CORR Insights®: How Does the Subchondral Bone Density Distribution of the Distal Humerus Change Between Early and Advanced Stages of Osteoarthritis?

Where Are We Now?

There are important differences of opinion about the genetic basis of osteoarthritis (OA), as well as whether risk of the disease (or disease progression) is reduced or increased by use of the joint. The joint under most investigation at present is the knee, because of the high prevalence of OA in older patients, and because of the association of knee OA with soccer players and marathon runners [2, 5, 13]. Changes in the subchondral bone can predict subsequent symptoms or structural progression [3, 14], and recently it has been shown that not only local joint inflammation but also low-grade systemic inflammation may contribute to the OA disease process [1, 9].

In this month’s issue of Clinical Orthopaedics and Related Research®, Hwang et al. [6] focus on the relationship between subchondral bone density, OA, and the carrying angle at the elbow. Although Li et al. [10] reviewed the interrelationship between bone structure, bone density, and bone metabolism about 10 years ago, there has been little investigation of this topic since. Hwang et al. [6] found that in patients with more advanced elbow OA, subchondral bone density was more radially deviated. The authors also found a link between an increased carrying angle and radial deviation of stress. Based on these findings, surgeons and researchers should further explore whether this might be more biomechanically related or a consequence of secondary biological effects by carrying out good-quality investigations with well-designed research.

Where Do We Need To Go?

It is interesting to see the drift toward radiocapitellar OA with increasing carrying angles but the question remains: Is this a cause and effect or is it a consequence? The research in this month’s CORR® [6] was carried out in South Korea. I did wonder whether differences in carrying angle in the contralateral elbow could have been informative, as others have found differences in skeletal alignment between patients of Asian descent and those of other races [4, 8]. I note that a study from Malaysia found “that the left arm has a greater carrying angle then the right arm in both genders” [11], which was a novel finding, as most previous studies had shown the right arm had a wider carrying angle than the left arm. Validation of these carrying angle findings in other patient populations would be interesting.

The dynamics of subchondral bone biology and morphology are constantly changing, and they are influenced by mechanical factors. For example, in their study, Martinez-Catalan and Sanchez-Sotelo [12] highlighted that “most patients with primary osteoarthritis of the elbow report a history of heavy lifting with the affected upper extremity,” so it is important for this to be considered as a causative factor, though this is hardly going to be the last word on the topic. And it is well recognized that in the proximal femur, mechanical stresses influence the trabecular orientation as well as the contour and shape of subchondral bone. Researchers now need to tease out whether the drift toward valgus in elbow arthritis is the cause of changes in subchondral morphology and biology or whether biological changes to the articular cartilage are caused by more rigid subchondral bone that develops either as a consequence of changes in biology or indeed are genetically influenced.

How Dost We Get There?

This research into OA development is focused on whether subchondral bone rigidity is the cause of articular cartilage deterioration or whether articular cartilage deterioration is the cause of subchondral bone changes. This is a classic “Is the cart before the horse” conundrum. This will be challenging to determine, but once we start to understand this, we must focus on preventative measures that reduce OA progression. We need to explore to what degree repetitive injury causes OA, and which particular aspects of mechanical stress is most important in that pathogenesis. The challenge is very similar to that facing the researchers studying head trauma in sport and its link to long-term brain injury. We know they are related, and we need to work out the most important factors and develop mitigation schemes to reduce or even eliminate the risk.

To date, no treatments to reverse cartilage stiffening and the resulting damage have been identified. Current treatments—exercise, weight loss, physical therapy, medications, injections, and joint replacement surgery—are more focused on reducing pain and improving mobility. Much has remained unknown about the molecular causes of this damage and how to treat it, but perhaps there is now some light at the end of the tunnel.

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Lessons are being learned from current biological research focusing on the more common OA of the knee.

• An animal study found a new mechanism that links age-related cartilage tissue stiffening with the repression of a key protein associated with longevity [7]. This study offers new potential treatment targets to restore cartilage health, and the results may explain why epigenetic factors caused by aging affect other tissues throughout the body.