The coefficient of friction (COF) of articular cartilage is thought to increase with osteoarthritis (OA) progression, and this increase may occur due to a decrease in lubricin concentration. The objectives of this study were to measure the COF of guinea pig tibiofemoral joints with different stages of OA and to establish relationships between COF, lubricin concentrations in synovial fluid, and degradation status using the Hartley guinea pig model. Both hind limbs from 24 animals were harvested: seven 3-month-old (no OA), seven 12-month-old (mild OA), and 10 that were euthanized at 12 months of age after undergoing unilateral ACL transection at 3 months of age (moderate OA). Contralateral knees served as age-matched controls. COFs of the tibiofemoral joints were measured using a pendulum apparatus. Synovial fluid lavages were analyzed to determine the concentration and integrity of lubricin using ELISA and Western blot, and the overall articular cartilage status was evaluated by histology. The results showed that the mean COF in the ACL-deficient knees was significantly greater than that of the no OA (p < 0.01) and mild OA knees (p < 0.01). Lubricin concentrations in the ACL-deficient knees were significantly lower than that in both of the other groups (p < 0.01). No significant differences in COF or lubricin concentration were found between the no OA and mild OA knees. Histology verified the extent of cartilage damage in each group. ß

The purpose of this study was to investigate the mechanical consequences of proteoglycan 4 (Prg4) deficiency on intervertebral disc mechanics using a Prg4 knockout mouse model. Prg4, also called lubricin, was first identified as the boundary lubricant in synovial fluid but has subsequently been localized within a number of musculoskeletal tissues in areas subjected to shear and tensile stresses, including the intervertebral disc. The function of lubricin in the intervertebral disc has not been determined. Lumbar level 1–2 vertebral body-disc-vertebral body motion segments were isolated from Prg4 null mice and wild type (WT) litter mate controls. Disc dimensions were measured and motion segments were tested in axial loading and torsion. Torque measurements and disc dimensions were used to calculate the torsional apparent modulus for discs from Prg4 null and WT discs. Discs from Prg4 null mice had a significantly smaller mean transverse disc area (p=0.0057), with a significantly larger proportion of this area occupied by the nucleus pulposus (p<0.0001), compared to WT specimens. Apparent torsional moduli were found to be elevated in Prg4 null lumbar discs compared to WT controls at 10–10° (p=.0048) and 10–30° (p=0.0127) rotation. This study suggests a functional role for Prg4 in the murine intervertebral disc. The absence of Prg4 was associated with an increased apparent torsional modulus and the structural consequences of Prg4 deficiency in the intervertebral disc, with expansion of the area of the nucleus pulposus relative to the transverse disc area in Prg4 null specimens.

Painful and inflamed joints result from joint trauma involving disruption of the cartilage [1]. The pathogenesis of post-traumatic osteoarthritis is not well understood but is most likely multifactorial. Other factors, such as inflammation, may be a critical precursor for post-traumatic arthritis. Transient acute synovitis and inflammation following a traumatic event can persist for months and may be representative of a serious joint injury [2]. Joint effusion aspirates from patients in the acute phase of injury have a higher level of activated leukocytes and an increased rate of reactive oxygen species (ROS) production relative to autologous peripheral blood [3]. In an in vitro study, the presence of inflammatory leukocytes caused more chondrocyte death isolated from traumatized matrix region relative to impacted cartilage alone [4]. Our previous study showed that severe trauma may not be a good predictor for the development of post-traumatic arthritis since chondrocyte death and matrix loss was minimal up to seven days post-trauma [5].