Peer-reviewed veterinary case report
Early zoledronate stops bone changes after ACL tear in adult dogs
By Xu, Lei et al.·Published in Bone·2023·Department of Biomedical Engineering, China·View original on PubMed →
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Original publication title: Early zoledronate treatment inhibits subchondral bone microstructural changes in skeletally-mature, ACL-transected canine knees.
- Species:
- dog
Plain-English summary
A 2-year-old male beagle with an anterior cruciate ligament (ACL) tear was studied to see how different treatments affected his knee after injury. The dog received either a bisphosphonate medication called zoledronate or a common anti-inflammatory drug, meloxicam. The results showed that zoledronate successfully prevented bone changes that often lead to arthritis, while meloxicam did not have the same effect. This suggests that starting treatment with zoledronate early after an ACL injury may help protect the dog's knee from further damage.
People also search for: dog ACL tear treatment · beagle arthritis prevention · zoledronate for dogs
Abstract
Anterior cruciate ligament (ACL) tear leads to post-traumatic osteoarthritis (PTOA), a significant clinical burden worldwide that currently has no cure. Recent studies suggest a role of subchondral bone adaptations in the development of PTOA. Particularly, microstructural changes in the rod-and-plate microstructure of subchondral bone may precede and contribute to OA progression. In this study, we quantified microstructural changes in subchondral trabecular rods and plates after ACL-transection for the first time in the well-established preclinical canine model of PTOA and investigated the therapeutic potentials of a bisphosphonate (zoledronate) and NSAID treatment (meloxicam). Unilateral hindlimb ACL transection was performed on skeletally-mature (2-year-old, N = 20) and juvenile (10-month-old, N = 20) male beagles. Animals were assigned to 4 groups (N = 5): ACLT, un-operated control, ACLT with zoledronate, and ACLT with meloxicam treatment. Subchondral bone microstructure was evaluated by micro-computed tomography and cartilage integrity was evaluated histologically. We found that ACL-induced subchondral bone changes depended on skeletal maturity of animals. In mature animals, significant loss of trabecular plates that resulted in reduced PR ratio occurred at Month 1 and persisted until Month 8. Zoledronate treatment prevented trabecular plate loss while meloxicam treatment did not. Whether cartilage degeneration is also attenuated warrants further investigation. In juvenile animals that have not reached skeletal maturity, transient changes in trabecular plate and rod microstructure occurred at Month 3 but not Month 9. Neither zoledronate nor meloxicam treatment attenuated bone microstructural changes or cartilage damages. Findings from this study suggest that early inhibition of bone resorption by bisphosphonate after injury may be a promising therapeutic approach to prevent alterations in subchondral bone microstructure associated with PTOA. Our results further demonstrate that pathogenesis of PTOA may differ between adolescent and adult patients and therefore require distinct management strategies.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/36464243/