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ID PMID Title PublicationDate abstract
11798731 [Specific antibodies for the early diagnosis of rheumatoid arthritis]. 2000 Jan OBJECTIVE: To assess the specificity and sensitivity of antiperinuclear factor (APF), anti-keratin antibody (AKA), anti-Sa antibody and anti-RA33 antibody in the diagnosis of RA. METHODS: 128 patients with RA, whose durations were within 1 year, were included. APF and AKA were detected by indirect immunofluorescence on the human buccal mucosa cells and the straum corneum of Wistar rat esophagus. Anti-Sa antibody and anti-RA33 antibody were examined by Western blotting. Sa antigen was extracted from human placenta while RA33 antigen from Ehrlich cells. RESULTS: (1) The specificities and sensitivities of APF, AKA, anti-Sa antibody and anti-RA33 antibody were 91.4% (224/245) & 35.2% (45/128), 90.2% (221/245) & 32.0% (43/128), 90.6% (222/245) & 33.6% (43/128), 89.8% (220/245) & 28.9% (37/128), respectively, versus 72.3% (177/245) & 44.5% (57/128) for rheumatoid factor (RF). There were no statistical differences in the specificity between the four antibody groups and RF until 1:128 were taken as positive titer. Among 71 patients with RF-negative RA, 15 (21.1%) were positive for APF, 18 (25.4%) positive for AKA, 21 (29.6%) positive for anti-Sa antibody and 17 (23.9%) positive for anti-RA33 antibody. (2) Specificity and sensitivity were 95.1% (233/245) and 46.1% (59/128) respectively when two of the four antibodies turned out to be both positive. If three or more kinds were detected simultaneously, specificity was as much as 99.6% (108/128). (3) Statistical difference was found among the four groups defined by the number of positive antibodies in radiographic stage and patients assessment of illness. CONCLUSION: (1) Dictation of APF, AKA, anti-Sa antibody and anti-RA33 antibody can greatly improve the specificity of diagnosis of early RA and serve as a complement when RF is negative. (2) Combined detection of the above four antibodies has a better discrimination ability as a laboratory criterion than that of RF. (3) Three or more positive antibodies may be an indicator of severe bone erosion and emergent demand for early treatment with better outcome.
10873961 Magnetic resonance imaging, radiography, and scintigraphy of the finger joints: one year f 2000 Jul OBJECTIVES: To evaluate synovial membrane hypertrophy, tenosynovitis, and erosion development of the 2nd to 5th metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints by magnetic resonance imaging in a group of patients with rheumatoid arthritis (RA) or suspected RA followed up for one year. Additionally, to compare the results with radiography, bone scintigraphy, and clinical findings. PATIENTS AND METHODS: Fifty five patients were examined at baseline, of whom 34 were followed up for one year. Twenty one patients already fulfilled the American College of Rheumatology (ACR) criteria for RA at baseline, five fulfilled the criteria only after one year's follow up, whereas eight maintained the original diagnosis of early unclassified polyarthritis. The following MRI variables were assessed at baseline and one year: synovial membrane hypertrophy score, number of erosions, and tenosynovitis score. RESULTS: MRI detected progression of erosions earlier and more often than did radiography of the same joints; at baseline the MRI to radiography ratio was 28:4. Erosions were exclusively found in patients with RA at baseline or fulfilling the ACR criteria at one year. At one year follow up, scores of MR synovial membrane hypertrophy, tenosynovitis, and scintigraphic tracer accumulation had not changed significantly from baseline; in contrast, swollen and tender joint counts had declined significantly (p<0.05). CONCLUSIONS: MRI detected more erosions than radiography. MR synovial membrane hypertrophy and scintigraphy scores did not parallel the changes seen over time in clinically assessed swollen and tender joint counts. Although joint disease activity may be assessed as quiescent by conventional clinical methods, a more detailed evaluation by MRI may show that a pathological condition is still present within the synovium.
10854227 The endogenous adjuvant squalene can induce a chronic T-cell-mediated arthritis in rats. 2000 Jun Squalene is a cholesterol precursor, which stimulates the immune system nonspecifically. We demonstrate that one intradermal injection of this adjuvant lipid can induce joint-specific inflammation in arthritis-prone DA rats. Histopathological and immunohistochemical analyses revealed erosion of bone and cartilage, and that development of polyarthritis coincided with infiltration of alphabeta(+) T cells. Depletion of these cells with anti-alphabeta TcR monoclonal antibody (R73) resulted in complete recovery, whereas anti-CD8 and anti-gammadelta TcR injections were ineffective. The apparent dependence on CD4(+) T cells suggested a role for genes within the major histocompatibility complex (MHC), and this was concluded from comparative studies of MHC congenic rat strains, in which DA.1H rats were less susceptible than DA rats. Furthermore, LEW.1AV1 and PVG.1AV1 rats with MHC identical to DA rats were arthritis-resistant, demonstrating that non-MHC genes also determine susceptibility. Some of these genetic influences could be linked to previously described arthritis susceptibility loci in an F2 intercross between DA and LEW.1AV1 rats (ie, Cia3, Oia2 and Cia5). Interestingly, some F2 hybrid rats developed chronic arthritis, a phenotype not apparent in the parental inbred strains. Our demonstration that an autoadjuvant can trigger chronic, immune-mediated joint-specific inflammation may give clues to the pathogenesis of rheumatoid arthritis, and it raises new questions concerning the role of endogenous molecules with adjuvant properties in chronic inflammatory diseases.
9374924 Effects of detraining subsequent to strength training on neuromuscular function in patient 1997 Oct The effects of detraining subsequent to strength training on neuromuscular function were examined in 39 recent-onset rheumatoid arthritis (RA) patients. Eighteen age- and sex-matched healthy people (H) served as controls. Patients were randomly allocated either to the experimental group (PE), who carried out progressive strength training for 6 months, or to the control group (PC), who maintained only their habitual physical activities. After 6 months, PE returned to their earlier physical activities and strength training was terminated. At baseline, the maximal strength of the trunk extensors (not significant), grip strength and maximal dynamic strength and the shape of the force-time curve of the knee extensors were lower in PE and PC (P < 0.05-0.001) than in H. Strength training in PE led to remarkable increases (P < 0.05-0.001) in the maximal strength of all muscle groups without changes in the shape of the force-time curve. The increases in muscle strength in PE obtained by strength training were lost to a great degree during the detraining period for the isometric trunk extension (P < 0.01) and flexion (P < 0.01) strength and for the dynamic knee extension strength (P < 0.05), but not for the grip strength. In PC, trunk extension and flexion strength decreased significantly throughout the study period. At the post-test, all the strength values in both patient groups were much lower than in H. RA is a chronic disease which seems to need continuous physical exercise with sufficient intensity to minimize/prevent the loss of muscle strength and functional capacity.
11263010 [The immunologic homunculus in rheumatoid arthritis. A new viewpoint of immunopathogenesis 2001 Feb Autoreactivity plays a major role in the pathogenesis of RA. The rheumatoid factor has been and still is for now more than 50 years the only autoreactivity that is clinically applied in the diagnosis of RA. This well reflects the current way of thinking that a single antigen or a single cause drives an individual into disease. Although by now many other autoantigens and autoreactivities have been described, their discovery was always on the search for the one and only autoreactivity that causes RA. This includes also immune reactivities directed against xenogenic antigens. But, none of the known RA-associated autoreactivities is present in all RA patients and none of them occurs exclusively in RA. Thus, the observed sensitivities and specificities are well below 100%. Therefore, RA has often been postulated to consist of various immunological subentities with similar clinical symptoms. Nevertheless, none of the autoreactivities correlates with a distinct clinical feature or course of disease. It is about time to say good-bye to the idea that a single antigen or immunoreactvity causes and maintains rheumatoid arthritis. In this paper we present RA as the clinical outcome of an immune system that has shifted from a healthy to an autoimmune steady state. This is accomplished by many different reactivities and autoreactivities that occur either in parallel or one after the other. The entirety of the known RA-associated reactivities and (auto)antigens is presented in detail. The major RA-relevant autoantigens comprise BiP, citrulline, the Sa-antigen, hnRNP A2, p205, IgG, calpastatin, calreticulin, collagen and the shared HLA-DR epitope. The accumulation of factor--involving autoreactivities, cytokines, environmental and genetic factors--that challenge the normal regulatory mechanisms of the immune system lead to a regulatory catastrophe. In individuals developing the clinical features of RA the immune system has been regulated to a new--autoimmune--steady state. This attractor "rheumatoid arthritis" has many features of what has originally been described by Irun Cohen as the immunological homunculus: The healthy immune system is configured such as to direct its attention to major self-antigens. Thus it creates an autoreactivity to many autoantigens as a prerequisite for regulatory mechanisms that are sufficient to control them. The shift from the normal to rheumatoid attractor involves the inflammatory cytokines TNF-alpha, IL-1 and IL-6, autoreactive T- and B cells directed at a variety of synovial and systemic antigens, activated dendritic cells and macrophages, tissue destruction and genetic factors such as the association with shared epitope. Environmental factors involved may also, but do not necessarily, include infection. With the appearance of clinical features of RA, naive, potentially autoreactive T cells infiltrate the synovial compartment and become activated by dendritic cells and other APCs. The autoantigenic peptides that are presented to these T cells are derived from inflammatory cell and tissue destruction as well as from tissue repair and remodeling processes. These T cells proliferate and either provide help to B cells with the specificity to the same antigens or cause direct cytopathic tissue damage. Thereby, more and novel antigens are generated, released and presented again to naive or primed autoreactive T cells. These processes involving cytokines, tissue destruction and autoreactive T cells are sufficient to maintain RA even without the permanent presence of a triggering agent. The recursive autoimmune processes are well consistent with the finding of the many different autoreactivities in RA and their respective sensitivities and specificities. The massive influx of T cells into the arthritic joint is accompanied by the anergization of over 90% of T cells in this compartment--which further substantiates the concept of the RA attractor within the self-regulating immune system. Thereby, the RA-attracted immune system is not able to completely downregulate the inflammation and the local tissue damage/repair. Thus, the immune system is permanently stimulated and suddenly by chance shifts to a stable state different from the healthy system--reaching the wide fields of rheumatoid arthritis which in itself is self-sustaining as the healthy state before disease onset.
9805191 Amyloidosis mimicking rheumatoid arthritis. 1998 A 49-year-old man presented a clinical picture suggesting seronegative rheumatoid arthritis. He developed severe joint contractions, pasty synovial swelling, macroglossia and proteinurie. Subsequent investigations disclosed light-chain multiple myeloma and A1-amyloid deposits in synovial tissue and skin. A1-amyloidosis should be considered in the differential diagnosis of patients with seronegative polyarthritis. Clues to the diagnosis of amyloid arthropathy are a carpal tunnel syndrome, early occurrence of joint contractures in combination with a relatively mild synovitis and a low ESR as well as the presence of other possible organ involvement with amyloidosis.
10778569 Malignancy in rheumatoid arthritis--a report of two cases. 1999 May The development of malignancy in the setting of pre-existing connective tissue disease is well known. We report two cases of rheumatoid arthritis who developed malignancy--multiple myeloma in one of them and carcinoma cervix in the other. Case 1 was a 62 year old man, who developed multiple myeloma three years after the onset of rheumatoid arthritis. Case 2 was a 61 year old female with history of rheumatoid arthritis for two years and who developed carcinoma cervix.
11333344 Anti-interleukin-1 therapy in rheumatic diseases. 2001 May Recent research has shown that in the processes of rheumatoid arthritis (RA), interleukin (IL)-1 is one of the pivotal cytokines in initiating disease, and the body's natural response, IL-1 receptor antagonist (IL-1Ra), has been shown conclusively to block its effects. In laboratory and animal studies inhibition of IL-1 by either antibodies to IL-1 or IL-1Ra proved beneficial to the outcome. To date, two large well-controlled studies in patients with RA led to the conclusion that IL-1Ra is clinically effective and that it slows progression of bone damage as measured radiographically. Being a specific, selective inhibitor of the IL-1 pathway, IL-1Ra could constitute an important new approach to treating patients with RA that significantly reduces the signs and symptoms of the disease, reduces joint destruction and up to now has proved safe and well tolerated.
9272302 Human cytomegalovirus infection and systemic lupus erythematosus. 1997 Jul OBJECTIVE: Viruses are considered possible aetiologic agents of autoimmune disease. Evidence suggests that human cytomegalovirus (HCMV) may be a pathogenetic factor in systemic lupus erythematosus (SLE). We undertook a seroepidemiological study to determine whether HCMV infection is increased in patients with SLE. METHODS: Sero-epidemiologic data, indicative of virus prevalence, were obtained by enzyme immunoassay. RESULTS: Eighty-eight of 97 serum samples (90.7%) taken from adult patients with SLE were seropositive for HCMV. By contrast, HCMV was detected in only 32 of 50 (64.0%) adult patients with rheumatoid arthritis (RA) and 42 of 97 (43.3%) normal controls. The odds ratio for HCMV prevalence in SLE/normal controls was 14.53 (95% CI is 6.39 to 33.04). For comparison, data for herpes simplex virus-I (HSV-I) seropositivity were obtained from the same three groups. Seventy-eight patients with SLE (80.4%), 40 patients with RA (80.0%) and 57 normal controls (58.8%) were seropositive for this closely-related herpesvirus. CONCLUSION: The data shows a specific and highly significant association between infection with HCMV and a clinical diagnosis of SLE.
9870878 Functional analysis of rheumatoid factor-producing B cells from the synovial fluid of rheu 1998 Dec OBJECTIVE: To understand the regulation of rheumatoid factor (RF) production in rheumatoid arthritis (RA), we studied IgM-RF production by B cells isolated from the synovial fluid (SF). METHODS: Highly purified SF and peripheral blood (PB) B cells were isolated by negative selection in a fluorescence-activated cell sorter (FACS) and then cultured with either L cells, CD40 ligand (CD40L)-transfected L cells, or type B synoviocytes in the presence or absence of interleukin-2 (IL-2), IL-4, or IL-10. Total IgM and IgM-RF were detected after 14 days by enzyme-linked immunosorbent assay. Enzyme-linked immunospot assays were performed to detect cells that spontaneously produced immunoglobulin. SF B cells were also phenotypically characterized by FACS analysis. RESULTS: Terminally differentiated CD20-,CD38+ synovial plasma cells (PC) present in the SF of RA patients secreted IgM-RF in the absence of a stimulus. IgM-RF production markedly increased when SF B cells were cultured in the presence of type B RA synoviocytes together with IL-10, but independently of CD40-CD40L interaction. Although CD20-,CD38+ PC could also be demonstrated in SF B cells from patients with other forms of arthritis, IgM-RF production was restricted to the SF B cell cultures of patients with seropositive RA. The frequency of IgM-RF-producing cells among IgM-producing PC in patients with seropositive RA was estimated to be as much as 50%. CONCLUSION: These data demonstrate that terminally differentiated CD20-,CD38+ IgM-RF-producing B cells are specifically present in the inflamed joints of patients with seropositive RA. There is evidence that the local environment in the rheumatoid joint favors RF production. The relatively high frequency of IgM-RF PC in the SF B cell population provides evidence of a dominant RA-specific antigen-driven response in the development of the synovial PC repertoire.
9008603 Accumulation of soluble Fas in inflamed joints of patients with rheumatoid arthritis. 1997 Jan OBJECTIVE: To examine the concentration of the soluble form of the Fas molecule (sFas) in the serum and synovial fluid of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). METHODS: The concentration of sFas in the serum of 15 normal subjects and in the synovial fluid and serum of 45 RA patients and 13 OA patients was determined. The erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) level, and the level of several cytokines in serum and synovial fluid were also determined. RESULTS: The synovial fluid concentration of sFas was higher in RA than in OA patients (P < 0.005). The synovial fluid level of sFas correlated weakly with serum levels of CRP (r = 0.541), the ESR (r = 0.499), and with synovial fluid levels of interleukin-2 (IL-2) receptor (r = 0.544), IL-6 (r = -0.529), and intercellular adhesion molecule 1 (r = 0.514). Reverse transcription-polymerase chain reaction analysis revealed that synovial cells and infiltrating mononuclear cells expressed sFas messenger RNA in RA patients. CONCLUSION: Our data suggest that accumulation of sFas in the joint cavity of RA patients may inhibit apoptosis and exacerbate the inflammatory process.
9781272 Evaluation of rheumatoid arthritis using a scoring system devised from magnetic resonance 1998 Aug We studied the magnetic resonance imaging (MRI) of 120 knees in 86 rheumatoid arthritis (RA) patients and of 14 unaffected knees in 12 control cases. We also developed a scoring system as a quantitative analysis method. We divided the MRI into 10 items, and classified the severity of the symptoms into 4 grades (score 0 to 3). The average total score increased according to the radiographic grade. Soft tissue lesions were clearly detected, even in the early stages of RA. Items such as synovial proliferation showed a high score even in the early stages, suggesting that it was the initial symptom of RA. The score also showed a correlation with the inflammatory signs. These results suggest that this scoring system is very sensitive and yields a good reflection of RA activity. We demonstrated that this system is simple and convenient for routine diagnostic use. We further demonstrated that it is useful for following the advancement of RA and for evaluating the response to treatment.
11160347 Serum amyloid A (apoSAA) expression is up-regulated in rheumatoid arthritis and induces tr 2001 Feb 15 The acute-phase reactant rabbit serum amyloid A 3 (SAA3) was identified as the major difference product in Ag-induced arthritis in the rabbit, a model resembling in many aspects the clinical characteristics of rheumatoid arthritis (RA) in humans. In Ag-induced arthritis, up-regulated SAA3 transcription in vivo was detected in cells infiltrating into the inflamed joint, in the area where pannus formation starts and, most notably, also in chondrocytes. The proinflammatory cytokine IL-1beta induced SAA3 transcription in primary rabbit chondrocytes in vitro. Furthermore, rSAA3 protein induced transcription of matrix metalloproteinases in rabbit chondrocytes in vitro. In the human experimental system, IL-1beta induced transcription of acute-phase SAA (A-SSA; encoded by SAA1/SAA2) in primary chondrocytes. Similar to the rabbit system, recombinant human A-SAA protein was able to induce matrix metalloproteinases' transcription in chondrocytes. Further, immunohistochemistry demonstrated that A-SAA was highly expressed in human RA synovium. A new finding of our study is that A-SSA expression was also detected in cartilage in osteoarthritis. Our data, together with previous findings of SAA expression in RA synovium, suggest that A-SAA may play a role in cartilage destruction in arthritis.
9756444 The association between ocular cicatricial pemphigoid and rheumatoid arthritis. 1998 Sep PURPOSE: To assess the pathogenesis, symptomatology, and severity of rheumatoid arthritis (RA) in patient's with concomitant ocular cicatricial pemphigoid (OCP). METHODS: We retrospectively analyzed the charts of eight patients seen at a single institution between the years 1972 and 1997 with concomitant RA and OCP. Patients with OCP secondary to medical therapy, radiation, or chemical burns, or Stevens-Johnson syndrome were excluded. RESULTS: The female-to-male ratio was 7:1. All patients had positive serum rheumatoid factors and immunohistochemical confirmation of OCP. The mean number of years of RA prior to OCP diagnosis was 19. The number of patients with stage II OCP was three of eight (37.5%). The number of patients with stage III OCP was five of eight (62.5%). All patients had radiologic evidence of degenerative joint disease and synovial thickening. All eight patients had keratoconjunctivitis sicca, five of eight patients (62.5%) had Sjögren's syndrome, and five of eight patients (62.5%) developed rheumatoid cornea necrosis leading to corneal perforation. CONCLUSIONS: The implication exists that RA and OCP may be linked via an immunologically mediated mechanism and that patients with severe extraarticular symptoms associated with RA may be more likely to develop OCP. Prompt recognition of overlying symptoms may facilitate proper therapy for control of both diseases.
11508587 Comparison of disability and quality of life in rheumatoid and psoriatic arthritis. 2001 Aug OBJECTIVE: There is controversy about the severity of peripheral psoriatic arthritis (PsA) compared to rheumatoid arthritis (RA). Early reports found PsA to be a milder disorder, excepting the mutilans form. Recent reports suggest that PsA can be as severe as RA. We compared severity, disability, and quality of life in patients with PsA and RA matched primarily for disease duration. METHODS: Data relating to the extent and severity of disease were recorded in a hospital clinic setting. Recent radiographs of hands and feet were read blinded to diagnosis, and information on function and quality of life was collected with the Health Assessment Questionnaire (HAQ) and EuroQol-5D, respectively. RESULTS: Forty-seven patients were matched for disease duration (median PsA 5 yrs, RA 7 yrs). The male/female ratio was 24/23 for PsA, 16/31 for RA, and median ages were 45 and 51 years, respectively. Patients with RA had significantly more joint involvement of metacarpophalangeal joints and wrists, whereas distal interphalangeal joints, spine, sternoclavicular joints, and sacroiliac joints were significantly more involved in PsA. No difference was found regarding Ritchie Articular Index, inflammatory markers, HAQ score, or EuroQol-5D. Patients with RA had significantly more damage on radiographs of hands and feet: median (range) Larsen score hands PsA 8 (0-91), RA 38 (0-125); feet PsA 4 (0-34), RA 11(0-56). Patients with RA were taking significantly more disease modifying drugs. CONCLUSION: Peripheral joint damage is significantly greater in RA than in PsA after equivalent disease duration, but function and quality of life scores are the same for both groups. The additional burden of skin disease in PsA may account for this.
10358459 [Minocycline in the treatment of rheumatoid arthritis]. 1998 Aug The author presents a review of contemporary knowledge on the treatment of rheumatoid arthritis with minocycline. He analyzes the assumed mechanism of action, dosage and the most frequently encountered undesirable effects of treatment. He informs the reader on the results of the most important studies with minocycline.
10649674 Cervical spine complications in rheumatoid arthritis patients. Awareness is the key to ave 2000 Jan Rheumatoid arthritis is associated with several pathologic changes in the cervical spine, including loss of articular cartilage, ligamentous destruction, and bone erosion. These changes may lead to one or a combination of complications, including atlantoaxial subluxation, cranial settling, subaxial cervical subluxation, and periodontoid pannus formation. Surgical management of these problems should focus on relieving pain, stabilizing the spine, and decompressing neural elements.
9059140 ICAM-1, E-selectin, and TNF alpha expression in labial salivary glands of patients with rh 1997 Jan OBJECTIVE: To assess the expression of ICAM1, VCAM1, E-selectin, CD44, and TNF alpha in labial salivary glands of patients with rheumatoid vasculitis. METHODS: Labial salivary glands from six patients with rheumatoid vasculitis before and after treatment, six aged matched rheumatoid arthritis patients without clinical evidence of rheumatoid vasculitis, 10 patients with primary Sjögren syndrome, 10 patients with rheumatoid arthritis and proven secondary Sjögren syndrome, and six controls were tested with specific antibodies. RESULTS: ICAM1, E-selectin, and TNF alpha were significantly expressed in endothelial cells and perivascular cellular infiltrate only in rheumatoid vasculitis before treatment. CONCLUSIONS: The expression of ICAM1, E-selectin, and TNF alpha allows an assessment of the activity of the vasculitic process in rheumatoid vasculitis. Labial salivary gland biopsy findings in patients with rheumatoid arthritis and visceral vasculitis without purpura or neuropathy (that is, mesenteric, coronary, or cerebral vasculitis) would be of interest and are examples where labial salivary gland tissue is more accessible than the affected tissue.
10374316 [10-year epidemiological study on rheumatic diseases in Shantou area]. 1997 Mar 22,049 adults were surveyed in a ten-year epidemiological study. The frequency of common rheumatic symptoms in Shantou population was much lower than that in northern China. The prevalence of ankylosing spondylitis, rheumatoid arthritis, osteoarthritis, osteoporosis and gout was 0.20%-0.32%, 0.20%-0.26%, 8.3%-10.8%, 12.4% and 0.15%-0.17% respectively. The frequency of HLA-B27 was 4.1% among general population and 90.6% in ankylosing spondylitis. The most commonly involved sites of osteoarthritis were lumbar spine, neck, and knee; but hands and hip were rarely involved. 85% subjects under investigation were found to be short of calcium intake. The differences between the north and the south of China in the prevalence of rheumatic symptoms may be related to the diversities in consciousness of seeking medical advice, reduction of bone content, climate and ergonomics.
11247872 Tensile properties of rat anterior cruciate ligament in collagen induced arthritis. 2001 Apr OBJECTIVES: To investigate the effects of collagen induced arthritis (CIA) on the tensile properties of rat anterior cruciate ligament (ACL). METHODS: The tensile strength, bone mineral density (BMD), and histology of ACL units from rats with CIA were investigated. RESULTS: The tensile strength of the ACL unit was significantly lower in the rats with CIA at 10 weeks after immunisation (ultimate failure load, 74.9% of the control; stiffness, 62.0% of the control). The major mode of failure was femoral avulsion, and the BMD was significantly lower in the rats with CIA. A histological examination of the ligament insertion in rats with CIA showed resorption of the cortical bone beneath the ACL insertion and an enlarged mineralised fibrocartilage zone. CONCLUSIONS: These findings indicate that the decrease in tensile strength of ACL units correlated with histological changes in the ligament-bone attachment, such as bone resorption beneath the ligament insertion site and an enlargement of the mineralised fibrocartilage zone.