Osteoarthritis (OA) is a common chronic painful joint disorder, occurring primarily ... It tends to affect distal interphalangeal joints, the trapezo-metacarpal, genu,.
Konferenca e IV kombetare e shkencave mjekesore ISBN 978-9928-4337-7-0
Osteoarthritis risk factors and clinical features Dr. Enida Xhaferi1, Asc.Prof. Teuta Backa Cico2, Msc. Alma Imami1, Dr. Irida Pano1, Msc. Miranda Cela1 1 2
University of Medicine/Faculty of Medical Technical Sciences, Tirana, Albania University Hospital Center “Mother Theresa”, Rheumatology Clinic, Tirana, Albania
Osteoarthritis (OA) is a common chronic painful joint disorder, occurring primarily in older people, which results in deformity and disability. It involves a complicated, cartilage and subchondral bone degradative and repair process, with a synovial inflammation - influenced by mechanical stress, biochemical and genetic factors. OA is characterized the presence of focal lesions of the articular cartilage, combined with sclerosis in the subchondral bone and new bone formation (osteophytes) at the joint margins. It tends to affect distal interphalangeal joints, the trapezo-metacarpal, genu, coxsofemoral and intervertebral facet joints while wrists, elbows, metacarpophalangeal joints and shoulders are usually less likely to be affected by OA Risk factors include : obesity (link is stronger in women) and metabolic disorders, age (OA increases sharply with age), female gender, sex hormones (develops more in menopause), low dietary intake of antioxidants, some carotenoids, vitamin C and low levels of vitamin D, occupational factors, acute injury and repetitive joint loading, muscle weakness and genetic predisposition. There are general and specific OA clinical features. Pain, stiffness, and locomotor restriction are the main general symptoms of OA. During physical examination crepitus, joint deformity, or joint swelling (caused by bony remodeling, excessive osteophytosis, or joint subluxation) can be observed. Affected joints are usually tender during active motion testing and under pressure. Pain is the first and most important symptom of OA. It occurs after joint use and is relieved at rest. As disease progresses, pain occurs during minimal motion or even at rest and during sleep. Cartilage has no nerve supply and the pain in OA must arise from non cartilaginous structures. Periarticular tissue such as tendon and fascia are also source of pain during the OA process. Stiffness is observed in the morning or after inactivity during the day. This type of stiffness, is often an essential feature, although morning stiffness is usually less severe and of shorter duration than that seen in individuals with systemic inflammatory arthropathies. Morning stiffness generally resolves after less than 15 minutes.
Konferenca e IV kombetare e shkencave mjekesore ISBN 978-9928-4337-7-0 Limitations of motion and function develops as OA progresses and patients report that they can not perform day-to-day activities, like kneeling for knee OA, or cutting one’s toenails for hip OA. OA can be classified as primary or secondary. The ACR has proposed a set of criteria for OA depending on each joint. These criteria’s specificity and sensitivity are very good to excellent. Eular has also developed recommendations sets for diagnosis of hand and knee OA. Key words : Osteoarthritis, ACR, Eular Referencat 1. Imhof H, Sulzbacher I, Grampp S et al. Subchondral bone and cartilage disease: a rediscovered functional unit. Invest Radiol 2000; 35: 581–588. 2. Henrotin Y, Pesesse L, Sanchez C. Subchondral bone in osteoarthritis physiopathology: state-ofthe art and perspectives. Biomed Mater Eng 2009;19:311–6. 3. Brandt KD, Flusser D: Osteoarthritis. In Bellamy N, editor: Prognosis in the rheumatic diseases, Lancaster, UK, 1991, Kluwer Academic Publishers, p 11. 4. Forman MD, Kaplan DA, Muller GF, et al: The epidemiology of osteoarthritis of the knee. In Peyron JG, editor: Epidemiology of osteoarthritis, Paris, 1980, Ciba-Geigy, p 243. 5. Felson DT, Zhang Y, Hannan MT, et al: The incidence and natural history of knee osteoarthritis in the elderly. The Framingham Osteoarthritis Study. Arthritis Rheum 38:1500–1505, 1995. 6. Hunter DJ, March L, Sambrook PN: Knee osteoarthritis: the influence of environmental factors. Clin Exp Rheumatol 20:93–100, 2002. 7. Kapoor M,Martel-Pelletier J, Lajeunesse D, Pelletier J-P, Fahmi H.Role of proinflammatory cytokines in the pathophysiology of osteoarthritis. Nat Rev Rheumatol 2011 Jan;7(1):33e42. 8. Loeser RF, Goldring SR, Scanzello CR, Goldring MB. Osteoarthritis: a disease of the joint as an organ. Arthritis Rheum 2012 Jun;64(6):1697e707. 9. Malemud CJ, Goldberg VM, Moskowitz RW, et al: Biosynthesis of proteoglycan in vitro by cartilage from human osteochondrophytic spurs. Biochem J 206:329–341, 1982. 10. Goldring MB, Otero M. Inflammation in osteoarthritis. Curr Opin Rheumatol 2011 Sep;23(5):471e8. 11. Bijlsma JWJ, Berenbaum F, Lafeber FPJG. Osteoarthritis: an update with relevance for clinical practice. Lancet 2011 Jun 18;377(9783):2115e26. 12. Felson, D. T. Clinical practice. Osteoarthritis of the knee. N. Engl. J. Med. 354, 841–848 (2006). 13. Sellam, J. & Berenbaum, F. The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis. Nat. Rev. Rheumatol. 6, 625–635 (2010). 14. Felson, D. T. et al. Osteoarthritis: new insights. Part 2: treatment approaches. Ann. Intern. Med. 133, 726–737 (2000). 15. Hannan MT, Felson DT, Pincus T: Analysis of the discordance between radiographic changes and knee pain in osteoarthritis of the knee. J Rheumatol 27:1513–1517, 2000. 16. Neogi T, Felson D, Niu J, et al: Association between radiographic features of knee osteoarthritis and pain: results from two cohort studies. BMJ 339:b2844, 2009. 17. Blagojevic, M., Jinks, C., Jeffery, A. & Jordan, K. P. Risk factors for onset of osteoarthritis of the knee in older adults: a systematic review and meta-analysis. Osteoarthritis Cartilage 18, 24–33 (2010). 18. Saville PD, Dickson J: Age and weight in osteoarthritis of the hip. Arthritis Rheum 11:635–644, 1968. 19. Altman R, Alarcon G, Appelrouth D, et al. The American college of rheumatology criteria for the classification and reporting of osteoarthritis of the hand. Arthritis Rheum 1990;33:1601–10. 20. Zhang W, Doherty M, Peat G, et al. EULAR evidence-based recommendations for the diagnosis of knee osteoarthritis. Ann Rheum Dis 2010;69:483–9. 21. Altman R, Alarcon G, Appelrouth D, et al. The American college of rheumatology criteria for the classification and reporting of osteoarthritis of the hip. Arthritis Rheum 1991;34:505–14. 22. Zhang W, Doherty M, Leeb BF, et al. EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT. Ann Rheum Dis 2009;68:8–17.
Konferenca e IV kombetare e shkencave mjekesore ISBN 978-9928-4337-7-0
Faktoret e riskut dhe manifestimet klinike te osteoartritit Dr. Enida Xhaferi1, Asc.Prof. Teuta Backa Cico2, , Msc. Alma Imami1, Dr. Irida Pano1, Msc. Miranda Cela1. 1 2
University of Medicine/Faculty of Medical Technical Sciences, Tirana, Albania University Hospital Center “Mother Theresa”, Rheumatology Clinic, Tirana, Albania
Osteoartriti (OA) eshte nje crregullim artikular i perhapur gjeresisht, i dhimbshem dhe kronik, qe prek kryesisht moshat e medha dhe shoqerohet me shfaqje deformimesh artikulare dhe invaliditeti. Patogjeneza eshte resultat i nje sere procesesh te komplikuara degraduese dhe rigjeneruese te kartilagos dhe kockes subkondrale me inflamacion sinovial - qe influencohen nga faktore gjenetik, biokimik dhe stresi mekanik. OA karakterizohet nga prania e lezioneve fokale ne kartilagon artikulare, te kombinuara me skleroze te kockes subkondrale dhe formimin e kockes se re (osteofite) ne periferine artikulare. Patologjia prek me shpesh artikulacionet distale interfalangeale, artikulacionin trapezo-metakarpal, genu, koksofemoral dhe artikulacionet zygapophyseale ndersa artikulacionet radiokarpale, cubiti, glenohumeral dhe metacarpofalangeale preken zakonisht me rralle. Faktoret e riskut perfshijne : pranine e obezitetit dhe crregullimeve metabolike, mosha (shfaqja e OA rritet ndjeshem me moshen), gjinia femerore, hormonet seksuale (patologjia eshte me shpeshte ne menopause), marrjen e ulet dietike e antioksidanteve, nivel i ulet i vitamines D dhe vitamines C, faktoret e lidhur me profesionin, pranine e demtimit akut dhe ngarkeses se vazhdueshme ne artikulacione, dobesine muskulare dhe predispoziten gjenetike. Manifestimet klinike te OA ndahen ne te pergjitheshme dhe specifike. Dhimbja, ngurtesimi artikular dhe kufizimet lokomotore jane shenjat kryesore te pergjitheshme te OA. Gjate ekzaminimit fizik vihet re prania e krepitacioneve, deformimeve ose enjtjes artikulare. Artikulacionet e prekura jane zakonisht te dhimbshme ne presion dhe gjate testimit te levizjeve aktive. Dhimbja eshte shenja e pare edhe me e rendesishme klinike e OA. Shfaqet pas perdorimit te artikulacionit dhe qetesohet ne inaktivitet. Me perparimin e semundjes, dhimbja shfaqet gjate levizjeve minimale ose ne qetesi gjate gjumit. Kartilagoja eshte strukture qe nuk permban mbaresa nervore dhe dhimbja i detyrohet strukturave jo kartilaginoze. Indet periartikulare si tendinet dhe fasciat jane gjithashtu burim dhimbjeje ne OA. Ngurtesimi artikular shfaqet ne mengjes dhe gjate dites ne qetesi. Ky lloj ngurtesimi eshte shpesh nje shenje klinike karakteristike, megjithese ngurtesimi mengjesor qe vihet
Konferenca e IV kombetare e shkencave mjekesore ISBN 978-9928-4337-7-0 re ne OA eshte shpesh me pak i rende dhe zgjat me pak se ai qe vihet re ne te semuret me artropati inflamatore sistemike. Ngurtesimi mengjezor zhduket pergjithesisht pas me pak se 15 min. Kufizimet e levizjeve dhe funksionit krijohen me perparimin e semundjes dhe pacientet referojne se nuk jane ne gjendje ti realizojne aktivitetet ditore si ulja ne gjunje per OA genu ose prerja e thonjeve te gishtave te kembes per pacientet me OA te artikulacionit koksofemoral. OA mund te klasifikohet ne primar dhe sekondar. Kolegji American i Reumatologjise ka propozuar nje set kriteresh klasifikues per OA te vecanta. Specificiteti dhe sensitiviteti i ketyre kritereve varion nga shume i mire ne i shkelqyeshem. Eular ka hartuar gjithashtu kritere diagnostike per OA te duarve dhe kembeve.
Fjale kyc : Osteoartrit, ACR, Eular
Referencat 1. Imhof H, Sulzbacher I, Grampp S et al. Subchondral bone and cartilage disease: a rediscovered functional unit. Invest Radiol 2000; 35: 581–588. 2. Henrotin Y, Pesesse L, Sanchez C. Subchondral bone in osteoarthritis physiopathology: state-ofthe art and perspectives. Biomed Mater Eng 2009;19:311–6. 3. Brandt KD, Flusser D: Osteoarthritis. In Bellamy N, editor: Prognosis in the rheumatic diseases, Lancaster, UK, 1991, Kluwer Academic Publishers, p 11. 4. Forman MD, Kaplan DA, Muller GF, et al: The epidemiology of osteoarthritis of the knee. In Peyron JG, editor: Epidemiology of osteoarthritis, Paris, 1980, Ciba-Geigy, p 243. 5. Felson DT, Zhang Y, Hannan MT, et al: The incidence and natural history of knee osteoarthritis in the elderly. The Framingham Osteoarthritis Study. Arthritis Rheum 38:1500–1505, 1995. 6. Hunter DJ, March L, Sambrook PN: Knee osteoarthritis: the influence of environmental factors. Clin Exp Rheumatol 20:93–100, 2002. 7. Kapoor M,Martel-Pelletier J, Lajeunesse D, Pelletier J-P, Fahmi H.Role of proinflammatory cytokines in the pathophysiology of osteoarthritis. Nat Rev Rheumatol 2011 Jan;7(1):33e42. 8. Loeser RF, Goldring SR, Scanzello CR, Goldring MB. Osteoarthritis: a disease of the joint as an organ. Arthritis Rheum 2012 Jun;64(6):1697e707. 9. Malemud CJ, Goldberg VM, Moskowitz RW, et al: Biosynthesis of proteoglycan in vitro by cartilage from human osteochondrophytic spurs. Biochem J 206:329–341, 1982. 10. Goldring MB, Otero M. Inflammation in osteoarthritis. Curr Opin Rheumatol 2011 Sep;23(5):471e8. 11. Bijlsma JWJ, Berenbaum F, Lafeber FPJG. Osteoarthritis: an update with relevance for clinical practice. Lancet 2011 Jun 18;377(9783):2115e26. 12. Felson, D. T. Clinical practice. Osteoarthritis of the knee. N. Engl. J. Med. 354, 841–848 (2006). 13. Sellam, J. & Berenbaum, F. The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis. Nat. Rev. Rheumatol. 6, 625–635 (2010). 14. Felson, D. T. et al. Osteoarthritis: new insights. Part 2: treatment approaches. Ann. Intern. Med. 133, 726–737 (2000). 15. Hannan MT, Felson DT, Pincus T: Analysis of the discordance between radiographic changes and knee pain in osteoarthritis of the knee. J Rheumatol 27:1513–1517, 2000. 16. Neogi T, Felson D, Niu J, et al: Association between radiographic features of knee osteoarthritis and pain: results from two cohort studies. BMJ 339:b2844, 2009. 17. Blagojevic, M., Jinks, C., Jeffery, A. & Jordan, K. P. Risk factors for onset of osteoarthritis of the knee in older adults: a systematic review and meta-analysis. Osteoarthritis Cartilage 18, 24–33 (2010). 18. Saville PD, Dickson J: Age and weight in osteoarthritis of the hip. Arthritis Rheum 11:635–644, 1968. 19. Altman R, Alarcon G, Appelrouth D, et al. The American college of rheumatology criteria for the classification and reporting of osteoarthritis of the hand. Arthritis Rheum 1990;33:1601–10.
Konferenca e IV kombetare e shkencave mjekesore ISBN 978-9928-4337-7-0 20. Zhang W, Doherty M, Peat G, et al. EULAR evidence-based recommendations for the diagnosis of knee osteoarthritis. Ann Rheum Dis 2010;69:483–9. 21. Altman R, Alarcon G, Appelrouth D, et al. The American college of rheumatology criteria for the classification and reporting of osteoarthritis of the hip. Arthritis Rheum 1991;34:505–14. 22. Zhang W, Doherty M, Leeb BF, et al. EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT. Ann Rheum Dis 2009;68:8–17.
