Progressive Joint Disease Research Articles

Late results of total shoulder replacement in patients with rheumatoid arthritis.

Rheumatoid arthritis of the shoulder is a progressive and destructive joint disease, and similar to arthritis in other joints, progression of the disease is unpredictable and may stop at any stage of involvement. Between 1983 and 1996, more than 500 shoulder prostheses were implanted in patients at the authors' institution. Total shoulder replacement yields satisfactory short and long term results even in patients with severely destructed joints. Pain relief is reliable and significant as reported in short and long term studies. In most patients the functional result is good or acceptable. Although range of motion is only slightly increased, a satisfactory overall range of motion is achieved by most patients because of the unaffected scapulothoracic motion. However, deteriorating results, emphasizing the complexity of shoulder arthroplasty, were seen with increasing observation time in patients with rheumatoid arthritis. Proximal migration of the humeral prosthesis attributable to rotator cuff failure, with secondary eccentric glenoid loading and progressive loosening, is latent in patients with chronic progressive rheumatoid disease and was by far the most common complication (42%) in the present series.

Evaluation of the Leeds-Keio Synthetic Replacement for the Cranial Cruciate Ligament in Dogs: An Experimental Study

SummaryEight conditioned research dogs, whose body weight was between 25 and 30 kg, had unilateral implantation of a Leeds-Keio (LK) synthetic implant (Dacron polyester) immediately after severance and removal of the cranial cruciate ligament (CCL). A rectangular- shaped autograft, composed of fascia lata, was placed within the LK implant in four of the eight dogs; the other four dogs received the LK implant only. Modified Robert Jones bandages were placed on the limbs that had been operated upon; the bandages were left in place for 48 hours. After that time the limbs were not splinted. The dogs were confined to 1.5 m X 3 m kennels, with twice daily leash walks for the duration of the study. Although the joints that received the LK implants were stable immediately after the operation, they all developed progressive effusion, crepitation and instability accompanied by clinically apparent lameness. All of the dogs were euthanatized three months after the operations. Gross examination of the eight joints that had been operated upon confirmed the presence of degenerative joint disease. Three of the eight dogs had “bucket handle” type tears of their medial meniscus in the joints with the LK implant, and the medial menisci in the other five stifle joints that received LK implants had a fibrillated surface texture. Five of the eight LK implants had either ruptured completely or were stretched and frayed to the point where mechanical testing was not justified. Mean breaking strength of the 3 intact LK implants was 6.6% of the contralateral, control CCL. Ingrowth of fibrous tissue into the LK implants was minimal. The synovium from all joints with LK implants had moderate to severely increased cellularity within the synovial villi and supporting stroma consisting predominantly of lymphocytes, plasma cells and macrophages. Multinucleated giant cells formed aggregates around irregular shaped strands of particulate material which was translucent and refractive. Under polarized light, these particles were bright yellow to green consistent with Dacron particles. It was concluded that the LK implant, as implanted in this study, was not a satisfactory replacement for the CCL in dogs.The Leeds-Keio synthetic replacement for the canine cranial cruciate ligament was implanted in eight dogs. All eight dogs developed progressive instability and secondary degenerative joint disease over a period of three months after the operation. It was concluded that the Leeds-Keio ligament, as implanted in this study, is not satisfactory for use in dogs.

Report of the 16th Meeting of the British Inflammation Research Association Topic: Measuring bone and joint disease progression: biochemical quantification

Report of the 16th Meeting of the British Inflammation Research Association Topic: Measuring bone and joint disease progression: biochemical quantification

A T cell receptor beta chain variable region polymorphism associated with radiographic progression in rheumatoid arthritis.

In rheumatoid arthritis (RA) genetic factors influence susceptibility to disease and progression. Identifying these genetic factors may give more insight into the aetiology and pathogenesis of this disease. Furthermore, if these genetic markers can predict progression in an early stage of disease, timely institution of more aggressive treatment in patients with a bad prognosis may help to prevent joint damage. Several studies have shown that HLA-DRB1 alleles are associated with RA, whereas others have indicated that genes not linked to the HLA complex are also involved. Candidates for such genes are the T cell receptor (TCR) alpha/beta genes. The association of a polymorphism in a TCR beta chain variable region gene (TCR-V beta 8) with both risk for RA and radiographic progression of joint disease was analysed after a three year follow up. A cohort of 118 white patients with a duration of disease shorter than one year at entry, and 110 white controls were typed for this (BamHI) TCR-V beta 8 polymorphism. The distribution of the two alleles, 2.0 and 23.0 kb, was identical in patients and controls. Radiographic progression (modified Sharp method) after a three year follow up, studied in 111 patients, was significantly less in the group possessing the 2.0 kb allele (p = 0.03). This does not confirm the reported association of the (BamHI) TCR-V beta 8 2.0 kb allele with RA. By contrast with previous findings in smaller studies, in the present study this 2.0 kb allele was protective against radiographic progression. Because well known prognostic variables in RA were corrected for, the findings indicate that the TCR-V beta 8 polymorphism studied is a new prognostic marker for this disease.

Triple arthrodesis in older adults. Results after long-term follow-up.

We studied the results for seventeen patients (eighteen feet) who had had a triple arthrodesis at an average age of sixty-six years (range, fifty-two to eighty years). There were twelve women and five men. The procedures had been performed to correct deformities of the hindfoot and midfoot caused by an untreated rupture of the posterior tibial tendon in ten patients; by rheumatoid arthritis in three patients (four feet); and by neuropathic arthropathy (associated with diabetes mellitus), trauma, old poliomyelitis, and a stroke in one patient each. The average duration of follow-up was forty-two months (range, twenty-seven to 156 months). At the most recent follow-up examination, three patients had a non-union (one, of the talonavicular joint and two, of the calcaneocuboid joint), six patients (seven feet) had progressive degenerative joint disease involving the ankle, seven had progressive degenerative changes in the mobile joints of the feet, two had had an infection but both infections had healed, and one had had postoperative collapse of the foot because of premature, unauthorized weight-bearing. In one patient, a staple across the subtalar joint had been removed because of pain caused by impingement of the staple on the tip of the fibula. Over-all, fourteen of the seventeen patients were satisfied with the result of the operation. All seventeen had less pain postoperatively, but eleven still had some discomfort.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone and joint disease progression: detection, imaging and quantification.

Bone and joint disease progression: detection, imaging and quantification.

Internal derangement of the temporomandibular joint: Radiologic staging with clinical, surgical, and pathologic correlation

The radiologic findings from 60 patients with 86 internally deranged temporomandibular joints (TMJ) upon whom sequential imaging procedures had been performed over a period of two months to ten years were analyzed and correlated with clinical, surgical (72 joints), and pathological observations. Internal derangement of the TMJ disc (meniscus) and osseous structures was found to be an irreversible and progressive disorder with characteristic stages. Internal derangements of the TMJ were divided into early (stage one), intermediate (stages two and three) and late stage (stages four and five) categories based upon radiologic findings obtained with radiography, lateral TMJ tomography and either two compartment arthrography or high field, surface coil MR. After sequential imaging studies, each patient and 72 deranged joints underwent surgical joint exploration and meniscectomy because of progressive joint disease and clinical disability. Surgically removed tissues underwent routine histological evaluation. Surgical and pathologic observations included disc displacement, deformity, hyalination, myxomatous degeneration, perforation of the disc attachments, capsular adhesions, synovitis and mandibular condyle lesions including osteochondritis dissecans (OCD), avascular necrosis (AVN), osseous remodeling and degenerative arthritis. There was excellent correlation between imaging studies and surgical observations. Internal derangement of the TMJ is an irreversible, generally progressive disorder which may be staged and followed with radiography, tomography and either two-compartment arthrography or high field, surface coil MR.

Sulfasalazine significantly slows joint damage and disease progression

Sulfasalazine significantly slows joint damage and disease progression

Pulse methotrexate therapy in rheumatoid arthritis. A controlled prospective roentgenographic study.

To assess whether weekly pulse methotrexate therapy alters radiographic progression of joint disease in patients with rheumatoid arthritis. Prospective, controlled study. Hand, wrist and foot roentgenograms obtained before, at the onset of, and during methotrexate treatment were scored for degree of joint-space narrowing and erosions by three rheumatologists using a standard method. Sequential sample of 24 patients with active definite or classical rheumatoid arthritis and previous unsuccessful treatment; of these, 3 were excluded due to drug ineffectiveness; 2, due to side effects; and 1, due to refusal to take methotrexate. Treatment with nonsteroidal anti-inflammatory drugs and prednisone was continued. Methotrexate was given weekly to control clinical evidence of disease in patients. After having had an average of 30 months of therapy, the 18 patients who continued to receive methotrexate therapy showed significant (p less than 0.05) clinical improvement, as evidenced by their decreased joint counts and joint scores, duration of morning stiffness, pain scales, and sedimentation rates. Despite patients' prolonged clinical improvement, the mean rate of development of erosions and joint-space narrowing during methotrexate therapy was not significantly different from the rate of radiographic progression before methotrexate therapy (0.043 compared with 0.041; p greater than 0.05). Weekly pulse methotrexate is effective for the long-term management of clinical disease activity in patients with refractory rheumatoid arthritis but may not be a disease-modifying agent by roentgenographic criteria.

RADIO-ISOTOPIC JOINT SCANS IN HAEMOPHILIC ARTHRITIS

The majority of severe haemophiliacs will develop a crippling arthritis consequent upon recurrent haemarthroses although the pathogenic mechanism remains unclear. We have carried out technetium-99 pertechnetate joint scans in the elbows, knees and ankles of 23 haemophilic patients and compared the isotope uptake of the 15 patients with clinical and radiological evidence of arthritis to that of eight patients without arthritis, to 13 age-matched healthy male controls, and to 10 age-matched males with active rheumatoid arthritis. Isotope uptake into the knee joints was significantly higher in haemophilic arthritis than in controls, haemophiliacs without arthritis, and patients with rheumatoid arthritis [median percentage uptake of administered technetium (Tc) dose X 10(3) in right knee = 9.4, 6.2, 6.4 and 6.6, respectively]: and the differences from haemophilic arthritis were all significant (p less than 0.01, Mann-Whitney U test). Similar differences were seen in the elbows and ankles. Increased Tc uptake correlated strongly with frequency of haemarthrosis, pain, synovitis, range of movement and radiological changes in knees and elbows, but poorly with the lesser changes seen in the ankles. These results would support the theory that haemophilic arthritis amongst the inflammatory arthropathies and that scanning is an appropriate technique for following progression of joint disease.

Observations and Research on Hip Dysplasia

Hip dysplasia affects man and all other domestic mammals. In man, 1.3 children in 1000 are affected. In dogs the prevalence may run over 50% in large dogs if control measures have not been practiced. Few data are available on the prevalence of hip dysplasia in other mammals, but it is thought to be low. The disease is undoubtedly rare in undomesticated animals. No specific genetic pattern of inheritance has been demonstrated in this variable disease. It has been demonstrated that both genetic and environmental influences contribute to development, regardless of the species affected [5, 9, 20, 21, 26, 47, 50]. Consequently, the disease has been designated as polygenic or multigenic. There is no evidence that a primary defect of bone exists but rather the disease is a failure of the muscles and other soft tissues to hold the hip joint in full congruity [20, 21]. This is further supported by the fact that bony dysplasia can be increased, decreased, or prevented by controlling the degree of joint instability and incongruity [35]. No other malformations are associated with the disease [52], which signifies that hip dysplasia is ‘many diseases that end up with common degenerative lesions of the hip joint’ [51]. Inborn metabolic errors of chemical and hormonal origin are not evident [34, 58]. The quantity of hormones needed to produce hip dysplasia experimentally far exceeded those that could be produced by any biological system [34, 36, 57]. A causal relationship between muscles and soft tissue defects or pathological changes other than lack of muscle mass or strength has not been established [25, 26]. Experimentally, hip dysplasia may be produced in many ways [27, 36, 47, 50, 58, 59]. These include any circumstances that contribute to an unstable hip joint, that is, adductor forces, lack of muscle strength, chemical relaxation of the pelvic soft tissues, traumatic injury to the hip joint, and overloading of the joint by weight. Hip dysplasia is a concentration of factors from a pool of genetic weaknesses and environmental stresses that fall into a programmed pattern of progressive remodelling and degenerative joint disease.

An experimental study of surface injury to articular cartilage and enzyme responses within the joint.

An experimental model of degenerative joint disease on chondromalacia consists of a surgically-scarified articular surface of the adult dog knee joint. In 52 dogs, evaluated by histologic and enzymatic assays over a period of 1 to 110 weeks post-surgery, the levels of acid hydrolase activity varied on various areas of articular cartilage within the same joint. There was a transient rise in most of the acid hydrolases in the synovium as a response to arthrotomy of the knee joint. All of the acid hydrolases studied did not respond uniformly to surgically created trauma. There was evidence of repair of the cartilage lacerations even when the subchondral zone was not breached. Lacerations in the central portion of the patella rarely showed healing in contrast to those placed more to the periphery of the articular surface. There was no gross or histologic evidence of progressive degenerative joint disease up to 2 years post-surgery. Thus an injury inflicted to the surface of the articular cartilage may be in itself insufficient in severity to produce destructive changes in the joint. This should not be too surprising, since, clinically, all joint surface injury does not lead to degenerative arthritis. The joint seems to have an injury threshold whereby chondrocytes are capable of repairing surface injury if the damage is not massive or repetitive. Insofar as lacerations in the center of the patella rarely healed, while the peripheral ones showed consistent signs of healing, the site of injury, as well as the magnitude of injury, may be critical.

THE INFLUENCE OF CORTICOSTEROIDS ON NORMAL AND PAPAIN-TREATED ARTICULAR CARTILAGE IN THE RABBIT

1. Because of the controversy over the clinical effects of corticosteroids on joint tissues a series of experiments on the knee joints of rabbits was undertaken. 2. The articular cartilage of the distal femoral epiphyses of normalcontrols has been compared with that of rabbits treated daily either with cortisone or with methyl prednisolone systemically or by intra-articular injections. 3. The changes caused by intravenous papain and their subsequent recovery have been described, and the adverse effect of corticosteroids on recovery has been assessed. 4. The biological mechanisms involved are discussed, and as a result caution is urged in the administration of corticosteroids in the presence of progressive degenerative joint disease.