Abstract
Abstract
Purpose
Several cytokines and growth factors start and progress the destruction process of joint hyaline cartilage and fibrosis formation. Captopril is classified as an Angiotensin-converting enzyme inhibitor in which several studies revealed that captopril significantly decreases fibrosis formation in some organs like the liver, heart, and kidney. This study aimed to evaluate the use of captopril in reducing the possibility of arthrofibrosis and osteoarthritis in an animal model.
Method
In this in-vivo animal model study, the anterior cruciate ligament of 24 rabbits was transected to induce osteoarthritis and arthrofibrosis. The control group contained 11 rabbits and the second group consisted of 13 rabbits. The second group was treated with 10 mg/ kilogram/day captopril through a nasogastric tube. The control group was treated with normal saline in the same way. Cartilage damage and osteoarthritis were evaluated by Osteoarthritis Research Society International (OARSI) scoring system. After 30 days, animals were sacrificed, and arthrofibrosis and cartilage damage were evaluated microscopically and macroscopically.
Results
According to macroscopic and microscopic evaluation, captopril dramatically reduced arthrofibrosis formation based on visual scoring and the Masson trichrome staining system. Cartilage damage was lower in the intervention group compared to the control group.
Conclusions
Captopril is an angiotensin-converting enzyme inhibitor that demonstrated to significantly decreases the possibility of arthrofibrosis. Although the beneficial preventive effect of captopril on osteoarthritis was not proved statistically, better results may be obtained if the route of administration or drug dosage is changed.
Publisher
Springer Science and Business Media LLC
Subject
Orthopedics and Sports Medicine
Reference42 articles.
1. Bhimani R, Shahriarirad R, Ranjbar K, Erfani A, Ashkani-Esfahani S (2021) Transportal versus all-inside techniques of anterior cruciate ligament reconstruction: a systematic review. J Orthop Surg Res 16:734
2. Bosch U (2002) Arthrofibrosis. Orthopade 31:785–790
3. Brower GL, Levick SP, Janicki JS (2007) Inhibition of matrix metalloproteinase activity by ACE inhibitors prevents left ventricular remodeling in a rat model of heart failure. Am J Physiol Heart Circ Physiol 292:H3057–H3064
4. Brunelli G, Longinotti C, Bertazzo C, Pavesio A, Pressato D (2005) Adhesion reduction after knee surgery in a rabbit model by Hyaloglide®, a hyaluronan derivative gel. J Orthop Res 23:1377–1382
5. Costa LE, La-Padula P, Lores-Arnaiz S, D’Amico G, Boveris A, Kurnjek ML et al (2002) Long-term angiotensin II inhibition increases mitochondrial nitric oxide synthase and not antioxidant enzyme activities in rat heart. J Hypertens 20:2487–2494