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Early Detection of OA Key to Treatment


Synovitis predates and is associated with the development of radiographic osteoarthritis, new findings suggest. Treating synovitis in knee OA may help reduce disease progression and relieve symptoms. Details here.

The following two studies examine various factors involved in properly diagnosing osteoarthritis (OA). One looks at synovitis as a potential predictor for developing knee OA and the second looks at how leptin is tied to cartilage loss, which may help detect early OA.

Synovitis: A Precursor of Radiographic Knee OA?

The presence of effusion-synovitis or Hoffa-synovitis significantly increases the risk of radiographic knee OA according to an international nested, case-control study.

The researchers selected 133 knees (from 120 persons) that developed radiographic knee OA, based on x-ray and MRI without contrast, within 48 months of having a Kellegren Lawrence grading (KLG) of 0 on knee radiographs. All case patients were enrolled in the OA Initiative, a multicenter, 8-year, prospective, observational cohort of subjects with knee OA or at high risk of developing knee OA.

At baseline, 69.92% of cases and 78.95% of controls were pain free or had infrequent knee pain; 40% of cases had frequent knee pain compared with 28% of controls, reported Inoshi Atukorala, MD, of University of Sydney and the University of Colombo in Sri Lanka, and colleagues.

At the onset of radiographic OA, 57.1% of cases had frequent knee pain and 25.6% had infrequent pain. A history of injury was reported by 20.3% of cases and 12.8% of controls at baseline, and a history of knee surgery by 3.76% and 3.01%, respectively. The KLG of cases at the time of radiographic OA was 2 in 75.9%, 3 in 22.6%, and 4 in 1.5%, whereas 97.7% of controls remained at a KLG of 0 and only 2.3% reached KLG 1, they wrote online in Annals of Rheumatic Diseases.

Effusion-synovitis in the year prior to occurrence of radiographic knee OA tripled the odds of subsequent incident radiographic knee OA (52.80% in cases versus 29.60% in controls, odds ratio 3.23, 95% CI 1.72-6.06). This relationship persisted (OR 4.70, 95% CI 2.35-9.34) at the time of onset of radiographic OA.

Whereas synovitis in OA was previously believed to be a consequence of underlying joint damage, its discovery suggests "that synovial membrane inflammation plays a role early in the disease. These findings are further supported by previous research on knees without OA, which shows that synovitis and effusion increase risk for cartilage loss," the authors wrote.

"Therefore, our findings concur with previous findings which indicate at least an accelerating role of inflammation in disease initiation," they added.

Associations between Hoffa-synovitis and incident radiographic knee OA in cases (versus controls) achieved significance at baseline (46.21% in cases versus 30.83%, OR 1.80, CI 1.10-2.96), the year prior to a finding of radiographic OA (53.23% versus 30.40%, respectively, OR 2.47, CI 1.45-4.23), and concurrent with incident radiographic OA (OR 2.40, CI 1.43-4.04).

Adjusting for potential covariates in sensitivity analyses did not change the association between synovitis/effusion-synovitis and the occurrence of radiographic OA.

Because synovial inflammation was more marked in the year preceding development of radiographic knee OA, it suggests that synovitis predates, and is also associated with the development of radiographic OA, according to the authors.

They add that "treating synovitis in knee OA may have a role in reducing progression of the disease and providing symptom relief. Therefore, the results of this study are useful in identifying a targeted therapy to alter the pathogenesis of knee OA."

Limitations of the study were the use of non-contrast-enhanced MRI -- contrast-enhanced MRI is the "gold standard" for identifying synovitis -- and the retrospective study design.

Leptin May Be Key In Knee Cartilage Loss

Circulating leptin was linked to knee cartilage thinning in adults after adjusting for body mass index (BMI) and other factors, and may potentially explain the association between obesity and cartilage thickness.

Over 2.7 years, baseline levels of leptin and changes in leptin over time were negatively associated with changes in medial tibial cartilage thickness in a cohort of 163 subjects older than 50, reported Oliver P. Stannus, of the University of Tasmania in Australia, and colleagues in Annals of Rheumatic Diseases.

Leptin is a protein that influences body weight homeostasis and regulates immune and inflammatory processes. A previous study using MRI found serum leptin to be associated with reduced knee cartilage volume.

Because cartilage thickness may be more sensitive in detecting early OA, the authors sought to determine the cross-sectional and longitudinal associations between serum leptin levels and knee cartilage thickness.

The 163 patients were selected randomly from the Tasmanian Older Adult Cohort study, which sought to identify factors related to development and progression of OA. All had MRI images of the right knee at baseline and follow-up to assess knee cartilage thickness, and 157 had serum leptin measurements at baseline and follow-up for longitudinal analysis.

Forty-six percent of the participants were women; average age of the entire cohort at baseline was 62.6 years and their mean BMI was 27.5 kg/m2. The median and mean leptin levels were 8.65 pg/mL and 12.69 pg/mL, respectively.

After adjustment for age, sex, BMI, radiographic OA, lean mass, and smoking and disease status, cross-sectional analyses showed that leptin levels were significantly associated with knee cartilage thickness at all sites:

  • Femoral: beta -0.013 (95% CI -0.022 to -0.003)
  • Medial tibial: beta -0.009 (95% CI -0.018 to -0.001)
  • Lateral tibial: beta -0.012 (95% CI -0.021 to -0.003)
  • Patellar: beta -0.014 (95% CI -0.026 to -0.002)

Longitudinally, baseline leptin was negatively associated with change in cartilage thickness at the femoral, medial tibial, and lateral tibial sites, and the association with change in medial tibial cartilage thickness (beta -0.004, 95% CI -0.007 to -0.001) remained significant after adjustment for the same covariates above. Change in serum leptin was negatively associated with change in medial tibial cartilage thickness, and this association remained unchanged after multivariable analysis (beta -0.009, 95% CI -0.018 to -0.001).

Excess leptin may play a catabolic role that contributes to the pathological process of OA, the authors speculated. In animal studies, it appeared to be an important local and systemic factor that influenced cartilage degradation. Decreases in serum leptin with weight loss may explain the improvement in physical function and symptoms in patients with knee OA who lose weight.

Two other features of leptin in OA may have been elucidated in the current study.

"First, adiposity status as a risk factor for OA may be mediated by leptin," as participants with higher baseline levels of leptin had higher BMI, total body fat and trunk fat, and lower cartilage thickness than those with lower levels of leptin, the authors wrote. "We also found significant associations between adiposity measures and cartilage thickness, the magnitude of which decreased substantially at all sites after adjustment for leptin, providing support for this hypothesis of mediation."

Second, longitudinal results demonstrated that loss of media tibial cartilage thickness was most strongly associated with leptin, which may indicate that cartilage degradation is more common in the medial compartment.

The response rate of only 57% yielded a modest sample size, which represented a possible study limitation, the authors noted, but was offset by a high retention rate (82%). Comorbidities in the sample may have affected the associations, even though results were largely unchanged when adjusted for disease status or when subjects with other diseases were excluded from analysis. Also, leptin levels measured in serum do not allow for detection of local autocrine or paracrine effects of leptin, they said.

This article was first published on MedPage Today and reprinted with permission. (Free registration is required.)

The OAI is a public-private partnership between the National Institutes of Health (NIH) and private industry including Merck Research Laboratories, Novartis Pharmaceuticals, GlaxoSmithKline, and Pfizer.

Atukorala disclosed funding from the Osteoarthritis Research Society International Collaborative Scholarship. One co-author disclosed funding by an NHMRC Health Practitioner Fellowship.

Co-authors disclosed relevant relationships with Boston Core Imaging Lab (BICL), Novartis and, Astra-Zeneca.

The study by Stannus' group was supported by the National Health and Medical Research Council of Australia , the Tasmanian Community Fund, the Arthritis Foundation of Australia, and the University of Tasmania Grant–Institutional Research Scheme.

Stannus and co-authors disclosed no relevant relationships with industry.

Reviewed by Zalman S. Agus, MD Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner.


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