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- Author or Editor: Alan J. Nixon x
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Abstract
Objective—To investigate effects of β-aminopropionitrile and a combination of insulin-like growth factor (IGF)-I and β-aminopropionitrile on metabolism of equine tendon fibroblasts.
Sample Population—Flexor tendon explants from 3 horses.
Procedure—Explants received 1 of 4 treatments (control, IGF-I, β-aminopropionitrile, and IGF-I/β-aminopropionitrile) for 10 days, and message expression for collagen types I and III was assessed by use of in situ hybridization. Histologic findings, new protein production, and quantitative determinations of glycosaminoglycan, DNA, and de novo collagen synthesis were made.
Results—Insulin-like growth factor-I stimulated an anabolic response in tendon. Collagen synthesis and glycosaminoglycan and DNA content of explants were all increased. β-Aminopropionitrile significantly suppressed collagen synthesis, which was not ameliorated by concurrent IGF-I treatment. β-Aminopropionitrile caused alterations in cell morphology characterized by large round cells with eccentric nuclei and decreased density of collagen fibers. Protein production and collagen type-III mRNA expression were reduced in these cells.
Conclusion and Clinical Relevance—Treatment with β-aminopropionitrile resulted in decreased production of protein and collagen synthesis, which could be expected to suppress tendon healing. The negative effects of β-aminopropionitrile could not be abrogated by addition of IGF-I to the medium. Treatment resulted in alterations in cell morphology and matrix consistency, which could further delay tendon healing. β-Aminopropionitrile may impair tendon healing at a cellular level by decreasing collagen production or increasing rate of degradation of existing matrix. Because of reduced crosslinking during β- aminopropionitrile treatment, in combination with transiently decreased tensile strength, alterations in collagen content and structure may weaken the healing tendon. (Am J Vet Res 2001;62:1557–1562)
Abstract
Objective—To determine molecular changes in the expression of insulin-like growth factor-I (IGF-I) and transforming growth factor-β1 (TGF-β1) in horses with osteochondrosis, and to characterize expression of matrix aggrecan and collagen types I, II, and X in articular cartilage of affected joints.
Sample Population—Articular cartilage from affected stifle or shoulder joints of 11 horses with naturally acquired osteochondrosis and corresponding joints of 11 clinically normal horses.
Procedure—Harvested specimens were snap frozen in liquid nitrogen, and total RNA was isolated. Specimens were fixed in 4% paraformaldehyde for histologic examinations. Expression of matrix molecules was assessed by analysis of northern blots and in situ hybridization, using equine-specific cDNA probes and riboprobes, respectively. Expression of IGF-I and TGF-β1 was assessed by use of noncompetitive quantitative polymerase chain reaction, in situ hybridization, and immunohistochemical analysis.
Results—Cartilage obtained from osteochondrosis lesions had significantly greater expression of IGF-I, compared with normal cartilage. Expression of TGF- β1 and collagen type I were higher, but not significantly so, in affected tissues. Expression of aggrecan or collagen types II and X did not differ between affected and clinically normal cartilage.
Conclusions and Clinical Relevance—Increased expression of growth factors and collagen type I was found in cartilage from osteochondrosis lesions. However, this probably reflects a healing response to injured tissue rather than a primary alteration. Therefore, methods aimed at altering concentrations of growth factors in cartilage of growing horses would be unlikely to alter the incidence or progress of the disease. (Am J Vet Res 2001;62:1088–1094)
Abstract
Objective—To clone the 5' end of type III collagen and describe its pattern of mRNA and protein expression in normal and healing tendons in horses.
Animals—14 healthy adult horses.
Procedure—The tensile region of collagenase-injured superficial digital flexor tendons was harvested at intervals from 1 to 24 weeks after injury. Total RNA was reverse-transcribed into cDNA for cloning and sequencing of type III collagen. Equine-specific nucleic acid probes were developed and used for northern blot analysis and in situ hybridization. Type III collagen protein and cyanogen bromide-cleaved collagen peptides were assessedby gel electrophresis.
Results—Type III collagen mRNA expression and protein content increased immediately after injury and remained increased. Type III collagen was localized to the endotenon in normal tendon and in injured tendon at 1 week. At 8 and 24 weeks, expression became more widely distributed throughout the tendon parenchyma. Injured tendon contained 6 times more type I than type III collagen mRNA. Quantities of type III collagen protein were maximal in the first 4 weeks after injury (approx 33%) and then began to decrease.
Conclusions and Clinical Relevance—Type III collagen expression is increased initially in endotenon and subsequently in parenchyma of healing tendon; however, type III remains the minor collagen throughout the healing process. The role of type III collagen in tendon healing is not fully elucidated. (Am J Vet Res 2005;66:266–270)
Abstract
Objective—To determine the mRNA expression of bone morphogenetic protein (BMP)-6 and -2 and a BMP antagonist (Noggin) in horses with osteochondrosis.
Sample Population—Samples of articular cartilage from affected stifle or shoulder joints of 10 immature horses with naturally acquired osteochondrosis and corresponding joints of 9 clinically normal horses of similar age; additionally, samples of distal femoral growth plate cartilage and distal femoral articular cartilage were obtained from a normal equine fetus.
Procedure—Cartilage specimens were snap-frozen in liquid nitrogen, and total RNA was isolated. Adjacent specimens were fixed in 4% paraformaldehyde for histologic examination. Expression of BMP-6, BMP-2, and Noggin mRNA was evaluated by real-time quantitative polymerase chain reaction (PCR) assays. Spatial tissue mRNA expression of BMP-6 was determined by in situ hybridization.
Results—Nucleotide sequences were obtained for portions of the BMP-6 propeptide and mature peptide region, as well as the signal and mature peptide region of Noggin. Expression of BMP-6, BMP-2, and Noggin mRNA was found to be similar in cartilage from normal and osteochondrosis-affected horses. Spatial expression of BMP-6 correlated with the middle and deep layers of articular cartilage; no differences were observed in overall expression between cartilage specimens from the 2 groups of horses. No expression of BMP-6 was found in the superficial layer, subchondral bone, or osteochondrosis-affected cleft fibrous tissue.
Conclusions and Clinical Relevance—Although these signaling peptides may play important roles in cartilage differentiation, results did not provide evidence to suggest that they are involved in the disease process of osteochondrosis. (Am J Vet Res 2004;65:110–115)
Abstract
Objective—To determine clinical and radiographic findings, treatment, and outcome of horses with fractures of the palmar aspect of the radial carpal bone, with or without concurrent fractures of the palmar surfaces of the other carpal bones.
Design—Retrospective study.
Animals—10 horses.
Procedure—Medical records were reviewed to obtain information on history, signalment, clinical and radiographic findings, treatment, and outcome. Follow-up information was gathered from owners and referring veterinarians.
Results—7 horses became lame after recovery from general anesthesia for treatment of an unrelated problem. The remaining 3 horses developed a forelimb lameness after falling (1 horse) or being turned out in a pasture (2 horses). Fractures involved the palmar surface of the radial carpal bone in all 10 horses; in addition, the ulnar carpal bone was affected in 2 horses, the intermediate carpal bone in 2 horses, and the distal aspect of the radius in 4 horses. None of the 4 horses treated nonsurgically returned to work, and 3 were euthanatized because of recalcitrant lameness. In the other 6 horses, fragments were removed surgically. Two were euthanatized because of continued lameness, 1 was euthanatized for other reasons, 2 were sound enough for light work, and 1 returned to athletic work.
Conclusions and Clinical Relevance—Results suggest that fractures of the palmar aspect of the carpal bones are uncommon in horses. The prognosis appears to be poor for affected horses but may be better for horses that undergo arthroscopic removal of intra-articular fragments. (J Am Vet Med Assoc 2001;219:801–804)
Abstract
Objective—To evaluate outcome after intralesional injection of insulin-like growth factor-I (IGF-I) for treatment of superficial digital flexor (SDF) tendonitis in Thoroughbred racehorses.
Design—Retrospective case series.
Animals—40 Thoroughbred racehorses.
Procedures—Medical records of racehorses with SDF tendonitis treated within 13 weeks after injury by intralesional injection of IGF-I (25 or 50 μg every other day for 4 or 5 treatments) were reviewed. Outcome was determined via analysis of race records, owner follow-up, and examination.
Results—Mean age of the horses was 3.1 years (range, 2 to 7 years), and time from injury to treatment ranged from 8 to 90 days. Mean ± SD approximate lesion length on admission was 15.6 ± 6.0 cm, and mean percentage cross-sectional area of the tendon affected was 26 ± 18%. Twenty-six of the 40 horses underwent desmotomy of the accessory ligament of the SDF tendon. Echolucency was reduced in 23 of 26 horses by the end of the treatment period. Twenty-one of 34 (62%) horses for which race data were available raced at least once after treatment, including 10 (30%) horses that raced between 1 and 4 times and 11 horses (32%) that raced ≥ 5 times. Thirteen of 28 (46%) horses had a recurrence of tendonitis or developed tendonitis elsewhere.
Conclusions and Clinical Relevance—Results suggested that in Thoroughbred racehorses with SDF tendonitis, intralesional injection of IGF-I led to a decrease in ultrasonographic lesion severity, but treated horses had only a moderate prognosis for return to racing.
Abstract
Objective—To determine the clinical, radiographic, ultrasonographic, and arthroscopic findings associated with tenosynovitis of the carpal synovial sheath induced by exostoses that originate from the caudal surface of the physeal scar of the distal radius and determine the results of surgical removal of those exostoses in horses.
Design—Retrospective study.
Animals—10 horses.
Procedure—Medical records of horses with effusion in the carpal synovial sheath and lameness evaluated from 1999 to 2003 were examined.
Results—All horses had a history of intermittent mild to moderate effusion of the carpal synovial sheath and lameness of 1 forelimb. Results of regional perineural and intrathecal anesthesia of the carpal synovial sheath confirmed that the lameness originated in the carpal synovial sheath. Radiography revealed exostoses originating from the caudal cortex of the distal radius at the level of the closed physis. Arthroscopy was performed for confirmation and removal of exostoses that penetrated the carpal synovial sheath and impinged on the deep digital flexor tendon. All horses returned to previous athletic activity. One horse had a recurrence of clinical signs 12 months after surgery, which resolved with medical treatment.
Conclusions and Clinical Relevance—Tenosynovitis of the carpal synovial sheath and lameness were caused by impingement of exostoses of the caudal radius on the lining and contents of the carpal synovial sheath. Although the clinical signs and surgical treatment were similar to that caused by osteochondromas, these exostoses developed at the level of the closed physis of the distal radius and were not radiographically or histologically similar to osteochondromas. (J Am Vet Med Assoc 2004;224:264–270)
Abstract
Objective—To determine clinical and radiographic features of subchondral cystic lesions (SCL) of the proximal extremity of the tibia in horses that could be used to classify these lesions as being related to osteochondrosis or osteoarthritis and to evaluate results of surgical debridement.
Design—Retrospective study.
Animals—12 horses with 14 SCL.
Procedure—Medical records and radiographs obtained before and after treatment were reviewed.
Results—In 6 young horses (8 lesions), SCL were considered to be related to osteochondrosis; all involved the lateral tibial condyle. The remaining 6 horses were mature and had radiographic evidence of osteoarthritis in addition to SCL. Arthroscopic debridement was performed in 4 horses in which lesions were considered to be a result of osteochondrosis and in 3 horses with osteoarthritis. Three horses in which SCL were considered to be a result of osteochondrosis performed athletically after debridement. Two horses with moderate osteoarthritis returned to work after arthroscopic debridement but at a lower level of athletic performance. One horse with SCL related to osteochondrosis responded to medical treatment and went on to race.
Conclusions and Clinical Relevance—Results suggest that arthroscopic debridement of SCL is feasible in horses in which lesions involve the cranial portion of the lateral or medial tibial condyle, and that treated horses may be able to perform athletically. (J Am Vet Med Assoc 2001;218:408–413)
Abstract
Case Description—3 horses were referred for treatment of subchondral cystic lesions of 1 or both medial femoral condyles.
Clinical Findings—All horses had clinically apparent lameness confirmed to be due to a radiographically evident subchondral cystic lesion of the medial femoral condyle with a large articular component (> 15 mm) and shallow subchondral depth (< 10 mm). Arthroscopic assessment of affected cartilage revealed undulating cartilage with a relatively smooth surface and extensive residual perimeter attachment.
Treatment and Outcome—Resorbable polydioxanone pins were used arthroscopically to reattach the cartilage overlying the subchondral cystic lesions. A biologic graft (bone marrow aspirate concentrate or allogeneic chondrocytes) was injected into the depths of the cystic cavity following cartilage reattachment. Follow-up examination confirmed radiographic resolution of the lesion and elimination of clinical signs within the treated femorotibial joint.
Clinical Relevance—Lesions with a large area of affected articular cartilage have been associated with a decreased rate of return to athletic function following arthroscopic debridement, likely secondary to the loss of subchondral architecture and the production of imperfect fibrocartilage repair. Salvage of the affected cartilage in a select population of horses with progressively expanding but shallow subchondral cystic lesions of the medial femoral condyle is possible and may improve radiographic and clinical outcome.