Meniscal tears and malposition result in cartilage loss in patients with symptomatic knee osteoarthritis (OA), according to a study in the March issue of Arthritis & Rheumatism.¹ While the onset of knee OA after meniscectomy is fairly common and is traditionally considered a result of the joint injury, until now little was known about the effect of meniscal damage and abnormalities on cartilage loss in knees with a predisposition for the disease.

The new study showed that in the medial tibiofemoral joint, each measure of meniscal malposition was associated with an increased risk of cartilage loss. Moreover, there was a strong association between meniscal damage and cartilage loss. For example, correlation coefficients between meniscal damage, height, and proportion of coverage in the medial compartment ranged from 0.69–0.87 (P <.0001), whereas correlations of meniscal measures were weaker in the lateral compartment and ranged from 0.20–0.45 (P <.0001). Since meniscal coverage and meniscal height diminished with subluxation, less coverage and reduced height also increased the risk of cartilage loss, the authors report.

In the study of 257 subjects enrolled in the Boston Osteoarthritis of the Knee Study, researchers used magnetic resonance imaging (MRI) to measure the position of the meniscus and to evaluate and score the severity of meniscal damage. Among the MRI-assessed knees, 29% had a previous injury, 27% had a previous surgery, and 5% had a previous meniscectomy.

Study subjects had a mean age of 66.6 years and mean body mass index (BMI) of 31.5 ±  5.7 kg/m². All study participants met the American College of Rheumatology criteria for symptomatic knee OA, confirmed by X-rays and self-reports of frequent knee pain. Baseline assessments included knee MRI with follow-up MRI at 15 and 30 months. Cartilage and meniscal damage were scored on MRI in the medial and lateral tibiofemoral joints using the semiquantitative whole-organ MRI score. Tibiofemoral cartilage was scored on MRIs of all five plates of each tibiofemoral joint, and the meniscal position was measured using eFilm Workstation software.

"This study highlights the importance of an intact and functioning meniscus in subjects with symptomatic knee OA, since the findings demonstrate that the loss of function has important consequences for cartilage loss," conclude the researchers, led by David J. Hunter, MD, a rheumatologist at Boston University Medical Center in Boston, Massachusetts.

"At present, efforts are being made to preserve a damaged meniscus rather than remove it, and an industry of meniscal replacements is developing," Dr. Hunter concludes. "Our study points to the need for critical, prospective evaluation of these new therapeutic options."

More attention to the role of the meniscus in OA

"Meniscal disease as a cause of OA is well known," explains Kenneth D. Brandt, MD, professor emeritus of medicine and orthopaedic surgery at Indiana University School of Medicine in Indianapolis, Indiana. "Patients who have a meniscus injury and have it yanked out by an orthopaedist were known to be at an increased risk for developing OA, so in an epidemiological sense this is known," he says. "The meniscus also gets damaged as a result of OA—not just football or soccer players with acute injuries, but also patients with idiopathic OA."

The new study and others by the same group of investigators "have emphasized that because of MRI studies, you can see the meniscus is out of place and can't serve a proper mechanical function," Dr. Brandt tells CIAOMed. The role of the meniscus "has been insufficiently emphasized," he says. "OA is not simply a cartilage disease; it's a disease of an organ and all the tissues. Everything is involved. [The new study] puts mechanics right in the middle, and this is not given sufficient weight by people who try to design [disease-modifying] drugs for OA."

Reference

1. Hunter DJ, Zhang YQ, Niu JB, et al. The association of meniscal pathologic changes with cartilage loss in symptomatic knee osteoarthritis. Arthritis Rheum. 2006;54:795-801.