Osteoarthritis (OA) is a prevalent joint condition affecting millions globally, characterized by the breakdown of articular cartilage and changes in the underlying bone. This degradation leads to pain, stiffness, and reduced joint function, often progressing over time. Understanding its contributing factors helps recognize individual susceptibility and potential preventative strategies. Some factors are unchangeable, while others are influenced by lifestyle and overall health.
Inherent Risk Factors
Age represents the largest inherent risk factor for osteoarthritis, with its prevalence increasing with each decade of life. Cartilage naturally undergoes changes as people get older, including reduced cellularity and decreased capacity for repair, making it more susceptible to wear and tear.
Genetic predisposition plays a role in OA development, as the condition often runs in families. While no single gene has been identified as the sole cause, genetic variants related to cartilage extracellular matrix structure and bone density have been implicated. These genetic influences can affect joint structure, cartilage quality, or the body’s ability to repair joint tissues, increasing an individual’s susceptibility.
Sex differences are observed in OA prevalence, with the condition becoming more common in women after age 45, whereas it is slightly more common in men before this age. This shift in prevalence may be linked to hormonal changes, particularly the decline in estrogen levels following menopause, which can affect cartilage and joint metabolism. Congenital bone deformities, such as hip dysplasia or misaligned joints, can lead to uneven weight distribution and increased stress on specific areas of the joint. Such structural abnormalities accelerate cartilage degradation, contributing to earlier onset or more severe forms of OA.
Lifestyle and Activity-Related Factors
Excess body weight places increased mechanical stress on weight-bearing joints like the knees, hips, and spine, raising the risk of osteoarthritis. Additional load accelerates the wear and tear on articular cartilage, leading to its degradation. Beyond mechanical stress, obesity is associated with OA in non-weight-bearing joints, suggesting that metabolic factors may also contribute to cartilage damage.
Previous joint injuries, such as fractures, ligament tears, or meniscal damage, predict OA in the affected joint. These traumatic events alter the joint’s biomechanics, leading to abnormal loading patterns and increased friction within the joint. Minor injuries can compromise cartilage integrity over time, making it more vulnerable to further degradation.
Repetitive stress and certain occupational hazards contribute to OA risk. Jobs or sports that involve repeated strain, heavy physical workloads, frequent kneeling, stair climbing, or whole-body vibration accelerate cartilage breakdown. For instance, heavy physical work is a common occupational risk factor for knee, hip, and spine OA. This continuous mechanical loading overwhelms the cartilage’s capacity for repair, leading to microtrauma and progressive joint damage.
Contributing Health Conditions
Certain medical conditions increase susceptibility to osteoarthritis by directly or indirectly affecting joint health. Metabolic disorders, such as diabetes, have been linked to an elevated risk of OA. Diabetes impairs cartilage health and its repair processes, as advanced glycation end-product (AGE) accumulation can stiffen cartilage and make it more prone to damage.
Hemochromatosis, a condition characterized by iron overload, contributes to joint damage and subsequent OA. Excess iron deposits in the joints can lead to inflammation and direct injury to the cartilage and synovium, predisposing to arthritic changes. Other forms of arthritis, such as rheumatoid arthritis or gout, cause joint destruction. This pre-existing damage to the joint structures leads to secondary osteoarthritis.