Synovial nature of pathologic periarticular structures, including subcutaneous nodules. descent from embryonic arthrogenic fibroblasts: a hypothesis.

In the embryo the periarticular fibroblasts were the producers of the greater part of the joint they surround in later life, as well as of the tendon sheaths and bursae. It is postulated that adult fibroblasts have retained atavistic arthrogenic properties, and may react to traumatizing, inflammatory and oncogenic stimuli by forming periarticular joint-like structures: "arthromas" such as ganglia, meniscal cysts, synovial cysts, synovial sarcoma and subcutaneous nodules. The arthroid nature of these growths manifests itself by the presence of a central cavity, which can be identified as a synovial cavity by histologic, histochemical and electron-microscopic methods. In case of affection of the joint all of these adnexa may be involved. A resemblance of these structures to embryonic joint tissues has been noted for years. The nature of the subcutaneous nodule is discussed at some length. It may contain one or more synovial clefts; synovial elements may be found in its centre by histochemistry and electron-microscopy. Recent and personal findings shed a new light on palisading cells, which may be fibroblasts, having taken up again their embryonic task as synovioblasts. From periarticular fibroblasts thus three kinds of tumors may arise; benign (ganglia, cysts, subcutaneous nodules), malignant (synovial sarcoma) and "semi-malignant" (pannus in rheumatoid arthritis).

Ankylosing spondylitis and inflammatory bowel disease. II. Prevalence of peripheral arthritis, sacroiliitis, and ankylosing spondylitis in patients suffering from inflammatory bowel disease.

To establish the prevalence of peripheral arthritis, radiographic sacroiliitis, and ankylosing spondylitis in patients with inflammatory bowel disease, 58 consecutive patients suffering from ulcerative colitis (UC) and 51 with Crohn's disease (CD) underwent a detailed rheumatological examination. In addition, all patients were screened for the presence of the antigen HLA B27. Peripheral arthritis was found in 14 (8 UC, 6 CD) patients (12.8%); radiographic sacroiliitis was diagnosed in 11 (5 UC, 6 CD) (10.1%), of whom 10 were asymptomatic; and ankylosing spondylitis was diagnosed in 2 UC and 2 CD patients (3.7%). 18.9% of the UC and 3.9% of the CD patients were HLA B27 positive. One of the 11 patients with radiographic sacroiliitis and 2 of the 4 with ankylosing spondylitis had the HLA B27 antigen. Peripheral arthritis, radiographic sacroiliitis, and ankylosing spondylitis are apparently frequent manifestations in patients suffering from inflammatory bowel disease. Asymptomatic radiographic sacroiliitis in these patients appears to differ from idiopathic ankylosing spondylitis, both clinically and genetically. Evaluation of subjective rheumatological complaints, necessary for a confident diagnosis of ankylosing spondylitis, according to the New York criteria is difficult during a flare-up of the inflammatory bowel process, as was shown in 4 CD cases with marked limitation of lumbovertebral function and chest expansion, but no radiological abnormalities of the SI joints.

Ankylosing spondylitis and inflammatory bowel disease. III. Clinical characteristics and results of histocompatibility typing (HLA B27) in 50 patients with both ankylosing spondylitis and inflammatory bowel disease.

A study was made, in co-operation with several gastroenterology and rheumatology centres, of the clinical and genetic characteristics (HLA B27) of 50 patients suffering from both inflammatory bowel disease (38 Crohn's disease (CD), 12 ulcerated colitis (UC)) and ankylosing spondylitis (AS), the latter diagnosis being established according to the New York criteria. 20 CD (52.6%) and 8 UC (66.7%) patients were HLA B27 positive. The presence of HLA B27 was studied in relation to clinical parameters, such as first occurrence of symptoms of AS or inflammatory bowel disease (IBD), a history of peripheral arthritis, iridocyclitis, and a positive history of AS or IBD. Our patients were found to have heterogeneous clinical features: on one side of the spectrum a group of cases was distingiushed with the typical characteristics of idiopathic AS, often being HLA B27 positive. On the other side a smaller group of HLA B27 negative patients was observed, with severe intestinal inflammatory pathology, lacking most of the typical clinical features of idiopathic AS ('secondary' form of AS). Finally, between these two extremes a group of patients was found with less pronounced clinical or genetic characteristics. These different clinical and histocompatibility patterns suggest a mixed aetiopathogenesis of AS in IBD patients. Such a 'syndrome' of AS might harbour both idiopathic AS and forms of AS 'secondary' to the intestinal inflammatory pathology.