الفهرس 
lntroductionOnly 14 pages are availabe for public view
 |  | from | 318 |  |  |
| | | from | 318 | | |
Abstract
Rheumatoid arthritis is characterized by chronic inflammation with progressive articular damage and is often associated with systemic manifestations. Lymphocytes, macrophages infiltrating the synovium have been reported to be involved in this process. Tissue destruction is caused be several mechanisms, including the production of monokines and matrix metalloproteinases Metalloproteinases are the proteases that participate in the degradation and remodeling of the extracellular matrix. Tissue inhibitors of metalloproteinases control their action (Klimiuk et al., 2002). Osteoarthritis is a joint disease characterized by progressive degradation of articular cartilage that leads to joint dysfunction, disability and pain. Erosion of the articular cartilage matrix is thought to be due to the increased synsthesis and activation of proteinases. Although all classes of proteinases may be involved, the matrix metalloproteinases are considered to play a pivotal role in cartilage destruction. Both the chondrocytes and the inflamed synovium contribute to the production of MMPs (DeGroot et al., 2001). Metalloproteinases are secreted by both the resident cells of joint tissues as well as by invading cells, they are active around neutral values of pH, and they have the combined ability to degrade all the components of the ECM. MMPs play significant roles in both developmental and repair processes, and it appears that aberrant regulation, which can occur at many levels, leads to their hyperactivity in diseases such as rheumatoid arthritis and osteoarthritis (Hembry et al., 1995). The aim of the study is: 1- To investigate whether plasma levels of matrix metalloproteinase 3 (MMP3), tissue inhibitor of metalloproteinase 1 (TIMP-1) are specifically elevated in (RA) and (OA). 2- To assess how these markers reflect the clinical activity of these disease. The study comprised 90 patients. They were divided into four groups. • Group I: Thirty patients with RA, they were 20 females and 10 males, their ages ranged from 18 to 65 years (mean 42 years). They were diagnosed according to the American college of Rheumatology (ACR) criteria (Arnett et al., 1988). • Group II: Twenty patients with knee osteoarthritis, they were 10 females and 10 males, their ages ranged from 42 to 70 years (mean 55 years). They were diagnosed according to the American college of Rheumatology (ACR) criteria (Altman et al., 1986). • Group III: Twenty patients with generalized osteoarthritis they were all females, their ages ranged from 53 to 70 years (mean 62 years). They were diagnosed according to the American college of Rheumatology (ACR) criteria (Altman et al., 1990). • Group IV: control group : 20 apparently healthy subjects they were selected from normal population. They were 10 females and 10 males their ages ranged from 20 to 30 years (mean 24.5 years). All patients of this study were subjected to the following: 1-Thorough history taking. 2-Thorough clinical examination: a- General examination: -Including all body systems (Head and Neck, skin, chest, cardiovascular, abdominal and neurological examination and genitourinary systems). b-Local examination including: -Inspection of skin overlying the joint for redness or swelling. -Palpation for joint hotness and tenderness and swelling. -Measurement of joint motion and deformity using a standard goniometer. -Detection of any muscle wasting and measurement of ms power. c-In cases of RA the following tests were performed: -Assessment of pain using (VAS) (Huskisson, 1997). -Assessment of tenderness using AI of Ritchie (Ritchie et al., 1968). -Assessment of grip strength (McRae, 1983). -Assessment of disease severity using clinical spread severity index (Walker et al., 1985). -Assessment of disease activity using Mallya and Mace activity score (Mallya and Mace, 1981). -Assessment of functional ability using (HAQ) (Fries et al., 1980). d- In cases of OA the following test were performed: -Assessment of joint pain using (VAS) (Huskisson, 1974). -Assessment of disease severity using total clinical severity score (Zaki et al., 1987). -Assessment of disease activity using Lysholm score (Lysholm, 1984) -Assessment of functional ability using Womac functional capacity score (Bellamy et al., 1995) e- In cases of GOA the following tests were performed: -Assessment of joint pain using VAS (Huskisson, 1974). -Assessment of functional ability using Dreiser’s functional index (Dreiser et al., 1995) - Assessment of grip strength (Mc Rae, 1983) - Assessment of tenderness (Ritchie et al., 1968) 3-Investigations: a-Radiology: 1- In RA: Plain radiography for hands, feet and other affected joints. The radiological assessment was done according to (steinbrocker et al., 1949). 2- In KOA: Plain radiography for knees the radiological assessment was done according to (chandnani and Resnick, 1992). 3- In GOA: Plain radiography for hands and other affected joints. The radiological assessment was done according to (Kellgren, 1963). b-Laboratory: 1- Full blood picture. 2- ESR (nm/h) (Dacie and Lewis, 1984). 3- RF by Latex fixation test (Singer and Plotz, 1956). 4- CRP (mg/liter) by latex agglutination (Kind and Pepys, 1984). 5- Estimation of serum matrix metalloproteinase 3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1) by Eliza. Our study showed that: In RA: There was a highly significant difference between MMP-3 and TIMP-1 levels in RA vs control (P=<0.001). MMP-3 level had significant correlation with VAS (P=.000), AI of Ritchie (P=.000), CSSI (P=.000), Mallya and Mace activity score (P=.001), functional disability of the patients (P=.000), radiographic damage of the patients joints (P=.003) and ESR (P=.004). TIMP-1 level had significant correlation with pain score (VAS) (P=.000), AI of Ritchie (P=.000), severity of the disease (P=.000), disease activity (P=.000), functional disability of the patients (P=.000), radiographic damage of the patients joints (P=.000) and ESR (P=.006). In KOA: There was a highly significant difference between MMP-3 and TIMP-1 levels in KOA vs control (P=<0.001). MMP-3 level had significant correlation with disease activity (P=.000), severity of the disease (P=.000), functional disability of the patients (P=.000) and radiographic damage of the patients joints (P=.000). TIMP-1 level had significant correlation with disease activity (P=.000), severity of the disease (P=.000), functional disability of the patients (P=.000) and radiographic damage of the patients joints (P=.000). In GOA: There was a highly significant difference between MMP-3 and TIMP-1 levels in GOA vs control (P=<0.001). MMP-3 had significant correlation with disease duration (P=.003), pain score VAS (P=.000), functional disability of the patients (P=.000) and radiographic damage of the patients joints (P.000). TIMP-1 had significant correlation with disease duration (P=.001), pain score VAS (P=.000), functional disability of the patients (P=.000) and radiographic damage of the patient joints (P=.000). CONCLUSION: From this study we can conclude that: 1- In rheumatoid arthritis patients, serum levels of MMP-3 and TIMP-1 are elevated and they are significantly correlated with disease activity, disease severity, functional disability of the patients and radiological damage of the patients joints. So these enzymes are involved in articular cartilage destruction and they are good indicators of inflammation and joint destruction. 2- In Osteoarthritis patients, serum levels of MMP-3 and TIMP-1 are elevated in both KOA and GOA and they are significantly correlated with disease activity, disease severity, functional disability of the patients and radiological damage of the patients joints. So these enzymes are involved in the pathogenesis of osteoarthritis and they are good indicators of joint destruction. 3- Serum levels of MMP-3 and TIMP-1 are more elevated in RA than OA so they are good indicators of inflammation.