive non-calcified cartilage damage. Subchondral trabecularbone becomes sclerotic. The sclerosis of periarticular mineralized tissues may bea biomechanical compensational adaptation to the widespread cysts and microdamagein subchondral bone, which render subchondral bone structure more fragile.
Mentions: Despite the numerous pathophysiological alterations detected in subchondral bone withOA, we still lack a clear understanding of the mechanisms underpinning these phenomenaand how these different aspects are interrelated to each other. Based on the currentstate of knowledge, one hypothesis for the pathogenesis of OA emerges (FigureĀ 5). Subchondral bone plays an important role in the pathogenesis ofOA, manifesting both microarchitectural and histopathological changes (BMELs, SBCs andmicrodamage). These histopathological changes not only have intimate interactions witheach other, but also have a close relationship with bone remodeling that wouldsubsequently lead to microarchitectural changes in the subchondral bone and theoverlying cartilage.

Bottom Line: Importantly, we discuss risk factors influencing subchondral bone integrity.We also focus on the microarchitectural and histopathological changes of subchondral bone in OA, and provide an overview of their potential contribution to the progression of OA.A hypothetical model for the pathogenesis of OA is proposed.

View Article: PubMed Central - HTML - PubMed

ABSTRACT
Osteoarthritis (OA) is a major cause of disability in the adult population. As a progressive degenerative joint disorder, OA is characterized by cartilage damage, changes in the subchondral bone, osteophyte formation, muscle weakness, and inflammation of the synovium tissue and tendon. Although OA has long been viewed as a primary disorder of articular cartilage, subchondral bone is attracting increasing attention. It is commonly reported to play a vital role in the pathogenesis of OA. Subchondral bone sclerosis, together with progressive cartilage degradation, is widely considered as a hallmark of OA. Despite the increase in bone volume fraction, subchondral bone is hypomineralized, due to abnormal bone remodeling. Some histopathological changes in the subchondral bone have also been detected, including microdamage, bone marrow edema-like lesions and bone cysts. This review summarizes basic features of the osteochondral junction, which comprises subchondral bone and articular cartilage. Importantly, we discuss risk factors influencing subchondral bone integrity. We also focus on the microarchitectural and histopathological changes of subchondral bone in OA, and provide an overview of their potential contribution to the progression of OA. A hypothetical model for the pathogenesis of OA is proposed.

Show MeSH
Related in: MedlinePlus