Quadriceps Contracture and Fracture Disease
Immobilization of a limb can lead to many structural, biomechanical, biochemical, and metabolic changes in the affected tissues. Fracture disease, a complication of fracture treatment and immobilization, is defined as atrophy of bone, soft tissues, nails, skin, and cartilage. This condition is most often seen in dogs with quadriceps contracture, also known as quadriceps "tie down," stiff stifle, post-trauma stifle stiffness, hyperextended stifle, hindlimb rigidity, ischemic contracture of the quadriceps, and Sudeck's disease. Distal femoral fractures treated by extension splints often result in a stiffened stifle in immature dogs. This syndrome is a common, often irreversible postsurgical complication, and the clinical signs, surgical anatomy, etiology, pathophysiology, and treatment will be reviewed.
Patients with fracture disease present with severe lameness of one of the hindlimbs. The affected limb is held in rigid extension and is generally not used when walking (Fig. 1). At rest, it is carried cranially in relation to the nonaffected hindlimb. The stifle may be bent caudally in "genu recurvatum." Close examination of the leg shows variable degrees of muscle atrophy and leg shortening. A careful orthopedic examination should always be performed to evaluate the entire leg. With fracture disease, neither the hock nor the stifle can be flexed: The range of motion of the stifle varies between 10° and 30°. The patella is drawn proximally in the trochlear groove and may be luxated medially. Palpation of the thigh muscles reveals atrophy and a hard quadriceps muscle. A careful examination of the hip joint is mandatory in younger dogs. The hip joint may be painful in full extension and in adduction, and inward and outward rotation may be limited. There may be a positive Ortolani sign.
The quadriceps muscle extends between the pelvis and femur proximally and the patella and tibial tuberosity distally. This muscle covers the femur cranially, laterally, and medially. Distally, the quadriceps muscle forms a tendon that includes the patella and ends on the tibial tuberosity. The quadriceps muscle is covered medially and cranially by both heads of the sartorius muscle (Fig. 2). The quadriceps femoris muscle consists of the rectus fernoris, the vastus lateralis, the vastus medialis, and vastus intermedius. The rectus femoris muscle is enclosed between the vasti (Fig. 3). The vastus lateralis is inseparably united with the rectus femoris and its terminal tendon except proximally. The vastus medialis extends from the proximal femur medially and covers the distal portion of the rectus femoris medially. Above the patella, its tendinous elements fuse with those of the rectus femoris (Fig. 4). The vastus intermedius muscle is the weakest portion of the quadriceps muscle and covers the medial, cranial, and lateral aspect of the femur, lying just under the rectus femoris (Fig. 5). The vastus intermedius muscle is separated from the femur by a very loose, thin connective tissue. The femoral nerve enters the quadriceps femoris muscle between the rectus femoris and the vastus medialis, supplying all four heads. The quadriceps muscle plays a major role in the extension of the stifle.
The changes following immobilization have been reproduced experimentally in different species including rats, rabbits, monkeys, cats, and dogs. Various techniques of immobilization have been used including casting, splinting, extension springs, internal extra-articular pinning, paw transection, nerve and tendon transection. Joints are immobilized either in full extension or in flexion. All these experiments have demonstrated changes in bones, muscles, articular cartilage, synovium, ligaments, and other periarticular structures as well as growth disturbances.
The effects of long- and short-term periods of immobilization on the bony skeletal structures are well known. Lack of movement and muscular unloading of normally loaded limb bones will cause a loss of bone mass (osteoporosis) due to disuse and an associated negative calcium balance. Nontraumatic immobilization of a young adult Beagle's foreleg for 60 weeks produced 66 per cent trabecular bone loss in the distal metaphysis of the third metacarpus, a 50 per cent loss in the radius, and a 25 per cent loss in the humerus. Compact bone loss in the bones of the same dog amounted to 58 per cent, 20 per cent, and 7 per cent, respectively. In young adult dogs, the loss is most prominent on the periosteal surface, there is a marked decrease in cortical area and thickness. Bone loss from the spongiosa appears to be due to a thinning and loss of trabeculae. In older dogs, the bone loss is slightly less important, and there is a marked expansion of the bone and marrow cavity and thinning within the cortex. Disuse osteoporosis is observed in dogs as early as 2 weeks after immobilization and may occur at an approximate rate of 5 per cent loss per month. Bone loss as a result of disuse occurs at rates 5 to 20 times greater than loss caused by other metabolic disorders affecting bone. Disuse osteoporosis is reported as a sequela of quadriceps contracture in growing dogs. Cortices may be extremely thin, with large intracortical resorption cavities appearing 10 weeks after immobilization. Pathologic fracture may be observed. Disuse osteoporosis results from an abnormal bone remodeling. Under normal circumstances, bone undergoes continuous turnover on the periosteal and endosteal surfaces and within the cortices, resulting in the deposition of new units of bone tissue. In disuse osteoporosis, there appears to be a decreased number of osteoblasts and an increased recruitment of osteoclasts. Despite the fact that cortical bone represents 80 per cent of the whole skeleton by volume, cancellous bone carries some 90 per cent of the total bone surface in the skeleton; the greater endosteal surface-to-volume ratio in the spongiosa, as compared with that in the cortical bone, may explain the earlier and consequently greater bone loss in the spongiosa. The initiating cause of disuse osteoporosis is not well understood. Lack of muscular activity, increased vascular supply to the affected limb, and absence of weight-bearing, which decreases the piezo-electric action of crystals on bone cells, are important factors in inducing bone atrophy. The reversibility of disuse osteoporosis is controversial. The reversibility of osteoporotic changes upon remobilization is probably tied to the severity of the changes and the length of immobilization periods. Recovery of loss may take as much as 5 to 10 times longer than the period of immobilization. However, more permanent changes occur with immobilization periods exceeding 12 weeks. Recently, disuse osteoporosis has been prevented experimentally by intracast quadriceps muscle stimulation in cast-immobilized rabbits.
Fibrous adhesion tying down the vastus intermedius appears to be the initiating factor of most quadriceps contractures. Immobilization causes muscle disuse atrophy evaluated by histologic, histochemical, and functional studies. Biopsies from dogs with quadriceps contracture show muscle atrophy more pronounced in the vastus lateralis muscle. Histochemical analysis shows type I fiber atrophy. Experimental studies in cats suggest that muscles maintained in a shortened position atrophy more rapidly, with greater loss of contractile function and myofibrillar (contractile) and sarcoplasmic (cytoplasmic) proteins than the stretched and neutrally positioned muscles. Disuse muscle atrophy is reversible. Immobilized skeletal muscles have a good regenerative potential that is not affected by the duration of immobilization. The recovery period may be 2 to 4 times longer than the period of immobilization. Although the bony and muscular atrophic changes are reversible, most of the articular and periarticular changes are irreversible.
Articular and Periarticular Changes
Joint immobilization results in a progressive contracture of the capsule and periarticular structure, with a subsequent decrease in the joint space. After prolonged immobilization, fatty connective tissue envelops the cruciate ligaments and completely fills the joint cavity. Adhesions form between the fibrous tissue and the nonarticulating surfaces of articular cartilage. In rats, adhesions cover virtually all unapposed articular cartilage at 60 days. In dogs, adhesions are not observed 8 weeks after immobilization, but they become obvious at 3 months (Fig. 6). Other changes are observed in the articular cartilage, synovium, ligaments, and periarticular structures.
Joint immobilization results in morphologic, biochemical, and metabolic changes even a few days after immobilization. Rigid, sustained pressure on the articular cartilage of rabbit knee joints results in chondrocytic death. In the noncontact areas of articular cartilage, the interface between fibrous tissue and hyaline cartilage is initially distinct, but with time this interface is replaced by a pannus as early as 2 weeks after immobilization and by mature fibrous tissue. When articular cartilage surfaces are in apposition, microscopic changes have been observed as early as 4 days after immobilization. Biochemical and metabolic changes occur concomitantly with these early changes. Some studies have demonstrated an increased glycoaminoglycan (GAG) synthesis, but decreased GAG content as early as 4 to 10 days after immobilization, whereas others have demonstrated a reduction in proteoglycan synthesis after 6 days of immobilization. With time, various cartilaginous changes are observed, including fibrillation, deep erosion, fibrous ankylosis, and sometimes cartilaginous or even bony ankylosis (Fig. 7). The late changes of cartilaginous and bony ankylosis are observed only after months of immobilization).
These morphologic, metabolic, and biochemical changes appear to be the result of reduced joint motion and loading. Intermittent joint loading stimulates the formation and circulation of synovial and interstitial fluids that nourish and lubricate the cartilage. Joint immobilization may compromise the metabolic exchange needed for proper structure and function of the articular cartilage. Recent experiments suggest that joint motion alone is not sufficient to maintain cartilage health. Degenerative changes occur in stifle joints of dogs even in the presence of joint motion if the joint remains unloaded. Joint motion without joint loading during the immobilization period will not prevent deterioration of the articular cartilage. The reversibility of articular cartilage changes depends upon the length of immobilization and the extent to which movement is really restricted during immobilization. Morphologic and biochemical cartilage changes are fully reversible if the immobilization period is less than 4 weeks. The time required for cartilage to recover may be many times longer than the initial immobilization period. After 7 weeks of immobilization, the articular cartilage defects may be permanent and may continue to progress, even upon remobilization. Recently, articular cartilage changes have been prevented in short-term cast immobilization by intercast muscle stimulation and intra-articular injection of hyaluronic acid.
Synovial, Ligamentous, and Periarticular Connective Tissue Changes
The metabolic activity in the joint capsule increases markedly as early as 4 days after immobilization. Thickening of the joint capsule is one of the first microscopic changes. There is a nonspecific fibrous hyperplasia of the joint capsule (Fig. 8) and proliferation of the type B synoviocytes in the synovial membrane.
Immobility leads to a progressive contracture of the joint capsule and periarticular fibrous connective tissue, patellar tendon, ligaments, and fascia. The biochemical composition of periarticular fibrous connective tissues has been demonstrated following immobilization of synovial joints. These changes consist mainly in a reduction of water and glycoaminoglycans and an alteration in collagen cross-linking. No changes in collagen mass or collagen type between control and immobilized fibrous connective tissue has been detected. The failure to demonstrate collagen accumulation and the lack of type III collagen in periarticular connective tissue supports the concept that inflammation is not the basis of the contracture. The biomechanical properties of these joint components are altered following a period of immobilization. A decrease of 57 per cent in the stiffness of the rabbit medial collateral ligament is reported after 40 days of immobilization. Hyaluronic acid loss in periarticular connective tissues correlates with some physical measures of stiffness. Hyaluronic acid may not be necessary for articular cartilage lubrication, but it may be important for the lubrication of soft tissues in and around the synovial joints. Motion of connective tissue matrix appears to inhibit the contracture process through several mechanisms: stimulation of proteoglycan synthesis, which favors lubrication; ordering the deposition of new collagen fibers so as to resist tensile stresses; and prevention of abnormal cross-linking in the matrix. Osteoarthritis of the immobilized synovial joints appears as the end result of capsular and periarticular connective tissue contracture. The severity of degenerative joint disease is directly related to the duration of immobilization. The increased intra-articular pressure in the stifle seems to be due to contracture of periarticular tissues and to muscle contraction in the shortened position, causing static compression of the articular cartilage. There is "pressure necrosis" of the articular cartilage. The position in extension or in flexion of the immobilized joint appears important as only a few cases of osteoarthritis have been observed when rabbits knees are immobilized in flexion. Joint stiffness secondary to immobilization was inhibited by intra-articular hyaluronic acid injection in experimental joint contracture in rabbits. Injected hyaluronic acid appears to have a significant protective effect on the immobilized tissue by stimulating hyaluronic acid synthesis by fibrous connective tissue, by minimizing the loss of GAGs, and by reducing joint stiffness.
The influence of immobilization has been described in growing dogs in which quadriceps contracture was observed, and in experimental studies Immobilization of the stifle in dogs younger than 3 months of age induces multiple changes throughout the affected limb including hip subluxation, bone hypoplasia, and increased femoral torsion. Hip subluxation is consistently evident after 8 to 10 weeks of cast immobilization with the stifle in hyperextension. Immobilization of the knee in extension in the presence of intact hamstring muscles results in an unstrained pull of these muscle groups across the hip joint, with subsequent hip subluxation or dislocation. Other coxofemoral changes are also found, including hypertrophy of the ligament of the femoral head, significant decrease in blood flow of the femoral head," and progressive degenerative changes developing in the dislocated hip. Bone hypoplasia is more severe in distal bones of the limb.' Absence of mechanical stimulation from normal weight-bearing decreases osteoblastic activity and epiphyseal growth. As a result, changes resulting from immobilization of a limb in very young dogs are more pronounced than in adults. In addition to the changes observed in mature animals, there may be disturbance of the growth of bones and joints including hip subluxation, abnormal bone torsion, and bone hypoplasia.
The prognosis for dogs with a quadriceps contracture is guarded to poor depending upon the duration of immobilization, the age of the animal, and the nature of the possible associated lesions such as disuse osteoporosis, osteoarthritis of the stifle, patellar luxation, limb shortening, hip subluxation or dislocation, and infection. Because no satisfactory method has been proposed for preventing disuse osteoporosis, degenerative joint disease of the stifle, and growth disturbances secondary to immobilization, the treatment of recognized cases of quadriceps contracture in young dogs is rarely satisfactory. The treatment may improve the gait, but the patient will rarely be without lameness.
Quadriceps contracture cases should not be considered only as a stifle problem, and the entire affected leg should be evaluated before any treatment. All the bony, muscular, and articular changes should be recorded. Because active physical therapy cannot be initiated as in human beings, most treatments are surgical. Treatment is directed at restoring movement to the knee by (1) freeing the adhesions between the vastus intermedius and the distal femur, (2) lengthening the quadriceps femoris mechanism, (3) releasing the periarticular connective tissue contracture, and (4) positioning the stifle in a physiologic weight-bearing position. There are two major contraindications for surgical treatment: (1) major limb shortening, and (2) combination of limb shortening, hip subluxation, and severe disuse osteoporosis in young dogs. Several surgical techniques have been de-scribed including (1) Z plasty of the quadriceps muscles, (2) quadriceps plasty, using plastic sheeting, (3) sliding myoplasty, (4) vastus intermedius excision, (5) stifle arthrodesis, and (6) limb amputation. Currently the author uses only the last three procedures. The vastus intermedius excision procedure is used only in the first few weeks of quadriceps contracture before the appearance of irreversible cartilage changes. The patient is positioned in dorsal recumbency. A craniomedial approach to the femur and stifle joint is used. The skin incision is made on the craniomedial aspect of the thigh from the proximal third of the femur, and it ends distally over the medial aspect of the tibial tuberosity. The subcutaneous fat and fascia are incised and cleared from the area so that the separation between the cranial and caudal parts of the sartorius muscle can be clearly visualized. The fascia between these two parts is incised. The cranial part of the sartorius muscle is reflected laterally and the caudal part medially. The rectus femoris and vastus medialis muscles are separated by incising the tendinous elements of the vastus medialis where it fuses distally with that of the rectus femoris (Fig. 9). The incision may be extended distally in the medial retinaculum, exposing the medial joint capsule. The cranial and medial aspects of the vastus intermedius muscle appear after a medial retraction of the vastus medialis muscle and lateral retraction of the rectus femoris muscle (Fig. 9). The excision of the vastus intermedius starts just above the joint capsule and extends dorsally on the cranial lateral and medial aspects of the femur. The strong adhesions are excised, exposing the femoral callus; the excision of the lateral part of the vastus intermedius may be facilitated by a medial arthrotomy and lateral luxation of the patella (Fig. 10). At this stage, the stifle may be bent in 45° to 60° of flexion. Further flexion may be facilitated by a releasing incision in the lateral retinaculum. In immature animals, care must be taken to avoid avulsion of the tibial tuberosity. Excess callus is removed using rongeurs and bone rasps. After a joint lavage using lactated Ringer's solution, the patella is relocated in its femoral trochlear groove. Closure consists of suturing the vastus medialis muscle to the rectus femoris muscle using simple interrupted sutures. The medial retinaculum is sutured with the stifle in flexion. The subcutaneous tissues and skin are closed in a routine manner. Postoperatively, an Ehmer sling is applied for 4 days. On the fourth day, the patient is anesthetized, the sling is removed, and the limb is flexed and extended. The sling is reapplied until the seventh day. Physical therapy is initiated daily between the 8th and 14th day, and exercise is encouraged.
Indications for stifle arthrodesis are: (1) failure of the aforementioned surgical procedure, (2) advanced stage of osteoarthritis of the stifle, (3) osteomyelitis of the distal femur, and (4) septic arthritis of the stifle. The surgical technique for arthrodesis of the stifle has been described. Amputation is recommended in advanced stages of quadriceps contracture, generally in very young dogs when multiple problems are observed, such as a stiff stifle associated with hip subluxation, short bones, and pathologic fractures. All the pathophysiologic changes occurring in bones, muscles, and joints following immobilization should be kept in mind. Because no satisfactory method can prevent these changes and because most surgical treatments are unsatisfactory, the clinician should consider all recent investigations to prevent this condition. Stable fixation of fractures allows an early return to functional weight-bearing without immobilization. When an external support is used, the leg is fixed in a flexed walking position. The use of electric muscle stimulation to maintain musculoskeletal health should be evaluated in early cases of fracture disease. Intra-articular hyaluronic acid injection may be a useful therapeutic approach to prevent joint contractures in which injuries or diseases result in enforced immobilization.
1. Akeson WH, Woo SLY, et al: The connective tissue response to immobility: Biochemical changes in periarticular connective tissue of the immobilized rabbit knee. Clin Orthop 93:356-362, 1973 2. Akeson WH, Amiel D, Mechanic GL, et al: Collagen cross-linking alterations in joint contractures: Changes in the reducible cross-links in periarticular connective tissue collagen after nine weeks of immobilization. Connect Tissue Res 5:15-20, 1977 3. Amiel D, Akeson WH, Harwood FL, et al: The effect of immobilization on the type of collagen synthetized in periarticular connective tissue. Connect Tissue Res 8:27-32, 1980 4. Amiel D, Woo SLY, Harwood FL, et al: The effect of immobilization on collagen turnover in connective tissue: A biochemical-biomechanical correlation. Acta Orthop Scand 43:325-332, 1982 5. Amiel D, Frey C, Woo SLY, et al: Value of hyaluronic acid in the prevention of contracture formation. Clin Orthop 196:306-311, 1985 6. Bardet JF, Hohn RB: Quadriceps contracture in dogs. J Am Vet Med Assoc 183:680-685, 1983 7. Bardet JF, Hohn RB: Subluxation of the hip joint and bone hypoplasia associated with quadriceps contracture in young dogs. J Am Anim Hosp Assoc 20:421-428, 1984 8. Basset CAL, Becker RO: Generation of electric potentials by bone crystals in response to mechanical stress. Science 137:1063-1064, 1969 9. Bennett GE: Lengthening of the quadriceps tendon. J Bone Joint Surg 4:279-241, 1922 10. Binkley JM, Peat M: The effects of immobilization on the ultrastructure and mechanical properties of the medial collateral ligament of rats. Clin Orthop 203:301-308, 1986 11. Braund KJ, Shires PK, Mikeal RL: Type I fiber atrophy in the vastus lateralis in dogs with femoral fractures treated by hyperextension. Vet Pathol 17:166-177, 1980 12. Brinker WO, Piermattei DL, Flo GL: Handbook of Small Animal Orthopedics and Fracture Treatment. Philadelphia, WB Saunders Co, 1983 13, Burr DB, Frederickson RC, Pavlinch C, et al: Intracast muscle stimulation prevents bone and cartilage deterioration in cast-immobilized rabbits. Clin Orthop 189:264-278, 1984 14. Cooper 11G: Alterations during immobilization and regeneration of skeletal muscles in cats. J Bone Joint Surg 54:919-953, 1979 15. Drake JC, Hime JM: Two syndromes in young dogs caused by Toxoplasma gondii. J Small Anim Pract 8:621-626, 1967 16. Enneking WF, Horowitz M: The intra-articular effects of immobilization on the human knee. J Bone joint Surg 54:973-985, 1972 17. Evans EB, Eggers GWN, Butler JK, et al: Experimental immobilization and remobilization of rat knee joints. J Bone Joint Surg 42:737-758, 1960 18. Evans HE, Christensen GC: Miller's Anatomy of the Dog. Edition 2. Philadelphia, WB Saunders Co, 1979, pp 385-386 19. Finsterbush A, Friedman B: Early changes in immobilized rabbit knee joints. A light and early microscopic study. Clin Orthop 92:305-319, 1973 20. Finsterbush A, Friedman B: Reversibility of joint changes in rabbits. Clin Orthop 111:290-298, 1975 21. Geiser M, Trueta J: Muscle action, bone rarefaction and bone formation. J Bone Joint Surg 40:282-311, 1958 22. Goldspink PF: The influence of immobilization and stretch on protein turnover and rat skeletal muscle. J Physiol (London) 264:267-282, 1977 23. Gritzka TL, Fry LB, Cheesman RL, et al: Deterioration of articular cartilage caused by continuous compression in a moving rabbit joint. J Bone Joint Surg 55:1698-1720, 1973 24. Hall MC: Articular changes in the knee in adults rats after ending immobilization. Clin Orthop 34:184-185, 1964 25. Herron AJ: Fracture disease. In Bojrab MJ (ed): Pathophysiology in Small Animal Surgery. Philadelphia, Lea & Febiger, 1981, pp 550-552 26. Holliday TA, Olander JH, Wind AP: Skeletal muscle atrophy associated with canine toxoplasmosis. Cornell Vet 53:288-301, 1963 27. Howell JA: An experimental study of the effect of stress and strain on bone development. Anat Rec 13:233-256, 1917 28. Jaworski ZFG, Liskova-Kiar M, Uhthoff HK: Effect of long-term immobilization on the pattern of bone loss in older dogs. J Bone Joint Surg 62:104-110, 1980 29. Jokl P, Konstadt S: The effect of limb immobilization on muscle function and protein composition. Clin Orthop 174:223-229, 1983 30. Jurvelin J, Kiviranta I, Tammi M, et al: Softening of canine articular cartilage after immobilization of the knee joint. Clin Orthop 207:246-256, 1986 31. Lagier R, Van Linthoudt D: Articular changes due to disuse in Sudeck's atrophy. Int Orthop 3:1-8, 1979 32. Langenskiöd A, Michelson JE, Videman T: Osteoarthritis of the knee in rabbit produced by immobilization. Acta Orthop Scand 50:1-14, 1979 33. Leighton RL: Muscle contractures in the limb of dogs and cats. Vet Surg 10:132-135, 1981 34. Leighton RL: Quadriceps contracture (ischemic contracture of the quadriceps). In Bojrab MJ (ed): Pathophysiology in Small Animal Surgery. Philadelphia, WB Saunders Co, 1981, pp 925-926 35. Main BJ: Effects of immobilization on the skeleton. In Owen R, Goodfellow J, Bullough P (eds): Scientific Foundation of Orthopedics and Traumatology. Philadelphia, WB Saunders Co, 1980, pp 426 435 36. Mazess RB, Whedon GD: Immobilization and bone. Calcif Tissue Int 35:265-267, 1983 37. Michelson JE, Langenskiöld A: Dislocation or subluxation of the hip. Regular sequels of immobilization of the knee in extension in young rabbits. J Bone Joint Surg 54:1177-1186, 1972 38. Milton JL: Surgery of muscle and tendon. In Bojrab MJ (ed): Current Techniques in Small Animal Surgery. Philadelphia, Lea & Febiger, 1983, pp 495-516 39. Nicoll EA: Quadricepsplasty. J Bone Joint Surg 45:483-490, 1963 40. Noyes FR, Torvik PJ, Hyde WB, et al: Biomechanics of ligament failure II: An analysis of immobilization, exercise, and reconditioning effects in primates. J Bone Joint Surg 56:1406-1418, 1974 41. Palmoski M, Perricone E, Brandt KD: Development and reversal of a proteoglycan aggregation defect in normal canine knee cartilage after immobilization. Arthritis Rheum 22:508-518, 1979 42. Palmoski MJ, Colyer RA, Brandt KD: Joint motion in the absence of normal loading does not maintain normal articular cartilage. Arthritis Rheum 23:325-334, 1980 43. Paukkonen K, Jurvelin MBJ, Helminen HJ: Effects of immobilization on the articular cartilage in young rabbits. Clin Orthop 206:270-280, 1986 44. Schoenecker PL, Lesker PA, Ogata K: A dynamic canine model of experimental hip dysplasia. J Bone Joint Surg 66:1281-1288, 1984 45. Shires PK, Braund KG, Milton JL, et al: Effect of localized trauma and temporary splinting on immature skeletal muscle and mobility of the femorotibial joint in the dog. Am J Vet Res 43:454-460, 1982 46. Stead AC, Camburn MA, Gunn HM, et al: Congenital hindlimb rigidity in a dog. J Small Anim Pract 18:39-46, 1977 47. Steinberg ME, Trueta J: Effects of activity on bone growth and development in rats. Clin Orthop 156:52-60, 1981 48. Thaxter GH, Mann RA, Anderson CE: Degeneration of immobilized knee joints in rats. J Bone Joint Surg 47:567-585, 1965 49. Thompson TC: Quadricepsplasty to improve knee function. J Bone Joint Surg 26:366-379, 1977 50. Uhthoff HK, Jaworski ZFG: Bone loss in response to long term immobilization. J Bone Joint Surg 60:420-429, 1978 51. Uhthoff HK, Sékaly G, Jaworski ZFG: Effects of long-term nontraumatic immobilization on metaphyseal spongiosa in young adult and old Beagle dogs. Clin Orthop 192:278-283, 1985 52. Videman T, Michelson JE, Rauhamaki R, et al: Changes in 35 S—sulfate uptake in different tissues in the knee and hip regions of rabbits during immobilization, remobilization and the development of osteoarthritis. Acta Orthop Scand 47:290-298, 1978 53. Videman T, Eronen 1, Friman C, et al: Glycoaminoglycan metabolism of the medial meniscus, the medial collateral ligament, and the hip joint capsule in experimental osteoarthritis caused by immobilization of the rabbit knee. Acta Orthop Scand 50:465-470, 1979 54. Videman T, Eronen I, Friman C: Glycoaminoglycan metabolism in experimental osteoarthritis caused by immobilization. Acta Orthop Scand 52:11-21, 1981 55. Woo SLY, Mattheus JV, Akeson WH, et al: Connective tissue response to immobility: Correlative study of biomechanical and biochemical measurements of normal and immobilized rabbit knees. Arthritis Rheum 18:257-264, 1975 56. Wright RJ: Correction of quadriceps contractures. Calif Vet 1:7-10, 1980 57. Young DR, Niklowitz WJ, Steck CR: Tibial changes in experimental disuse osteoporosis in the monkey. Calcif Tissue Int 35:304-308, 1983