What happens to bones in patients with osteoarthritis?

Bone Changes in Osteoarthritis

In osteoarthritis, bones undergo active remodeling characterized by osteophyte formation, subchondral bone thickening and sclerosis, cortical bone thickening, and increased bone mineral density—changes that paradoxically occur alongside cartilage destruction and represent an integral pathological component of the disease rather than a secondary phenomenon. 1, 2, 3, 4

Primary Bone Alterations

Osteophyte Formation and Hypertrophy

• Osteophytes (bone spurs) develop at joint margins as part of the hypertrophic bone response characteristic of osteoarthritis 1, 5
• In facet osteoarthritis of the spine, osteophytes develop alongside hypertrophy and sclerosis of the facet joints 1
• These bony outgrowths represent the body's maladaptive attempt at joint stabilization during progressive cartilage loss 2, 3

Subchondral Bone Remodeling

• Progressive cartilage loss triggers active bone remodeling in the subchondral bone (the bone layer directly beneath the cartilage) 2, 3, 4
• Subchondral bone undergoes both catabolic and anabolic remodeling processes in response to altered mechanical loading and biochemical signals 6
• The subchondral bone architecture changes at cellular and molecular levels, not just structurally 4

Cortical Bone Thickening and Sclerosis

• In advanced hip osteoarthritis, cortical bone thickening occurs on the medial or lateral side of the femoral neck, resulting in increased bone mineral density 1
• Sclerosis (abnormal hardening and increased density) of bone tissue develops as part of the disease process 1
• This thickening represents an attempt to redistribute mechanical loads across damaged joint surfaces 2, 3

Increased Bone Mineral Density

• Paradoxically, bone mineral density (BMD) increases in osteoarthritic joints despite the destructive nature of the disease 1
• In spine osteoarthritis, approximately 40% of women aged 55 and 85% of those over 75 years demonstrate increased BMD due to osteophytes, hypertrophy, and sclerosis 1
• This increased BMD can create diagnostic challenges on DXA scans, as it may mask concurrent osteoporosis 1

Pathophysiological Mechanisms

Altered Load Distribution

• Cartilage erosion alters load distribution over the joint surface, leading to abnormal mechanical stress on underlying bone 2, 3
• In knee osteoarthritis specifically, approximately 70-80% of joint load passes through the medial compartment during mid-stance phase of gait, creating asymmetric loading patterns 2, 7
• This malalignment drives compensatory bone remodeling in an attempt to adapt to altered biomechanics 2, 3

Bone-Cartilage Communication

• Increased vascularization and formation of microcracks in joints facilitate molecular communication between cartilage and bone 6
• Cartilage and subchondral bone actively communicate through signaling pathways to regulate joint homeostasis under pathological conditions 6
• Changes in bone are not merely secondary manifestations but active components of disease progression 6, 8

Inflammatory Component

• Synovial inflammation contributes to bone remodeling alongside mechanical factors 2, 3
• The entire joint undergoes structural and functional alterations, with bone changes representing an integral part of the disease process 9, 8

Clinical Implications

Diagnostic Considerations

• Vertebrae affected by significant osteoarthritic changes should be excluded from bone density measurements when they differ by more than a T-score of 1.0 from adjacent vertebrae 1
• The increased BMD from osteoarthritis can spuriously elevate bone density readings, potentially masking true osteoporosis 1
• Hip osteoarthritis causes less BMD artifact than spine osteoarthritis but still requires careful interpretation 1

Impact on Disease Progression

• Bone remodeling contributes to joint deformity development, including flexion deformities that commonly occur in advanced disease 2, 3
• The combination of cartilage loss, bone remodeling, and osteophyte formation collectively drives malalignment and functional impairment 2, 3
• Ligamentous laxity develops as bone and joint architecture changes, further reducing joint stability 2

Common Pitfalls

The most critical pitfall is assuming bone changes are merely secondary to cartilage damage—bone actively participates in disease pathogenesis and progression through bidirectional communication with cartilage 4, 6, 8. Clinicians must recognize that:

• Increased bone density on imaging does not indicate bone health in osteoarthritic joints 1
• Bone changes begin early in the disease process, not just in advanced stages 3, 6
• Therapeutic strategies targeting only cartilage preservation miss the active role of bone in disease progression 4, 6, 8