A study of 11 1 cases of cranial cruciate ligament disease, seen over a three year period has been made. Fifty-five of these dogs were under four years of age (average age 21.4 months) and most were of the larger breeds, particularly the rottweiler (25 per cent). The onset of clinical signs was sudden in 53 per cent and gradual in 47 per cent of these cases; bilateral disease was present in 31 per cent. The severity of the lameness was variable. The pathogenesis of the disease appears to involve a gradual stretching, partial rupture and eventually a complete rupture of the cranial cruciate ligament. The term cruciate disease has been used to cover this spectrum of ligament pathology and the clinical signs can appear at any stage during this ligament degeneration. Slight anterior drawer .movement can often be detected during the earlier stages of stretching and partial rupture but this can only be appreciated under general anaesthesia. Osteoarthritis is initiated during the early stages and may be well established by the time the cruciate completely tears. The predisposition to cruciate disease in these young dogs of the larger breeds is difficult to explain but may be related to inadequate exercise during puppyhood.
The prevalence of radiographic signs of degenerative joint disease (including appendicular osteoarthritis) among a hospital population of 218 cats was 33.9 per cent (74 cats), and the prevalence of signs of appendicular joint osteoarthritis was 16.5 per cent (36 cats). Half of the cases of appendicular joint osteoarthritis had no apparent radiographic or historical cause, and clinical signs of lameness were recorded in only six of them, all of which had an apparent radiographic cause. The 74 cats with radiographic signs of degenerative joint disease were on average significantly older than the 144 cats in which there were no radiographic signs of the disease.
Bacterial infections of joints produce an inflammatory arthropathy. Most cases appear to be due to the haematogenous localisation of bacteria in a joint and trauma may predispose a joint to infection. Two clinical syndromes are identified; the classic acute onset case and a more chronic local grade infection syndrome. Affected joints are usually thickened and show pain on manipulation. The synovial fluid has increased numbers of white cells, most of which are polymorphonuclear leucocytes. Peripheral blood analysis may be normal and only a few dogs show systemic illness. Radiography in the early stage, will only show soft tissue changes; periosteal new bone and bony destruction are seen in longer standing cases. The carpus was the most frequently affected joint and the larger breeds, particularly the males, were over‐represented. Various organisms were isolated but haemolytic Streptococcus and Staphylococcus intermedius were the most common. Culture of the synovial membrane was more sensitive than the synovial fluid. Antibiotic therapy for several weeks was generally successful providing an early diagnosis was made. In a few cases, steroid responsive synovial inflammation persisted in the absence of viable bacterial organisms.
Medical and/or surgical management were usually successful in resolving infection (94 per cent). However, they were frequently unsuccessful in restoring full joint function; this may in part have been due to the nature of the underlying joint
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