Lymphoplasmacytic Synovitis Research Articles

Histologic evidence for a humoral immune response in synovitis associated with cranial cruciate ligament disease in dogs.

To investigate histopathological features of synovium from dogs with cranial cruciate ligament disease (CCLD) to seek mechanisms of osteoarthritis (OA) associated with CCLD. Retrospective, single-institution case series. Thirty client-owned dogs. Synovial biopsies (n=30) obtained from stifles with CCLD were assessed by using two synovitis histopathology grading systems (Krenn and Hospital for Special Surgery [HSS]). The Krenn synovitis score was interpreted as "no synovitis," "low-grade," or "high-grade," while inflammatory subtype (low, mixed, or high) was determined by a computational algorithm within the HSS system. Comparison of synovitis scores was based on degree of CCL rupture and presence of meniscal tears. Histopathological changes and synovitis scores were similar regardless of degree of rupture (partial n=5, complete n=25) or presence of meniscal injury (n=12) and were characterized by hyperplastic and lymphoplasmacytic synovitis with increased vascularity (30/30) and the presence of hemosiderin deposits (28/30), binucleated plasma cells (28/30), mucoid change (25/30), and Mott cells (16/30). Thirteen (43%) specimens were consistent with high-grade synovitis according to the Krenn system, while 11 (37%) specimens fit into the high-inflammatory subtype with the HSS system. Synovitis associated with canine CCLD in this study population was lymphoplasmacytic and was often highly inflammatory, with the presence of cells pertaining to humoral immunity. Humoral immune responses may play key roles in the synovitis associated with CCLD. Modulation of biological factors that provoke humoral immune responses may mitigate symptoms of OA that persist and progress even after surgical treatment of CCLD in dogs.

Subarticular Inflammatory Pseudoabscesses: A Pathologic Study With Clinical Correlation.

Abnormal accumulation of neutrophils in a subarticular bone usually raises the concern for osteomyelitis or septic arthritis, a disabling and potentially life-threatening medical condition. At the pathology department of a specialized orthopedic institute, we observed a distinct pattern of subarticular inflammation mimicking infection characterized by collections of neutrophils, macrophages, and fibrin in pseudocystic spaces of variable size and extent in the superficial subarticular bone not accompanied by granulation tissue or necrosis. We coined the term "inflammatory pseudoabscess" to describe these accumulations. From 1997-2015, we reported inflammatory pseudoabscesses in 157 primary arthroplasty/osteotomy specimens from 143 patients without penetrating trauma or hardware in the affected joint. The predominant gross and histologic features were those of destructive/inflammatory joint disease, including lymphoplasmacytic synovitis (95.3%), subchondral osseous chronic inflammation (80.3%), exudative synovitis (58.0%), synovial pannus (52.0%), and marginal erosions of articular cartilage and/or subarticular bone (43.3%). Clinical information was available in 137 (95.8%) patients, 107 (overall: 74.8%) of whom had preoperatively or postoperatively diagnosed inflammatory arthropathy, most commonly rheumatoid arthritis. The remaining 30 (overall: 21.0%) patients had no documented inflammatory disorders, but some had bilateral or multijoint arthropathy, hands/feet involvement, lymphoplasmacytic synovitis, ulcerative colitis, or family history of inflammatory arthropathy. There was no documented infection-associated implant failure. We believe that inflammatory pseudoabscess represents an intraosseous manifestation of noninfectious inflammatory disorders of joints. This feature should be recognized by pathologists and used to suggest further clinical evaluation for undiagnosed inflammatory joint diseases.

Feline histoplasmosis presenting with bone and joint involvement: clinical and diagnostic findings in 25 cats.

The aim of this study was to describe clinical and diagnostic findings in cats with bone and joint disease associated with histoplasmosis. Medical records from between 2011 and 2017 were reviewed. Inclusion criteria required: (1) diagnosis of histoplasmosis by cytology, histology, urine or serum Histoplasma antigen testing, or culture; and (2) lameness or joint effusion as a presenting complaint or physical examination finding. Twenty-five cases met the inclusion criteria. Four had incomplete records, but available data were included when applicable. Lameness was a presenting complaint in 17/21 cats and was the only complaint in 9/21 cats. Initial diagnosis was made by cytology in 22/25 cats and by culture, urine antigen and necropsy in one case each. Diagnostic cytology samples included synovial fluid (n = 13), lymph node (n = 5), skin (n = 2), lung (n = 1) and bone (n = 1). Two additional cases had synovial fluid examined but no organisms present. Inflammation was present in all synovial fluid samples examined. Biopsy was obtained in two cats and histologic diagnoses included osteomyelitis with no infectious organisms identified and severe lymphoplasmacytic synovitis suggestive of feline periosteal proliferative polyarthritis. Histoplasma urine antigen test was positive in 7/12 cats. Inflammatory arthritis is common in cats with histoplasmosis, with lameness a common presenting complaint. Organisms are found in synovial fluid cytology in most cases. If not, appropriate additional diagnostics must be pursued.

Cruciate ligament degeneration and stifle joint synovitis in 56 dogs with intact cranial cruciate ligaments: Correlation of histological findings and numbers and phenotypes of inflammatory cells with age, body weight and breed

The majority of dogs with ruptured cranial cruciate ligaments (crCLs) have inflammatory changes of the stifle joint suggesting that synovitis is an important factor which is involved in the development of degenerative ligament changes. Detailed information is not available concerning the possible occurrence of inflammatory changes in the stifle joint synovium of dogs with macroscopically intact crCLs and its correlation with presence and severity of degenerative changes of the crCLs. Therefore, the purpose of this study was to examine post mortem tissue samples of 56 dogs with non-ruptured crCLs histologically for the presence of inflammatory and degenerative changes of the stifle joint synovium and cruciate ligaments, respectively. In 25/56 (44.6%) dogs, histology showed that both lymphoplasmacytic synovitis and degenerative alterations of the crCLs were present. In these dogs, there was a significant positive statistical correlation between the severity of synovitis and degenerative crCL lesions. The results suggest that synovitis in the stifle joints of dogs with non-ruptured crCLs is a frequent event and probably is involved in the development of degenerative lesions occurring in canine crCLs. Also, the severity of crCL degeneration in these 25 dogs was significantly correlated with their age and body weight. In 2/56 (3.6%) cases, only lymphoplasmacytic synovitis was found in the absence of degenerative crCL lesions. In 15/56 (26.8%) dogs, only degenerative lesions of the crCLs without synovitis were present. Statistically, a significant correlation was found between the severity of degenerative alterations and age and body weight of these dogs. Phenotyping of inflammatory cells by immunohistochemistry showed that the synovium of dogs which histologically had lymphoplasmacytic synovitis was infiltrated with CD3+ T lymphocytes, CD79+ B lymphocytes, major histocompatibility class II antigen (MHC class II)+ cells and macrophages expressing CD163 or S100/A8/S100A9 (calprotectin), while tartrate-resistant acid phosphatase (TRAP)+ cells were absent. Quantification and statistical evaluation of inflammatory cell types in the inflamed synovium revealed that the numbers of lymphocytic cells and macrophages were significantly correlated with the severity of synovitis. These findings indicate that, besides T and B lymphocytes, both pro- and anti-inflammatory macrophages play a role in the development of degenerative crCL alterations.

Shaggy Lame Fox Syndrome in Pribilof Island Arctic Foxes ( Alopex lagopus pribilofensis), Alaska.

A previously unrecognized condition is described in wild free-ranging Pribilof arctic foxes ( Alopex lagopus pribilofensis) from the Pribilof Islands, Alaska, USA. This condition is called shaggy lame fox syndrome (SLFS) denoting the primary clinical signs first observed. Criteria used to suspect SLFS on gross examination included emaciation, failure to shed winter pelage and moderate to severe polyarthritis. Criteria used to confirm SLFS histologically included polyarthritis (characterized by lymphoplasmacytic synovitis, tenosynovitis, bursitis, periosteal bony proliferation, and periarticular lymphoplasmacytic vasculitis) and systemic leukocytoclastic vasculitis. Other histological lesions often found included renal cortical infarcts, myocarditis with myocardial infarcts, lymphoplasmacytic meningitis, lymphoplasmacytic cuffing of meningeal and a few cerebral vessels, and cavitating infarcts of the brainstem and thalamus. The cause of SLFS is not known at this time; however, the gross and histological lesions suggest that the cause of SLFS may be a bacterial polyarthritis with a secondary immune-mediated vasculitis. These lesions are consistent with changes described with Erysipelothrix rhusiopathiae in domestic dogs; E. rhusiopathiae was identified from the synovial membrane of a swollen stifle joint and the kidney from one fox using real-time polymerase chain reaction and with culture from a fox that had gross and histological lesions of SLFS. Therefore, E. rhusiopathiae is a possible etiological agent for SLFS.

Prevalence of lymphoplasmacytic synovitis in dogs with naturally occurring cranial cruciate ligament rupture

To determine the prevalence of lymphoplasmacytic synovitis (LPS) in dogs with naturally occurring cranial cruciate ligament (CCL) rupture and compare clinical, radiographic, cytologic, and histologic findings in dogs with and without LPS. Cross-sectional study. 110 dogs with naturally occurring CCL rupture. Histologic examination of synovial biopsy specimens obtained at the time of surgical treatment was used to identify dogs with LPS. Clinical, radiographic, cytologic, and histologic findings were compared between dogs with and without LPS. 56 (51%) dogs had histologic evidence of LPS. There were no significant differences in age, body weight, duration of lameness, severity of lameness, severity of radiographic signs of degenerative joint disease, extent of CCL rupture (partial vs complete), or gross appearance of the medial meniscus between dogs with and without LPS. Mean tibial plateau angle was significantly lower in dogs with LPS than in dogs without LPS, and dogs with LPS were significantly more likely to have neutrophils in their synovial fluid. Lymphocytes were seen in synovial fluid from a single dog with LPS. Results suggested that LPS was common in dogs with naturally occurring CCL rupture. However, only minor clinical, radiographic, cytologic, and histologic differences were identified between dogs with and without LPS.

Inflammatory response in dogs with spontaneous cranial cruciate ligament rupture

SummaryThe inflammatory response in 73 dogs with spontaneous rupture of the cranial cruciate ligament was studied. Collagen I and II antibodies (CI, CII), antinuclear antibodies (ANA) and anti-neutrophil cytoplasmic antibodies (ANCA) in synovial fluid (SF) and serum were analysed, as well as serum thyroxine (T4) and free thyroxine (fT4). The type and degree of synovitis did not affect the concentration of antibodies to CI&II. The histological findings of the synovial membranes in 47 dogs were graded as mild non-specific synovitis in 21%, moderate nonspecific synovitis in 32%, moderate lymphoplasmacytic synovitis in 36% and nodular lymphoplasmacytic synovitis in 11% of the dogs. Of 45 dogs four had lower than normal concentration of T4 and fT4. There was not any evidence of a primary autoimmune response.

Histopathological evaluation of canine stifle joint synovial membrane collected at the time of repair of cranial cruciate ligament rupture.

Synovial membranes from 54 dogs were collected at the time of surgery to stabilize the stifle joint following rupture of the cranial cruciate ligament. Histological evaluation revealed lymphoplasmacytic synovitis with the formation of distinct, nodular aggregates in 36 synovial membranes. The remainder had evidence of chronic synovitis with variable numbers of diffuse, mononuclear cells. The presence of a potentially immune-mediated synovitis in the majority of cases suggests the need for further study.

Medial patellar luxation in 16 large dogs. A retrospective study.

Unilateral medial patellar luxation was diagnosed in 10, and bilateral medial patellar luxation in six, large and giant-breed dogs (22 stifles). Lameness occurred in five dogs after trauma or surgery, and 11 dogs had no known predisposing history. The mean age at presentation was 25 months, and the mean time from initial onset of clinical signs to diagnosis was 13 weeks. All traumatic or iatrogenic luxations (five dogs) were unilateral. Luxations presumed to be congenital were unilateral in five dogs and bilateral in six. The grades of medial patellar luxation were I (1 stifle), II (11 stifles), III (9 stifles), and IV (1 stifle). Preoperative function was good (1 dog), fair (9 dogs), and poor (6 dogs). Surgical correction was performed in dogs with grades II, III, and IV luxations (21 stifles). Complications included one wound dehiscence and trochlear wedge migration, one pin loosening, and one persistent lameness caused by lymphoplasmacytic synovitis. Long-term follow-up was available in 13 dogs (18 stifles). Function was judged by owners to be excellent in seven dogs, good in five dogs, and poor in one dog. Surgical treatment of grades II and III luxations yielded good (8 stifles) and excellent (9 stifles) results, while one grade IV luxation had a poor long-term outcome.

Acromegalic Arthropathy of the Hip

The changes in gross morphology of the femoral head, specimen radiograms, cut sections of the femoral heads, and histopathology of the synovium were examined in 11 surgical specimens from six acromegalic patients who were treated by total hip arthroplasty. The pathologic changes in six age- and sex-matched patients also undergoing 11 total hip arthroplasties for idiopathic degenerative joint disease were examined for comparison. The hip joint changes in acromegaly represent a peculiar arthropathy, which is characterized by prominent, proboscis-like medial osteophytes, moderate chronic lymphoplasmacytic synovitis, an irregular pitting of the subchondral bone observed roentgenographically, and osteopenia. When compared with idiopathic degenerative joint disease, these changes are distinctive in extent, if not in quality. The pathophysiologic relationship between these entities remains obscure.