Feline chondromalacia is a disorder of endochondral ossification of articular and epiphyseal cartilage. The disease occurs mainly in fast-growing large and giant dogs (4 to 8 months of age). It can develop in many articular and epiphyseal cartilages throughout the body. It is characterized clinically by a history of no trauma, lameness, and pain. ⒈ exfoliative osteochondrosis: abnormal thickening and cracking of articular cartilage, which in turn separates from the subchondral bone to form cartilage flaps or free cartilage pieces. It occurs mainly in the shoulder joint (posterior edge of the humeral head), elbow joint (medial humeral condyle), knee joint (internal and external femoral condyles) and tarsal joint (talar talus slide). The elbow prominence does not close: the center of elbow prominence ossification and the proximal ulnar epiphysis do not close for a long time (epiphyseal growth plate cartilage does not ossify), making the elbow joint unstable and prone to secondary elbow degenerative joint disease. Splitting of the ulnar coronoid process: The ulnar coronoid process splits into several pieces and does not heal with the ulna, which can lead to degenerative joint disease. Delayed closure of the secondary ossification centers of the long bones, such as delayed closure of the distal ulnar ossification center and normal closure of the distal radius ossification center, results in unsynchronized radial and ulnar bone growth, leading to angular deformity of the radius and ulna or subluxation of the elbow joint. The etiology is not well understood. Injury may be a factor, causing limited damage to the cartilage. Osteonecrosis due to hypernutritional hypertrophy, calcitonin, hormonal imbalance and other joint diseases can also cause this disease. There may also be a genetic link. Although some have no history of injury, there is a family history of the disease, as it occurs mostly in certain large breeds of dogs, such as the St. Bernard, German Shepherd, Golden Retriever, and Newfoundland. The main symptom is lameness. The lameness gradually increases and is persistent, often with inflexible joints after rest or lameness aggravated after exercise. Most of the joints of one limb develop, but several joints can develop at the same time. Joint extension of the affected limb can cause a painful response, with shoulder joint pain being more pronounced. In chronic cases, a “clicking” sound can be heard in the joints and muscle atrophy can be observed. If left untreated, persistent claudication can lead to degenerative joint disease. Diagnosis is based on body type, age, medical history and clinical symptoms to make a preliminary diagnosis, and X-ray examination is required to confirm the diagnosis. In early stages of the disease (4-6 months of age), a flattened subchondral bone is visible on X-ray because the separated cartilage has not yet calcified; as the epiphysis grows further, the defect takes on a shallow butterfly shape (6-7 months of age at this time); subsequently, the cartilage flap begins to calcify, but it remains in the joint surface defect (7-8 months of age or older); in severe cases, the calcified cartilage flap protrudes from the surface of the humeral head or even falls off to the posterior humeral head In severe cases, the calcified cartilage flaps protrude from the surface of the humeral head or even fall off to the back of the humeral head. Treatment methods 1. Clinical symptoms are mild, the course of the disease does not exceed 1 month, X-ray examination does not find calcified cartilage flap, conservative treatment can be used. The animal is forced to rest for 6 weeks, or the affected limb is suspended to limit the activity. If the pain is severe, anti-inflammatory analgesics can be used, but the animal still needs to rest forcibly, otherwise it will aggravate the disease. 2. If the cartilage flap has been found on X-ray examination or has been detached, surgery should be used as early as possible to remove it and remove the cartilage defective tissue of the humeral head that has been necrosed.
