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Managing Bone Cysts

Dr Jonathan Lumsden is a registered specialist in equine surgery and is the resident surgeon at the Randwick Equine Centre. His special interests are respiratory and arthroscopic surgery and lameness evaluation of racing and sport horses. His referral practice includes scintigraphic examinations as an adjunct to lameness evaluations. He has written articles, proceedings and book chapters and is a regular speaker in Australia and overseas

http://randwickequine.com.au/contact


Figure 1 & 2 - Show radiographs of the stifle of a 2-year-old thoroughbred which developed a hind-limb lameness soon after entering training. A large ovoid defect in the bone represents a medial femoral bone cyst

Figure 3 - Shows the arthroscopic appearance of the joint surface opening of a bone cyst, with a typical sunken crevice-like defect in the articular cartilage

Figure 4 -Arthroscopic appearance of the cyst in Figure 3 after removal of the cystic contents, linaing and unsupported cartilage at the joint opening.

Lameness in racing Thoroughbreds is a major cause of poor performance, interrupted racing schedules and premature retirement from racing. While osteoarthritis is the most common cause of lameness, there are several developmental bone abnormalities which may lead to joint pain requiring treatment, particularly in the juvenile racehorse. A common manifestation of developmental joint abnormalities is the formation of bone cysts or subchondral cyst-like lesions.

The most common site at which bone cysts are encountered in Thoroughbred racehorses is the stifle (the equivalent of the human knee). Specifically, bone cysts are found in the main weight bearing aspect of the stifle (the medial femoral condyle) and rarely at other locations within the joint (proximal lateral tibia and lateral femoral condyle). Although commonly referred to as bone cysts, they are not truly cystic structures by strict definition, but the term has become ensconced in the veterinary literature; despite this they are aptly named as they typically represent an oval or dome-shaped defect devoid of bone on radiographs. Bone cysts are identified on radiographs and are typically located just beneath the joint surface and commonly communicate with the joint cavity. The size of a medial femoral cyst varies from shallow dome-shaped defects (approximately 8mm x 3mm) to large ovoid-shaped cysts of 40mm x 30mm.

The development of bone cysts appears to be the result of a combination of factors, many of which contribute to other recognised developmental bone abnormalities, such as osteochondrosis (OCD). Factors identified include growth rate and body size, hereditability, nutrition (energy/protein/copper levels) and exercise. The majority of stifle cysts appear to arise as a sequel to abnormal bone development, but occasionally they may form secondary to arthritic in older horses. The majority of cysts appear to develop within the first eight (8) months of life but occasionally they may arise in older horses.

Current theory on the cause of bone cysts suggests formation is a result of abnormal skeleton development that leads to retained cartilage rather than transformation to bone. The less resilient cartilage develops flaws and crevices, which then allows influx of joint fluid, which results in cavitation of the bone. Enlargement of the cyst has also been shown to result from cells producing enzymes in the lining of developed cysts capable of causing bone resorption.

Recently published research investigating the cause of developmental orthopaedic disease and osteochondrosis indicates that stifle cysts may be more prevalent in foals that have exercise restricted to stall rest for extended periods. Further to this, research investigating stifle cysts and other forms of developmental orthopaedic diseases has shown that joint defects are more likely to persist, rather than spontaneously heal, in foals that have low dietary copper.

Lameness may develop as a result of a stifle cyst at any age, but the most typical scenario is a sudden onset of hindlimb lameness at the time of introduction to training, whether it be during breaking-in or preliminary training. Lameness may also be recognised prior to or during yearling preparation for sale. Conversely, the presence of a cyst may not result in any overt lameness, and may be an incidental finding on radiographs. In this regard, the advent of pre-sale survey radiographic examinations has identified a number of yearlings with
subtle changes to the shape of the femur at the typical weight-bearing site of cyst development. Predicting whether these changes, such as shallow concavities, develop into lameness causing bone cysts is difficult.

Radiographic evidence of active bone remodelling at the margins of the concavity, seen as a white rim of bone and radiating decalcification, is indicative of potential cyst enlargement. Despite the lack of reliable prediction, anecdotally, many of the observed subtle radiographic changes do not develop into significant bone cysts and performance limiting problems.

Treatment options for stifle bone cysts causing lameness include long term rest, anti-arthritic and intra-articular corticosteroid therapy and surgery. Conservative therapy, which may require nine to twelve months of paddock rest, has been associated with resolution of lameness and return to racing. Unfortunately the number of horses managed by conservative therapy that have been evaluated in the veterinary literature is very limited, but success rates are approximately 50%. Anecdotal evidence suggests conservative therapy is associated with a more protracted convalescence and a less predictable outcome than following surgical treatment.

Numerous surgical techniques have been used in the treatment of bone cysts. Current recommended treatment involves arthroscopic removal (curettage) of the cystic contents, cyst lining and the overlying unsupported cartilage. Additional techniques to use in an attempt to enhance healing and improve outcome have included bone drilling and grafting, both of which are now considered to offer no
benefit.

Presently, additional techniques to arthroscopic curettage which appear promising in improving surgical success are post-surgical intra-articular corticosteroid therapy and joint resurfacing techniques which use laboratory grown cartilage cells combined with growth factors to fill the bone defect. The current success rate for return to performance in horses following arthroscopic surgery is 50-74%. A recent review of yearlings and unraced 2-year-old Thoroughbreds undergoing arthroscopic surgery for stifle cysts indicated that 64% of treated horses raced compared to 77% of unaffected maternal siblings, indicating the majority of treated horses went on to race. When these two (2) groups were further compared, horses which had stifle cysts and underwent arthroscopic surgery earned less money per start in their 2-year-old and 3-year-old racing years but earned equal amounts in their 4-year-old racing season compared to the unaffected though related group. This finding is consistent with the long convalescence associated with this condition, i.e. 6-12 months following surgery.

A further interesting finding from this Kentucky based study was that depth of the cyst was not as important as the diameter of the cyst opening at the joint surface in influencing a successful outcome. Horses that had cysts with a joint surface diameter greater than 1.Scm had a significantly poorer outlook for racing.

Future research evaluating new joint resurfacing surgical treatments is likely to reduce convalescence time and improve racing prospects for horses with this common condition. Furthermore, with the advent of pre-sale radiographic examinations, follow-up studies will allow veterinarians to better predict which of the observed subtle radiographic bone changes are likely to result in bone cyst development. Similarly, such studies will help determine which bone cysts are likely to cause performance-limiting lameness, and how they are best managed when detected.