Effects of calcitonin on subchondral trabecular bone changes and on osteoarthritic cartilage lesions after acute anterior cruciate ligament deficiency.
Because SBM may contribute to cartilage breakdown in OA, experimental OA was induced in dogs by transecting the anterior cruciate ligament of the knee and treating with either CT or a placebo. CT significantly reduced both SBM and cartilage lesions. This study supports the use of CT in the treatment of canine experimental OA.


BACKGROUND
Because subchondral bone remodeling (SBM) may contribute to cartilage breakdown in osteoarthritis (OA), we evaluated to what extend calcitonin (CT) might affect cartilage and bone changes in the early stages of canine experimental OA.


METHODS
Twelve dogs underwent transection of the anterior cruciate ligament (ACLT) of the right knee. After ACLT, each animal received a daily nasal spray delivering either 400 U of CT (CT-treated group; n = 6) or a placebo (PL-treated group; n = 6). At day 84 after surgery, animals were killed, and cartilage changes were graded. BMD and volume fraction (BVF) were assessed by pQCT in different regions of interest (ROIs) of the subchondral cancellous bone of tibial plateaus (TPs). Statistics included a 2 x 2 factorial analysis with +/-CT as one factor and +/-ACLT as the other.


CONCLUSIONS
Nonoperated (N-OP) knees were normal in both groups. In the PL-treated group, ACLT knees all exhibited OA changes, which predominated in the medial knee compartment. Furthermore, compared with N-OP knees, the BMD and BVF of ACLT joints were both markedly reduced in medial TP but not in lateral TP. In contrast, in the CT-treated group, cartilage OA lesions of ACLT knees were significantly reduced, and there was no difference in BMD and BFV between N-OP and ACLT knees. These findings suggest that the loss of subchondral trabeculae contributes to cartilage breakdown, possibly by enhancing cartilage deformation on joint loading. By counteracting bone loss, CT reduced cartilage OA lesions, and thus, might be useful in the treatment of OA in cruciate-deficient dogs.
Department of Anatomy, Université Catholique de Louvain, Brussels, Belgium.
Catherine
C
Behets
James M
JM
Williams
Daniel
D
Chappard
Jean-Pierre
JP
Devogelaer
Daniel-Henri
DH
Manicourt
D000818:Animals; D016118:Anterior Cruciate Ligament / Q000473:pathology*; D001851:Bone Diseases, Metabolic / Q000473:pathology; D002116:Calcitonin / Q000494:pharmacology*; D002356:Cartilage / Q000378:metabolism / Q000473:pathology*; D004285:Dogs; D010003:Osteoarthritis / Q000188:drug therapy* / Q000473:pathology*; D010919:Placebos; D012474:Salmon / Q000378:metabolism; D013977:Tibia / Q000378:metabolism / Q000473:pathology
D010919:Placebos; D002116:Calcitonin