IntroductionOsteoporosis (OP) increases cartilage damage in a combined rabbit model of OP and osteoarthritis (OA). Accordingly, we assessed whether microstructure impairment at subchondral bone aggravates cartilage damage in this experimental model.MethodsOP was induced in 20 female rabbits, by ovariectomy and intramuscular injections of methylprednisolone hemisuccinate for four weeks. Ten healthy animals were used as controls. At week 7, OA was surgically induced in left knees of all rabbits. At 22 weeks, after sacrifice, microstructure parameters were assessed by micro-computed tomography, and osteoprotegerin (OPG), receptor activator of nuclear factor-κB ligand (RANKL), alkaline phosphatase (ALP) and metalloproteinase 9 (MMP9) protein expressions were evaluated by Western Blot at subchondral bone. In addition, cartilage damage was estimated using the histopathological Mankin score. Mann-Whitney and Spearman statistical tests were performed as appropriate, using SPSS software v 11.0. Significant difference was established at P < 0.05.ResultsSubchondral bone area/tissue area, trabecular thickness and polar moment of inertia were diminished in OPOA knees compared with control or OA knees (P < 0.05). A decrease of plate thickness, ALP expression and OPG/RANKL ratio as well as an increased fractal dimension and MMP9 expression occurred at subchondral bone of OA, OP and OPOA knees vs. controls (P < 0.05). In addition, the severity of cartilage damage was increased in OPOA knees vs. controls (P < 0.05). Remarkably, good correlations were observed between structural and remodelling parameters at subchondral bone, and furthermore, between subchondral structural parameters and cartilage Mankin score.ConclusionsMicrostructure impairment at subchondral bone associated with an increased remodelling aggravated cartilage damage in OA rabbits with previous OP. Our results suggest that an increased subchondral bone resorption may account for the exacerbation of cartilage damage when early OA and OP coexist simultaneously in same individuals.

Improvement of microstructural and remodelling parameters at subchondral bone by PTH [1-34] contributed to prevent cartilage damage progression in rabbits with early OPOA. These findings support the role of subchondral bone in OA. Further studies are warranted to establish the place of bone-forming agents as potential treatment in OA.

Intermittent administration of PTH [1-34] enhances the bone response around titanium implants in a rabbit model of ovariectomy and glucocorticoid-induced osteoporosis.

Diacerein does not seem to reduce but rather increase inflammatory mediators in synoviocytes, while it does not overall affect chondrocyte inflammatory profile.

Intermittent parathyroid hormone (PTH) administration has been shown to be a promising therapy for systemic bone loss. Accordingly, we hypothesized that PTH could have positive results in treating oral complications of osteoporosis. Hence, we evaluated both mandibular bone loss and its response to PTH in a rabbit model of osteoporosis induced by ovariectomy and glucocorticoid administration. There was a significant and marked decrease in bone mineral density (BMD), bone mineral content (BMC), and calcium content in ash from the osteoporotic peri-alveolar region, which influenced global jaw loss. Remarkably, PTH (1-34) administration to osteoporotic rabbits almost completely reversed BMD, BMC, and calcium content fall in the peri-alveolar region, subsequently reducing global mandibular bone loss. Thus, although the peri-alveolar region is particularly susceptible to osteoporosis, it also responds well to intermittent PTH. Therefore, these results suggest that PTH might represent a valid therapy for improving the osseointegration of dental implants in persons with osteoporosis.