Path. vet. 5: 436-441 (1968) From the Department of Veterinary Pathology, School of Veterinary Medicine, Washington State University, Pullman Localized Nodular Tenosynovitis in the Horse W.L. RAGLAND 1x1 When JAFFE ef al. (1941) presented their description of pigmented villonodular synovitis, bursitis, and tenosynovitis, they brought order to a wide range of tumor-like conditions of the joints, bursae, and tendons of man. These authors placed xanthoma, xanthogranuloma, xanthomatous giant-cell tumor of tendon, giant-cell tumor of tendon, synovioma, and benign giant-cell synovioma in 1 major group by emphasizing their common pathogenesis. Although proliferative in character, these conditions are now generally considered the result of an inflammatory process. JAFFE (1958) reserved the term pigmented villonodular ienosynovifis for an uncommon, diffuse form of the lesions of tendons, designating the more common type of lesion localixed nodular tenosynovitis. Although none of the lesions of this type has been reported in domesticated animals, the report by DANKS and OLAF- SON (1939) of a giant-cell sarcoma in a 7-year-old mule was probably a case of localized nodular tencsynovitis. The lesion was located on the anterior surface of the right stifle and did not cause lameness. The authors considered the lesion to Ee a sarcoma but malignancy was not unequivocably established. The present communication describes 2 cases of localized nodular tenosynovitis in the horse. Case Histories Case 1. In June 1964, a mass was surgically excised from the subcutis of the posterolateral region of the right stifle of an 18-year-old, palomino, cross-bred Arabian-Thoroughbred stallion. The lesion had been present for 2 months and caused no apparent evidence of pain or impaired movement. Repeated attempts to obtain information on recurrence or non-recurrence have been unsuccessful. Case 2. In August 1962, a nodular mass was surgically excised from the subcutis at the point of the right shoulder of an 8-year-old, hay, Thoroughbred stallion. The lesion had been present for l year, increasing slowly in size without pro- Fig. I. Small round to fusiform cells and multinucleated giant cells lying in a loose fibrillary matrix. Giant cell in lower right hand corner was apparently still in the process of development. Case 1. H & E, x 105. Fig. 2. Giant cell containing both lipid material and hemosiderin. Case 1. H & E, x 650. Fig. 3. Clefts representing remnant of villonodular pattern. Case 1. H & E, x 260.
RAGLAND 111 437
438 RAGLAND 111 ducing any evidence of pain or impairment of motion. No recurrence has been observed during the succeeding 3 years. Gross Pathology About 2 cm in maximum dimension, tissue from Case 1 was irregular, soft, and homogeneous. Most of the tissue was bright orange but several, poorly defined areas were bright or dark red. The tissue along 1 edge was gray and slightly firmer than the rest. The tissue from Case 2 was an irregularly shaped mass of firm, light gray tissue having a maximum dimension of about 5 cm. Its multinodular character was revealed by cross-sectioning the mass, which exposed less firm, darker gray foci, mottled with red and orange, and separated by dense fibrous tissue. Histopathology Case 7. This 2-month-old lesion was composed principally of small round to fusiform cells and giant cells lying in a loose, fibrillary network (Figs. 1-3). The small cells were more common and were uniformly distributed throughout the tissue. They were round, oval, or fusiform and contained small, darkly stained round, oval, or elongate nuclei. They often had indistinct boundaries, but in many instances the cytoplasm was continuous with the delicate collagenous fibers which made up the loose fibrillary matrix. In some areas, groups of fusiform cells were arranged in linear fashion, apparently in the process of forming thin, collagenous bundles. Whereas some of the small round cells had differentiated toward collagenous tissue, others had become phagocytic and were forming multinucleated giant cells. Both small round cells and giant cells contained considerable amounts of lipid material and some hemosiderin (Fig. 2). Giant cells contained up to several dozen nuclei. The giant cell in the lower right hand comer of Figure 1 was apparently still in the process of being formed. In 1 area, interconnecting clefts coursed through the tissue (Fig. 3). Lipid material (identified with oil red 0 stain) was more abundant than hemosiderin, accounting for the orange color. The red areas observed in the fresh specimen were the result of recent hemorrhage. Inflammatory cells were uncommon. Case 2. Desmoplasia was considerably more pronounced in this lesion and had isolated the active process into many discrete, nodular foci (Fig. 4). Most of this collagenous tissue was mature and contained scattered foci of siderophages surrounding small blood vessels, but very few inflammatory cells were evident. The cytologically more active foci were composed of round cells, slightly larger than those in Case 1, which had formed syncytial sheets and distinct multinucleated giant cells (Fig. 5). These cells contained less lipid material and hemosiderin than their counterparts in Case 1. The fibrillary network and fusiform cells of Case 1 were not present. There was, however, a differentiation to large fibroblastic cells at the margins of many nodules and some nodules had been completely replaced by these cells (Fig. 6). Scattered foci, in the active nodules, of round cells laden with hemosiderin pigment revealed the phagocytic capacity of these cells. The mottled color of this lesion was due mostly to recent and old focal hemorrhage, both in the active centers as well as in the surrounding desmoplastic tissue. Clefts could not be found in this older lesion.
Localized Nodular Tenosynovitis in the Horse 439 Fig. 4. Multiple foci of nodular tenosynovitis surrounded by desmoplastic tissue. Case 2. H & E, x30. Fig. 5. Round cells forming syncytial sheets and giant cells in active nodules of advanced lesion. Case 2. H & E, x260. Fig. 6. Fibroblastic area at the margin of an active nodule. Case 2. H & E, x 260.
440 RAGLAND 111 Discussion The full range of similar lesions as found in man have been grouped together and discussed in detail by JAFFE (1958). Regardless of location, the lesions could usually be classified as diffuse or ZocaZixed. Localized nodular tenosynovitis, the most common type, was usually a solitary nodule, located characteristically in the digits, and apparently occurred more often in females. Children were the least commonly affected. The condition was seldom related to pain or impaired motion. The diffuse form (pigmented villonodular tenosynovitis) has apparently been rare. Synovitis, the second most common type, was usually found in the knee joint, and had a slight predilection for males. Nodular and diffuse forms were of about equal frequency. Young adults were most frequently affected, with intermittent pain and swelling the chief complaints. Primary pigmented villonodular bursitis without synovial involvement was rare. The few cases observed were all of the diffuse type. JAFFE (1958) convincingly supported his view that these lesions were but slightly varying expressions of the same basic disorder. He argued, with less conviction, that they were the result of an inflammatory reaction rather than true benign neoplasms of synovioblasts. He preferred to view the round to elongate cells, the major cell type, as having their origin from subsynovial macrophages. As these cells proliferated, they differentiated to form fibroblasts, or large macrophages and giant cells. As this process continued, the synovium was raised irregularly and eventually disrupted and entrapped in the mass. The result at this stage was a spongy, villonodular lesion having a yellow to light brown color, depending on the relative amounts of lipid material or hemosiderin, respectively. This process continued until all that remained of the villonodular pattern in older lesions were clefts in the tissue. Finally, even these became obliterated by the fibroblastic process. The histologic appearance of these lesions varied so much, depending on their stage of development when they were removed for diagnosis, that their interrelationship could not be appreciated until a large collection had become available for study. Although the lesions in the 2 equine cases reported here were not recognized by the surgeons to have a definite relationship to tendons or tendon sheaths, classifying them as localized nodular tenosynovitis could be justified. JAFFE (1958) stated that, whereas an association with tendon or tendon sheath frequently could not be determined on gross inspection, it became evident on microscopic examination. He even commented that some of these lesions may have had their origin in the fascial and ligamentous tissues adjacent to the tendon sheaths, in which case it would be virtually impossible to determine the site of origin on gross inspection. In both Case 1 and Case 2, the lesions were located in the proximity of tendons. Furthermore, there was no pain, swelling of the joint, or lameness, all of which might have been expected had the lesions been in the synovium of the joints. On the basis of the characteristic histologic appearance, the general anatomic location, and the clinical history of these 2 equine lesions, it seems most likely that the site of origin was tendon sheath or adjacent fascia rather than joint or bursal synovium. The histology of the lesions was consistent with their duration. The 2- month-old lesion was soft, less cellular, and had a delicate, loose, fibrillar matrix.
Localized Nodular Tenosynovitis in the Horse 441 Clefts even existed in 1 area, suggesting the remains of a recent villonodular stage. On the other hand, the older lesion was firm and contained considerably more dense connective tissue which had apparently obliterated all evidence of a villonodular process. These observations are compatible with the descriptions of early and advanced localized nodular tenosynovitis ( JAFFE, 1958). It is difficult to determine how frequently lesions of this type have occurred in horses. Tendons of horses are subject to frequent trauma. However, nodules of this type have perhaps not often been removed for histologic examination, and may in time have resolved into scar tissue. As lesions of this type in man were originally considered neoplasms, a view still held by some pathologists, undoubtedly such lesions would have been designated, in some cases at least, as giant cell tumors. The report by DANKS and OLAFSON (1939) is probably a case in point. Since reactive giant cells may readily be formed in tissues of the horse, it is also possible that such lesions in the past might have been considered foreign body granulomas. Strmmary Subcutaneous nodules, removed from the shoulder of 1 and the stifle of another mature stallion, were identified histologically as localized nodular tenogno- &is. Neither horse exhibited any evidence of pain or impaired movement. One lesion had been present for 2 months, the other for 1 year. These nodules resulted from a proliferation of small round to fusiform cells with differentiation to fibroblasts or active phagocytes, including multinucleated giant cells. The older lesion had undergone considerable collagenization. Z~sammenfa~strng Subkutane Knoten, die von der Schulter eines ausgewachsenen Hengstes und dem Kniegelenk eines anderen entfernt waren, wurden histologisch als lokalisierte knotenfrmige Tenosynovitis identifiziert. Keines der Pferde zeigte irgendein Anzeichen von Schmerz oder Einschrankung der Bewegungsfreiheit. Eine Veranderung war 2Monate, die andere 1 Jahr vorhanden gewesen. Die Knoten waren durch Proliferation kleiner runder bis langgestreckter Zellen entstanden mit Differenzierung zu Fibroblasten oder aktiven Phagozyten, einschliesslich mehrkerniger Riesenzellen. Die altere Veranderung wies eine betrachtliche Kollagenbildung auf. Acknowledgments This study was supported by the State of Washington Initiative Measure No. 171 and U.S.P.H.S. Grant No. 5TIGM414. References 1. DANKS, A.G. and OLAFSON, P.: Giant-cell sarcoma. Cornell Vet. 29: 68-70 (1939). 2. JAFFE, H.L. ; LICHTENSTEIN, L. and SUTRO, C. J. : Pigmented villonodular synovitis, bursitis, and tenosynovitis. Arch. Path. 31: 731-765 (1941). 3. JAFFE, H.L.: Tumors and Tumorous Conditions of the Bones and Joints, pp. 532-557. (Lea and Febiger, Philadelphia 1958). Author s address: Dr. W.L. RAGLAND, Department of Pathology, University of Wisconsin, Mudisan, Wis. 53706 (USA).