Universidad de Murcia. Departamento de Biología Celular e Histología
Abstract
Osteoporosis (OP) is a major health problem
characterized by compromised bone strength.
Osteoarthritis (OA) is a joint disease that progresses
slowly and is characterized by breakdown of the
cartilage matrix. Alendronate (ALN), a nitrogencontaining bisphosphonate (BIS), inhibits bone loss and
increases bone mineralization, and has been used
clinically for the treatment of OP. It is still controversial
whether BIS is effective in inhibiting the progression of
OA. Chondrocyte apoptosis has been described in both
human and experimentally induced OA models. In our
study we aimed to detect whether ALN could protect
articular cartilage from degeneration and reduce
apoptosis rates in experimentally OA induced rats. For
this rats were ovariectomized (ovex), nine weeks after
operation rats were injected 30 μg/kg/week ALN
subcutaneously for six weeks. After six weeks articular
cartilages were obtained. We did Safranin O staining and
Mankin and Pritzker scorings to evaluate degeneration
and investigated the expressions of p53, cleaved caspase
3, Poly ADP-ribose (PAR), Poly ADP-ribose polymerase
1 (PARP 1), and applied TUNEL technique to determine
apoptotis rates. We found a significant decrease in
glycosaminoglycan (GAG) amount and increased
apoptosis which indicates damage on articular cartilages
of ovex rats. GAG amount was higher and apoptosis rate
was lower on articular cartilages of ALN treated ovex
rats compared to the ovex group. In contrary to studies
showing that early ALN treatment has a protective
effect, our study shows late ALN treatment has a
chondroprotective effect on articular cartilage since we
treated rats nine weeks after ovariectom