Getting to the Core of Bone Marrow Lesions

This post comes from Fred Nelson, MD, an orthopaedic surgeon in the Department of Orthopedics at Henry Ford Hospital and a clinical associate professor at Wayne State Medical School. Some of Dr. Nelson’s tips go out weekly to more than 3,000 members of the Orthopaedic Research Society (ORS), and all are distributed to more than 30 orthopaedic residency programs. Those not sent to the ORS are periodically reposted in OrthoBuzz with the permission of Dr. Nelson. 

The terms “bone marrow edema,” “bone marrow lesion” (BML), and “bone bruise” are often used interchangeably to refer to areas in cancellous bone that have hyperintense marrow signal in fluid-sensitive, fat-suppressed MRI sequences. Although most commonly observed in knee MRIs, BMLs can be seen in a variety of joints. In the hip, they are seen in transient osteoporosis and rapid-onset osteoarthritis. The term “bone bruise” is often specifically applied in the setting of an injury, such as lateral tibial plateau hyperintense changes that are seen after an anterior cruciate ligament rupture.

In the setting of knee osteoarthritis, BMLs are a response to degeneration of menisci, articular cartilage, synovium, or bone itself. One of the mechanisms associated with BMLs seems to be secondary to circulatory response and bone turnover. In one study covered in a 2017 review article¹, patients with OA and associated BMLs were randomized to receive the bone antiresorptive agent zoledronic acid (ZA) or placebo. At 6 months, VAS pain scores in the ZA group were reduced by ZA, the reduction in BML area was greater in the ZA group than in the placebo group, and a greater proportion in the ZA group achieved a clinically significant reduction in BML size (39% vs. 18%, p <0.044). A larger study is planned to further define the relationship between reduction in BML size and pain scores.

Regarding “crosstalk” between subchondral bone and articular cartilage in joint disease, recent data suggest that numerous canals and porosities connect the bone to cartilage at the interface. Treatment of the bone compartment with antiresorptives and anti-TGF-β at specific early time points has been shown to have chondroprotective effects in animal models. Additionally, one study identified s14-3-3ε, a short extracellular protein, as a mediator critical in the communication between subchondral bone and cartilage in OA. This may prove to be a potential target for therapeutic or prognostic use.

Numerous articles have outlined the abundance of trabecular microfractures seen in areas where BMLs are present. A commonly held hypothesis is that resorption cavities caused by bone remodeling can act as stress concentrations, promoting further microdamage and leading to a cycle of damage-remodeling-damage. Some individuals may be more prone to rapid bone turnover and thus more prone to developing bone edema.

When your clinical attention is directed to BMLs, their shape and extent may influence nonsurgical treatment decisions. Conservative management may be directed by a better understanding of how BMLs contribute to pain and OA progression.

Reference

1. Alliston T, Hernandez CJ, Findlay DM, Felson DT, Kennedy OD. Bone marrow lesions in osteoarthritis: What lies beneath. J Orthop Res. 2017 Dec 21. doi: 10.1002/jor.23844. [Epub ahead of print] PMID: 29266428