Role of bone architecture and anatomy in osteoarthritis

doi:10.1016/j.bone.2012.01.008

Bone

Volume 51, Issue 2, August 2012, Pages 197-203

https://doi.org/10.1016/j.bone.2012.01.008 Get rights and content

Abstract

When considering the pathogenesis of osteoarthritis (OA), it is important to review the contribution of bone in addition to the contribution of cartilage and synovium. Although bone clearly plays a role in determining the distribution of biomechanical forces across joints, which in turn plays a role in the initiation of OA, it has also more recently been appreciated that bone may contribute in a biological sense to the pathogenesis of OA. Far from being a static structure, bone is a dynamic tissue undergoing constant remodeling, and it is clear from a number of radiographic and biochemical studies that bone and cartilage degradation occurs hand in hand. Whether the initial instigating event in OA occurs in cartilage or bone is not known, but it is clear that bony changes occur very early in the pathogenesis of OA and often predate radiographic appearance of the disease. This review focuses on the structural variants of both hip and knee that have been associated with OA and the ultrastructural bone changes in these sites occurring in early OA pathogenesis.

This article is part of a Special Issue entitled “Osteoarthritis”.

Introduction

In considering osteoarthritis (OA) as a “whole joint” disease, it is important to acknowledge the contribution of bone in addition to cartilage and synovium to the pathogenesis of the disease. Well-known radiographic features of OA, such as bony sclerosis and osteophyte formation, are helpful in diagnosis of OA but are thought to be results of the disease process rather than causative. Changes in bone certainly occur as a result of OA, but changes in bone architecture and biology may also contribute to the development of OA. Not only does bone in part determine the distribution of biomechanical forces across the joint, but changes in the bone itself may contribute to the evolution of OA in ways that are now beginning to be appreciated. This review will highlight the emerging evidence that bone plays a key role in the pathogenesis of OA, with special focus on the hip and knee joints. We will highlight the role of bone shape as a risk factor for OA in the hip and knee. This subject has also been the topic of prior reviews by our research group and others [1], [2], [3], [4], [5], [6].

Section snippets

Does bone start the ball rolling in OA?

Bony changes appear very early in the course of OA and in some studies have been shown to precede cartilage changes. Petersson and colleagues studied subjects with chronic knee pain over a 3-year period and compared serum levels of bone and cartilage turnover markers between subjects that did and did not develop incident knee OA. Subjects with knee OA at baseline were excluded. They found that elevations in both bone sialoprotein (BSP) and cartilage oligomeric matrix protein (COMP) occurred

Changes in subcortical bone in early OA: a detailed look

A number of radiologic studies have supported the hypothesis that changes in subchondral bone may precede cartilage damage in OA. Using 3-Tesla, high-resolution magnetic resonance (MR) with parallel imaging, Bolbos and colleagues found a significant decrease in apparent bone volume to total volume (BV/TV) ratio in subjects with early knee OA as compared to healthy controls [23]. Both MR and multi-detector row CT images demonstrate that early in the course of knee OA, trabecular bone thins, with

Anatomic bone abnormalities associated with hip OA

Risk factors for OA of the hip include age, female sex, a history of hip injury, and exposure to sports and heavy mechanical loads [47], [48], [49], [50]. Genes also play an important role as risk factors for hip OA, as it is estimated that this disease has a heritability of approximately 60% in women [51]. In addition to these risk factors, it is now known that the geometry of the hip joint itself is an important risk factor for OA, with subtle architectural changes predating the radiographic

Anatomic abnormalities associated with knee OA

It has long been appreciated that altered distribution of forces across the knee joint is a predisposing factor for OA, though research on how knee shapes are associated with the presence or progression of OA is still in its early phases. Obesity is a clear risk factor for OA, presumably because of an increase in biomechanical load [81]. It has also been appreciated for some time that malalignment of the knee is a predisposing factor for knee OA and that malalignment may interact with increased

Molecular pathways implicated for their role in OA pathogenesis: the WNT/β-catenin and TGF-β/BMP pathways

It is clear that gene expression in bone is altered in OA. Hopwood and colleagues performed a microarray study of bone samples obtained from subjects undergoing joint replacement for hip OA or cadaveric controls without OA and found that, among the many genes that were differentially expressed, components of two major biologic pathways emerged: the WNT (wingless integration) pathway and the transforming growth factor-β (TGF-β)/bone morphogenetic protein (BMP) pathway [93]. Interestingly,

Conclusions

Increasing evidence suggests that bone and cartilage pathology are linked in osteoarthritis. Ideally, disease-modifying therapies for OA would target both bone and cartilage, as detrimental changes in these two compartments appear to be interconnected in the pathogenesis of OA.

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Patients with transfemoral amputation (TFA) are up to six times more likely to develop hip osteoarthritis (OA) in either or both the intact and residual limb, which is primarily attributed to habitually altered joint loading due to compensatory movement patterns. However, joint loading patterns differ between limbs, which confounds the understanding of loading-induced OA etiology across limbs. It remains unknown if altered loading due to amputation results in bony shape changes at the hip, which is a known etiological factor in the development of hip OA. Retrospective computed tomography images were collected of the residual limb for 31 patients with unilateral TFA (13F/18M; age: 51.7 ± 9.9 y/o; time since amputation: 13.7 ± 12.4 years) and proximal femur for a control group of 29 patients (13F/16M; age: 42.0 ± 12.27 years) and used to create 3D geometries of the proximal femur. Femoral 3D geometric variation was quantified using statistical shape modeling (SSM), a computational tool which placed 2048 corresponding particles on each geometry. Independent modes of variation were created using principal component analysis. 2D radiographic measures of the proximal femur, including common measures such as α-angle, head neck offset, and neck shaft angle, were quantified on digitally reconstructed radiographs (DRRs). SSM results were then compared to 2D measures using Pearson correlation coefficients (r). Two-sample t-tests were used to determine if there were significant differences between the TFA and control group means of 2D radiographic measurements (p < 0.05). Patients with TFA had greater femoral head asphericity within the SSM, which was moderately correlated to head-neck offset (r = −0.54) and α-angle (r = 0.63), as well as greater trochanteric torsion, which was strongly correlated to the novel radiographic measure of trochanteric torsion (r = −0.78), compared to controls. For 2D measures, the neck-shaft angle was smaller in the TFA group compared to the control group (p = 0.01) while greater trochanter height was larger in the TFA group compared to the control group (p = 0.04). These results indicate altered loading from transfemoral prosthesis use changes proximal femur bony morphology, including femoral head asphericity and greater trochanter changes. Greater trochanter morphologic changes, though not a known factor to OA, affect moment arm and line of action of the primary hip abductors, the major muscles which contribute to joint loading and hip stability. Thus, chronic altered loading of the amputated limb hip, whether under- or overloading, results in bony changes to the proximal femur which may contribute to the etiological progression and development of OA.
Hip adduction angle during wider step-width gait affects hip adduction moment impulse
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Decreasing an external hip adduction moment (HAM) impulse during stance is important to prevent the progression of hip osteoarthritis. A hip adduction angle (HAA) during walking influences the HAM impulse. Although a wider step-width (WS) gait is a gait modification to decrease a peak HAM, no study has reported the HAM impulse and HAA.
We investigated whether the HAA influences the peak HAM and HAM impulse during WS gait.
Twenty-six healthy young adults walked with normal step-width (NS) and WS comfortably. They were not instructed about hip adduction motion during gait, and the peak HAM, HAM impulse, HAA, and other gait parameters were evaluated using a 3D motion capture system. The participants were divided into two groups according to the HAA size during WS gait. The percentage reduction of HAM variables (the WS condition relative to the NS condition) and other gait parameters were compared between the groups.
No difference in gait parameters was found between the groups. The percentage reduction of the HAM impulse in participants with smaller HAA was significantly higher than that in participants with larger HAA (14.5 % vs. 1.6 %, p < 0.01). Also, during normal step-width gait, the large HAA group showed a significantly larger HAA compared to the small HAA group (about 3°).
Participants with smaller HAA could decrease the HAM impulse more effectively during WS gait compared with those with larger HAA. Thus, the HAA would influence the HAM impulse reduction effect on the WS gait. We recommend paying attention to the HAA to decrease the HAM with the WS gait.
Quantitative CT of the knee in the IMI-APPROACH osteoarthritis cohort: Association of bone mineral density with radiographic disease severity, meniscal coverage and meniscal extrusion
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Osteoarthritis (OA) is a highly prevalent chronic condition. The subchondral bone plays an important role in onset and progression of OA making it a potential treatment target for disease-modifying therapeutic approaches. However, little is known about changes of periarticular bone mineral density (BMD) in OA and its relation to meniscal coverage and meniscal extrusion at the knee. Thus, the aim of this study was to describe periarticular BMD in the Applied Public-Private Research enabling OsteoArthritis Clinical Headway (APPROACH) cohort at the knee and to analyze the association with structural disease severity, meniscal coverage and meniscal extrusion.
Quantitative CT (QCT), MRI and radiographic examinations were acquired in 275 patients with knee osteoarthritis (OA). QCT was used to assess BMD at the femur and tibia, at the cortical bone plate (Cort) and at the epiphysis at three locations: subchondral (Sub), mid-epiphysis (Mid) and adjacent to the physis (Juxta). BMD was evaluated for the medial and lateral compartment separately and for subregions covered and not covered by the meniscus. Radiographs were used to determine the femorotibial angle and were evaluated according to the Kellgren and Lawrence (KL) system. Meniscal extrusion was assessed from 0 to 3.
Mean BMD differed significantly between each anatomic location at both the femur and tibia (p < 0.001) in patients with KL0. Tibial regions assumed to be covered with meniscus in patients with KL0 showed lower BMD at Sub (p < 0.001), equivalent BMD at Mid (p = 0.07) and higher BMD at Juxta (p < 0.001) subregions compared to regions not covered with meniscus. Knees with KL2–4 showed lower Sub (p = 0.03), Mid (p = 0.01) and Juxta (p < 0.05) BMD at the medial femur compared to KL0/1. Meniscal extrusion grade 2 and 3 was associated with greater BMD at the tibial Cort (p < 0.001, p = 0.007). Varus malalignment is associated with significant greater BMD at the medial femur and at the medial tibia at all anatomic locations.
BMD within the epiphyses of the tibia and femur decreases with increasing distance from the articular surface. Knees with structural OA (KL2–4) exhibit greater cortical BMD values at the tibia and lower BMD at the femur at the subchondral level and levels beneath compared to KL0/1. BMD at the tibial cortical bone plate is greater in patients with meniscal extrusion grade 2/3.
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Temporomandibular joint osteoarthritis (TMJ-OA) is a degenerative disease of the joint. The early manifestations of TMJ-OA are abnormal remodeling of condylar subchondral bone. In bone tissue, bone marrow mesenchymal stem cells (BMSCs) and osteoblasts play important roles in the differentiation and maturation of most hematopoietic cells. MicroRNA-26b (miR-26b) is upregulated during the osteogenesis of BMSCs, and miR-26b overexpression leads to the activation of β-catenin and the enhancement of osteogenesis and cartilage formation. However, the pathologic mechanism remains unclear. In the present study, we used a rat model with OA-like changes in the TMJ induced by experimental unilateral anterior crossbite (UAC) and found that the level of miR-26b was markedly lower in BMSCs from the subchondral bones of UAC rats than in those from sham control rats. MiR-26b overexpression by agomiR-26b increased condylar subchondral bone osteogenesis in UAC rats. Notably, although agomiR-26b primarily affected miR-26b levels in the subchondral bone (but not in cartilage or the synovium), the overexpression of miR-26b in BMSCs in UAC rats largely rescued OA-like cartilage degradation, while the inhibition of miR-26b in BMSCs exacerbated cartilage degradation in UAC rats. We measured the expression levels of β-catenin and related osteogenic and osteoclastic factors after using miR-26b mimics and inhibitors in vivo. Moreover, BMSCs were treated with the β-catenin blocker Wnt-C59 and then transfected with miR-26b mimics or inhibitors. Then, we examined the expression of β-catenin as the direct target of miR-26b. The results of the present study indicate that miR-26b may modulate subchondral bone loss induced by abnormal occlusion and influence the osteogenic differentiation of subchondral BMSCs through β-catenin in the context of TMJ-OA progression.
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To study bone shape changes as a potential early feature of post-traumatic structural knee OA development, we estimated the association between meniscal status in the anterior cruciate ligament (ACL) injured knee and longitudinal condyle changes in bone surface area.
We used data from the KANON trial, including 121 young ACL-injured adults. We obtained baseline and 2-year follow-up knee MRIs. Our outcome was change in the bone surface areas (mean mm2, log-transformed) in 4 locations (femur, tibia, patella, and trochlea femur) in the medial and lateral compartment from baseline to 2 years. Meniscal pathology was defined as both present at baseline and newly developed (i.e., incident or progressed) using ACLOAS. We used multilevel linear regression adjusted for baseline bone area, age, sex, body mass index, treatment arm (i.e., early or optional delayed ACL reconstruction), and location. We analyzed medial and lateral compartment separately. We present results as percentage (%) bone area change difference with 95% confidence intervals (CI).
We analyzed 109 subjects (median 27 (18–36) years, 83% men) due to missing MRI information. The bone surface area increased on average by ∼2% over 2 years. The differences between knees with and without baseline meniscal pathology were 1.1% (95%CI 0.0–2.3%) and 1.4% (95%CI 0.6–2.2%) in the medial and lateral compartment, respectively, and 1.2% (95%CI 0.3–2.0%) and 1.3% (95%CI 0.6–2.0%) for medial and lateral newly developed pathology, respectively.
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Trial registration number ISRCTN 84752559.
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Coronal plane malalignment significantly affected the load distribution. Small changes in coronal tibial slope had less pronounced effects on the load distribution, but increased ligament strains. Transverse plane malalignment only minimally affected the load distribution.
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^☆: This work was supported by the NIH Academic Rheumatology and Clinical Immunology Training grant #AR007304 to J.C.B. and by 2K24-AR04884-06, R01 AR052000-01 A1, BAA-NHLBI-AR-10-06 grants and the Endowed Chair for Aging at U.C. Davis to N.E.L.

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ReviewRole of bone architecture and anatomy in osteoarthritis☆

Abstract

Introduction

Section snippets

Does bone start the ball rolling in OA?

Changes in subcortical bone in early OA: a detailed look

Anatomic bone abnormalities associated with hip OA

Anatomic abnormalities associated with knee OA

Molecular pathways implicated for their role in OA pathogenesis: the WNT/β-catenin and TGF-β/BMP pathways

Conclusions

Osteoarthritis Cartilage

Osteoarthritis Cartilage

Rheum Dis Clin North Am

Osteoarthritis Cartilage

Osteoarthritis Cartilage

Osteoarthritis Cartilage

Osteoarthritis Cartilage

Osteoarthritis Cartilage

Osteoarthritis Cartilage

Bone

Mayo Clin Proc

J Biomech

Osteoarthritis Cartilage

Osteoarthritis Cartilage

Comput Vis Image Underst

Osteoarthritis Cartilage

Osteoarthritis Cartilage

J Orthop Res

Magn Reson Imaging

J Biomech

Osteoarthritis Cartilage

Gene Expr Patterns

Osteoarthritis: is it a disease of cartilage or of bone?

Arthritis Rheum

Subchondral bone in osteoarthritis: a biologic link with articular cartilage leading to abnormal remodeling

Curr Opin Rheumatol

Bone, not cartilage, should be the major focus in osteoarthritis

Nat Clin Pract Rheumatol

The role of joint architecture in the etiology of arthritis

Osteoarthritis Cartilage

Relationship between joint shape and the development of osteoarthritis

Curr Opin Rheumatol

Changes in cartilage and bone metabolism identified by serum markers in early osteoarthritis of the knee joint

Br J Rheumatol

Evidence of altered bone turnover, vitamin D and calcium regulation with knee osteoarthritis in female twins

Rheumatology (Oxford)

99mTc HMDP bone scanning in generalised nodal osteoarthritis. II. The four hour bone scan image predicts radiographic change

Ann Rheum Dis

Prediction of the progression of joint space narrowing in osteoarthritis of the knee by bone scintigraphy

Ann Rheum Dis

Role of subchondral bone in osteoarthritis development: a comparative study of two strains of guinea pigs with and without spontaneously occurring osteoarthritis

Arthritis Rheum

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

Arthritis Rheum

Radiographic osteoarthritis of the hip and bone mineral density. The Study of Osteoporotic Fractures Research Group

Arthritis Rheum

The role of subchondral bone remodeling in osteoarthritis: reduction of cartilage degeneration and prevention of osteophyte formation by alendronate in the rat anterior cruciate ligament transection model

Arthritis Rheum

Subchondral bone changes in hand and knee osteoarthritis detected by radiography

Osteoarthritis Cartilage

Role of subchondral bone in the initiation and progression of cartilage damage

Clin Orthop Relat Res

Macroradiography using conventional radiographic X-ray equipment

Br J Radiol

Periarticular cancellous bone changes following anterior cruciate ligament injury

J Appl Physiol

Human adult chondrocytes express hepatocyte growth factor (HGF) isoforms but not HgF: potential implication of osteoblasts on the presence of HGF in cartilage

J Bone Miner Res

Alteration of cartilage metabolism by cells from osteoarthritic bone

Arthritis Rheum

Biochemical and mechanical properties of subchondral bone in osteoarthritis

Biorheology

Analysis of texture in macroradiographs of osteoarthritic knees using the fractal signature

Phys Med Biol

A robust and accurate method for calculating the fractal signature of texture in macroradiographs of osteoarthritic knees

Med Inform (Lond)

Trabecular morphometry by fractal signature analysis is a novel marker of osteoarthritis progression

Arthritis Rheum

Fractal analysis of trabecular bone in knee osteoarthritis (OA) is a more sensitive marker of disease status than bone mineral density (BMD)

Calcif Tissue Int

Review
Role of bone architecture and anatomy in osteoarthritis☆