Animal and in vitro studies suggest that parathyroid hormone (PTH) may affect articular cartilage. However, little is known of the relationship between PTH and human joints in vivo.
Longitudinal.
Barwon Statistical Division, Victoria, Australia.
101 asymptomatic women aged 35-49 years (2007-2009) and without clinical knee osteoarthritis, selected from the population-based Geelong Osteoporosis Study.
Blood samples obtained 10 years before (1994-1997) and stored at -80°C for random batch analyses. Serum intact PTH was quantified by chemiluminescent enzyme assay. Serum 25-hydroxyvitamin D (25(OH)D) was assayed using equilibrium radioimmunoassay. Models were adjusted for age, bone area and body mass index; further adjustment was made for 25(OH)D and calcium supplementation.
Knee cartilage volume, measured by MRI.
A higher lnPTH was associated with reduced medial-but not lateral-cartilage volume (regression coefficient±SD, p value: -72.2±33.6 mm(3), p=0.03) after adjustment for age, body mass index and bone area. Further sinusoidal adjustment (-80.8±34.4 mm(3), p=0.02) and 25(OH)D with seasonal adjustment (-72.7±35.1 mm(3), p=0.04), calcium supplementation and prevalent osteophytes did not affect the results.
A higher lnPTH might be detrimental to knee cartilage in vivo. Animal studies suggest that higher PTH concentrations reduce the healing ability of cartilage following minor injury. This may be apparent in the presence of increased loading, which occurs in the medial compartment, placing the medial cartilage at higher risk for injury.