Dr. H. Rawan Broto, SpPD (KR)Anggauta IRA Cabang Yogyakarta

1985 Dokter Umum FK UGM1999 Internist FK UGM2002 Konsultan Rheumatologist FK UI2002 Ka Subbag Reumatologi Bag PD FK UGM2002 Sekretaris Bagian PD FK UGM2004 Ketua SP3T Provinsi DIY2005 Manager Operasional RS Happyland Yogya2008 Ketua Komite Medis RS Happyland 2009 Dosen honorer FK-UMY 2012 Direktur RS Holistika Medika Yogyakarta

Penatalaksanaan OsteoarthritisRawan Broto

Bagian Ilmu Penyakit DalamFK UMY Jogjakarta

Arthritis affects many older adultsWomenMen53%37%

Myths & Truths about OAMyth: Once you get arthritis, you just have to live with it

Truth: you can manage your arthritis In many ways & live comfortably

Myths & Truths about OAMyth: No cure is available for most forms of arthritis

Truth: However, early diagnosis & management can help reduce impact of arthritis

BatasanOA adalah penyakit sendi yang ditandai dengan berbagai sindroma, karakteristik dengan menipisnya rawan sendi secara progresif, disertai respon pembentukan tulang baru/osteofit pada trabekula subkhondral atau tepi sendi

OsteoartritisMerupakan penyakit degeneratif ?

Konsep Wear and tear ?

Analogi dengan No acid no ulcer ?

Epidemiology

PopulationAge (yrs)Female (%)Male (%)English>357069US Caucasians>404443Alaskan Eskimos>402422Jamaican (rural)35-646254Pima Indians>307456Blackfoot Indians>307461South African Black>355360

Indonesia:

Penelitian berbasis masyarakatKota DesaMalang*10.0 % 13.5%Bandungan** 5.4%* Kalim H, cs 1994, ** Darmawan, 1992

Penelitian berbasis rumah sakit

RSCM (1991-1994)43.8% (total pasien reumatik)RSS (1995-2000) 54.6% (total pasien reumatik)Epidemiologi

The prevalence is higher in womenWomen are more likely to have inflammation of the proximal (Bouchards nodes) & distal interphalangeal joints of the hands (Heberdens nodes)OA of the hip occurs more frequently in menAfrican Americans experience more severe & disabling disease than CaucasiansChinese have; knee OA > hand OA > hip OA (rarely)

OSTEOARTRITIS NODULAR

Prevalensi Gambaran Radiologik OA Dalam Populasi Prevalensi (%)Usia (tahun)

Hal-hal Menarik dari Osteoartritis

Penyakit yang telah dikenal lama. (lihat Jurassic Park, The lost world, mummi di Museum Cairo)

Diagnosis relatif mudah.

Penyakit tampaknya sederhana, ternyata kompleks.

Faktor Risiko OAFaktor predisposisi umum: umur, jenis kelamin, kegemukan, hereditas, hipermobilitas, merokok, densitas masa tulang, hormonal, penyakit reumatik kronik

Faktor mekanik: trauma, bentuk sendi, penggunaan sendi, kurang gerak

Risk factors for primary OAOAObesityOccupationOld ageFamily history GeneticsTraumaJoint dysplasiaBone injuryGenderJoint injurySolomon L. 1997

Family history of diseaseRisk factors you cannot change

Family history of diseaseIncreasing age Risk factors you cannot change

Family history of diseaseIncreasing age Being femaleRisk factors you cannot change

Overuse of the jointRisk factors you can change

Overuse of the jointMajor injuryRisk factors you can change

Overuse of the jointMajor injuryOverweightRisk factors you can change

Overuse of the jointMajor injuryOverweightMuscle weaknessRisk factors you can change

Pandangan Terbaru Patogenesis OA

SynoviumSecretes the synovial fluidCapsuleLigaments hold the bones togetherSynovial fluidLubricates the joint capsuleBoneCartilageProtects the end of the boneAnatomy of a normal synovial jointMuscleTendonDieppe P. 1998

Normal Articular cartilage components and structureChondrocytes regulate the synthesis and degradation of cartilage by secreting enzymesCollagen and proteoglycan aggregates provide tensile strength, elasticity and recoilBoneTide mark separates articular cartilage from calcified cartilageArea of detail

Articular cartilage in actionNo loadLight loadHeavy loadReboundingUnaffected cartilageLight contactCartilage distortionCartilage and bone rebound when weight is removedCartilage

Modest, patchy chronic synovitisBone ends thickenBony outgrowths (osteophytes) formBone fragments may float in the joint spaceFluid filled cysts may form in the boneOA jointNormal jointCartilage:Pitted and frayed surfaceLoss of elasticityCartilage may wear away completelyThickening of capsuleCharacteristics of OADieppe P. 1998

ErosionArea of detailCartilage surface cracks and erodes. Small fragments break off into synovial fluidEventually the bone becomes exposedMore chondrocytes are produced resulting in an imbalance in the synthesis and degradation of cartilage componentsCollagen fibre structure is altered and the number and quality of proteoglycan aggregates decreasesBoneArticular cartilage in OA

Softening Stage

Fibrillation Stage

Fragmentation Stage

Joint = Bone + Cartilage + Synovial Fluid

Perubahan pada tulang

Perubahan pada cartilago

Perubahan pada cartilago

Joint tissues involved in OA

PATOGENESIS OA Bukan sekedar Wear and Tear :

Ada perbedaan dengan perubahan rawan sendi akibat proses penuaan (aging process)Dapat terjadi pada hewan muda yang dirangsang dengan zat kimia / traumaPerubahan-perubahan patologi berkaitan dengan perubahan kimiawi matriks

Stresses AbnormalNormal cartilageCartilage abnormalAgingGenetic and metabolic diseaseInflammationAdministration of toxinsImmune responseObesity, Developmental and anatomic abnormalitiesBony remodeling and micro fractureLoss of joint stabilityTraumaTheory A Biomaterial failure collagen networkfractureTheory BCell injuryIncrease of degradative responsesInhibitors reducedProteolytic enzymes increasedDestruction of prteoglycans collagenand other proteinsProteoglycan unravellingCartilage breakdown

RAWAN SENDI NORMALKOMPONEN MATRIKS EKSTRASELULER TERUS MENERUS TURN-OVER

PROTEOGLIKAN LEBIH CEPAT DEGRADASI DARI KOLAGEN

DILEPASKAN FRAGMEN PROTEOGLIKAN

BAGIAN YANG CLEAVAGE : INTI PROTEIN DEKAT G1 DAN G2

IKATAN HA-GLIKOSAMINOGLIKAN TERLEPAS

RAWAN SENDI OATerdapat gangguan keseimbangan degradasi dan sintesis (anabolik dengan katabolik) Walaupun ada sintesis (growth hormon) tetapi kualitas rawan sendi terbentuk burukStadium akhir:sintesis proteoglikan merosot, fungsi khondrosit sangat menurun. Peranan IL-1 sangat besar yaitu merangsang sekresi enzym katabolik stromelysin, kolagenase, gelatinase & tissue plasminogen inhibitor

Remodelling in OA

Hyaluronic acid Bone Bone CartilageOsteoclastOsteoblastChondrocytesHAHASynovial liningCapsuleSynthesis: Synoviocyte, chondrocyte

Hyaluronan in OA Synovial fluid

Hialuronan membentuk selubung yang berfungsi sebagai perisai viskoelastik guna melindungi kartilago tulang rawan dan sinovium dari stress mekanik, radikal bebas dan proses inflamasi. Hialuronan membentuk kerangka agregat proteoglican yang sangat penting untuk integritas struktur dan fungsi dari tulang rawan sendi.

INFLAMASI PADA OSTEOARTRITISUSAHA PEMBERSIHAN DEBRIS

KERADANGAN DEBRIS : KONDROITIN SULFAT DAPAT MENGAKTIFKAN FAKTOR HAGEMAN ------ JALUR KININ

KERADANGAN KARENA ARTRITIS LAIN : CONTOH : MILWAUKEE SHOULDER SYNDROM

PERAN IL-1 DAN TNF ALFA

Inflamasi pada Osteoarthritis

Penampakan rawan sendi saat pembedahan dan potongan lintangPembedahanPotongan lintang

Reduction of synovial membrane inflammationBefore treatmentAfter treatment

Kerusakan pada OsteoartritisMetabolisme khondrositKerusakan jaringan kolagenPeningkatan kadar airPenurunan proteoglikanPenurunan kualitas kolagen, proteoglikan

Classification of OAPrimary OAMost common formIs rare before age 40 years, prevalence increases with ageKnee joint most often affectedGenetic predisposition, particularly for hand arthritisSecondary OAPreceded by a predisposing disorder such as joint traumaOccurs in any joint

Solomon L. 1997

primary OA (idiopathic)Predominant form & occurs in absence of precipitating event & assumes a certain pattern; Localized (involving one or two sites)Generalized (involving three or more sites)Erosive

secondary OAoccurs when the disease is caused by congenital, developmental disorders, inflammatory, metabolic, or endocrine diseases, e.g.:Mechanical injury of joint (Congenital or posttraumatic)Prior inflammatory disease (RA, chronic gouty arthritis, etc )Metabolic disorder (Pagets disease)Endocrinopathies (DM, obesity, sex hormone abnormalities)Neuropathic disordersIntraarticular corticosteroid overuseothersLocalized OA is distinguished from generalized disease by the numberof sites involvedErosive disease is characterized byan erosive pattern of bone destruction and marked proliferation of interphalangeal joints of the hands.

Signs and symptoms of OASignsLoss of joint spaceJoint grinding/gratingBony outgrowths (osteophytes) Joint deformities e.g. Heberdens nodesSymptomsUse-related joint pain Joint stiffness after periods of inactivityLoss of joint movement/difficulty performing certain tasksJoint locking/giving wayFeeling of instabilityRestricted/painful movementsOxford Handbook of Clinical Medicine. 1998

Gambaran KlinisNyeri sendi: jalan, naik tangga, waktu malam, gerak lutut, kadang waktu diam (seperti sakit gigi di lutut).Hambatan gerakPembesaran sendiTanda keradangan minimalKrepitusSendi yang sering terkena: lutut, koksa, DIP, pergelangan kaki, tulang belakang.

Finger deformities in OADeformities occur at:The base of the thumb (Bouchards nodes) The middle joint of a finger (Bouchards nodes) The finger tip (Heberdens nodules)Heberdens nodules in a patient with OASciencephoto.com

OA PrimerOA Sekunder

Laboratory Tests No specific laboratory test or value is diagnostic for OA. The erythrocyte sedimentation rate (ESR) and hematologic & chemistry panels are usually unremarkable. Aspirated synovial fluid (if obtained) often displays leukocytosis & high viscosity.

Other Diagnostic Tests Radiologic evidence may be misleading because structural evidence of OA correlates poorly with symptoms. Radiographic changes are often absent in early OA. As the disease progresses, joint-space narrowing, subchondral bone sclerosis, & osteophytes may be detected. In late OA, there is gross deformity and possibly effusions.

Gambaran klinis (lanjutan)Secara klinis: Berat ringan gejala tidak berkorelasi dengan gambaran radiologik gambaran artroskopi

Gambaran radiologik OA Indeks Kellgren dan Lawrence (KL) KL-0 KL-1 (penyempitan celah sendi) KL-2 (osteofit) KL-3 (pembesaran tulang) KL-4 (deformitas)

Celah sendi menyempitOsteofitCelah sendi

Nyeri sendi degeneratif:Peningkatan tekanan interoseus akibat degenerasi rawan sendi akan menekan reseptor nociceptifMekanisme lain melalui reaksi nyeri inflamatif yang sama misal khondroitin sulfat merangsang XII mencetuskan jalur kininInfiltrasi sel MN dan hiperplasia vaskuler. Penebalan kapsul sendi menimbulkan rasa nyeri dan spasme ototSerpihan rawan juga bersifat antigenik.

Inilah proses kronisitas inflamasi pada OA

Kajian Pasien dengan OASumber Nyeri:mekanik - berkaitan dengan penggunaan sendiInflamasi - kekakuan, nyeri diperberat dengan istirahatNyeri malam hari - Hipertensi intraoseusNyeri memburuk dengan cepat - Pikirkan sepsis, avascular necrosis, fraktur, atau sinovitis kristal.

Pemeriksaan Klinis:Sumber nyeri dari persendian atau sekitar sendi?Nyeri menyeluruh? pertimbangkan fibromyalgiaAdakah deformitas?Adakah kelemahan otot?Tanda Inflamasi atau efusi lokal?OA generalisata atau lokal?Kajian Pasien dengan OA

PencegahanIdentifikasi faktor risiko untuk terjadinya OA.Modifikasi faktor risiko seperti berat badan (obesitas) dan trauma minor berulang.

Perubahan Gaya HidupUmumPertahankan berat badan optimal / ideal.Pertahankan aktifitas dan olah raga teratur.Pertahankan pendekatan positif.

KhususPenguatan otot.Berikan perhatian terhadap disabilitas spesifik (belanja, pekerjaan di rumah dan pekerjaan).

Balanced Diet Helps manage weightExtra pressure on some joints may aggravate your arthritis

Stay healthy

StrengtheningAerobicStretchingExercise is important

Aerobic ExercisesImprove cardiovascular fitnessHelps control weightMay help reduce inflammation in jointsFor those worried about advancement of arthritis, a Swedish study showed no progression of arthritis with moderate exercise.Walking, Biking

Walking AidesCaneWalkerHelps keep you balanced so you dont hurt other joints.

Suppress the signal transduction pathways of proinflammatory/catabolic mediators Exercices

Treatment is individualized (medical history, physical examination, radiographic findings, distribution & severity of joint involvement & response to previous treatment

Goals of therapy include (1) educating the patient and caregivers(2) relieving pain(3) maintaining or restoring mobility(4) minimizing functional impairment(5) Preserving joint integrity(6) improving quality of life.

OA Medications ! NSAIDs Nutritional Therapies Non Traditional therapy Future Therapies

Patient Perspectives !!!

Doctor Perspectives !!!

MedicationsAnalgesics, pain relievers, may provide temporary relief of arthritis pain.Must know what the side effect

OAINS : hanya menekan nyeri dan inflamasi, tidak dapat menghentikan perjalanan penyakit Kortikosteroid oral: tidak lazim diberikan pada OA Steroid injeksi IA diberikan dengan temporary Hyaluronan diberikan dengan pertimbangan tertentu DMARD (Disease Modified Anti-Rheumatic Drugs atau DC-ART (Disease Controlled Anti-Rheumatic Therapy) : dapat mengontrol dan menghentikan perjalanan penyakit

Farmakoterapi

ACR 2000 Guidlines-Drug Therapy Options in Osteoarthritis

Baseline program(Weight loss/exercise)

Mild/moderate Moderate/severePain pain/inflammation

AcetaminophenSteroids IA COX-2 specific Inhibitors

OTC NSAIDs Hyaluronans Traditional NSAIDs Tramadol (Hyalgan) (plus gastrorptection)Propoxyphene OpioidsSurgery

PENGOBATAN SIMPTOMATIKJangka Pendek

Obat anti inflamasi non steroid (NSAIDs)Analgetikum (Opioid, non-opioid)Muscle relaxan (eperison,dll)

Terapi medikamentosa penyakit reumatik :

Penting pemilihan NSAIDs secara rasionalPerlu pemahaman mekanisme kerja NSAIDsPerlu pemberian NSAIDs ?Pemilihan NSAIDs : perlu pertimbangan-pertimbangan tertentuTujuan : pengobatan yang efektif, aman / bebas dari efek samping yang merugikan

NSAIDs mana ?Sulit dijawab dengan singkat

- Efektifitas pada berbagai individu Individual- Efektifitas dan dosis optimal pada penyakit yang berbeda- Farmakokinetik- Efek samping- Kepatuhan penderita- Harga obat- Lain-lain : faktor yang mempengaruhi perjalanan suatu obat sebelum mencapai target organ, misalnya interaksi dengan makanan, interaksi dengan obat lain, bioavailibilitas dsb. Perhatikan perbedaan :

PERTIMBANGAN PEMBERIAN NSAIDs

Pertanyaan yang harus dijawab sebelum menuliskan resep NSAIDs : 1. Apakah penderita benar-benar memerlukan NSAIDs ?2. Apakah keluhan penderita dapat diobati dengan analgesik saja ?3. Adakah faktor risiko pada penderita yang perlu diperhatikan ?4. Apakah diperlukan NSAIDs dosis tinggi ?5. Bagaimana kombinasi NSAIDs dengan obat-obat lain seperti : - NSAIDs lain- analgesik - analog prostaglandin - antasida, antagonis H2 atau proton pump inhibitor

NSAID menekan proses inflamasi

- Tidak mempengaruhi perjalanan penyakit - Kerusakan sendi atau organ lain akibat penyakit reumatik berjalan terus

Mekanisme Kerja Lain NSAIDs:

Penghambatan kemotaksis terhadap sel-sel yang terlibat dalam proses inflamasiDaya antagonis terhadap mediator lainStabilisasi membran lisosomPenghambatan biosintesis mukopolisakaridaMempengaruhi translokasi Ca++Penghambatan terhadap produksi kolagenPenekanan fungsi limfosit

Disease Modifying Osteoarthritis Drugs (DMOAD)TetrasiklinGlycosaminoglycan polysulfuric acid (GAPS)Glycosaminoglycan peptide complexesPentosan polysulfateGrowth factors and sitokin (TGF-b)Terapi genetikTransplantasi stem cellOsteochondral GraftAnti TNF Alfa (Etanercept)

a. Topical NSAIDsb. Counterirritants

Advantages :Safe and effectiveBetter than placeboAs effective as NSAIDImproves patient assessed painLow rate of complication

Disadvantages : Patient with more severe radiographic grade have responded less Potential adverse event (rare): joint effusion, joint swelling, arthralgia, joint warm, injection site erythemaWang CT et al. J.Bone Joint SurbAm 2004.86A.538-545. Kemper F et al.CurrMed ResOpn2005.21.1261-1269. LussierA et al. J Rheumatol1996.23.1579-1583. VadVB et al.Arch Phys Rehab 2003.84.634-637. PetrellaRJ et al. Arch Intern Med 2002.162.292-298VISCOSUPLEMENT

KOMPLIKASI INJEKSI INTRAARTIKULERInfeksi 1 dari 1000-16.000 injeksiPerdarahanKerusakan rawan sendiNekrosis aseptikAtrofi kulit dan jaringan subkutanRuptur tendo atau ligamentum

New concepts in OA medicinesBio synthesis activity of chondrosit Inhibiting cytokin and free radicalInhibiting enzymes that account for joint damageRemoving lipid deposit in subchondral vascular Increasing sinovial hyaluronan

(Kalim, 1999)

Recent advancesWeight loss 3,9 kg improves symptom of OAQuadriceps exercises are beneficial in patients with OA of the kneeCox-2 selective drugs reduce the incidence of ulcersThe prevalence of OA necessitates a shared care approach to management between general practitioners and hospital specialistSeveral non surgical interventions to alleviate pain and disability : education, social support, physiotherapy and occupational therapy

Surgical : Osteotomy, Arthroplasty Cartilage cell replacement Stem cell transplantation Enzym engineering Nutritional Supplements : Glukosamin, Chondroitin sulfate, vit D and C

Other Interventions

Tujuannya mengoreksi deformitas Osteotomy, arthroplasty Sangat menolong pasien muda (Lavorgna et al., 1999)

Replaced Hip X-ray

Total Knee Joint ReplacementEnd surface of femur replaced with metalEnd surface of tibia replaced with metalPlastic liner is inserted between femur and tibia Patella is resurfaced with plasticThe entire knee is not removed as myth and lore would have it.This is a resurfacing procedure.

Total Knee Replacement

Canina Raphael of Minnara Cattery Yogyakarta

*Let the audience know the importance of this topic.

Here are some relevant facts about osteoarthritis that can be used with this slide:

Arthritis (using the general term for all the different types) is a common disease affecting adults aged 65 and over.It affects over 1/3 of men (37%) and just over half of women (53%) in this age group. Stated another way, 1 out of 2 older women have arthritis, and about 4 out of 10 older men have arthritis.

The graphs in this slide illustrate the prevalence of arthritis among young, middle-aged, and older adults.

Arthritis is the second leading cause of disability in the United States.

There are many different types of arthritis. In this discussion we are going to discuss osteoarthritis, which is a very common form of arthritis affecting many older adults as well as some younger adults.Right now, approximately 21 million people in the United States have osteoarthritis.****The prevalence of OA increases with age, rising from about 1% in those under 30 years to more than 70% in those over 70 years of age. Men and women are equally prone to OA, but more joints are affected in women. Obesity is a significant risk factor for the development and progression of OA, particularly OA of the knee. Joint injuries due to trauma, or as a result of repetitive occupational activities, are also strongly associated with OA. Frequently, patients with OA will have a family history of the disease and there is often a similarity in the type of OA that develops among family members.

ReferenceSolomon L. Clinical features of osteoarthritis. Textbook Rheum 1997;2:13831393.*Several of the currently identified risk factors for osteoarthritis cannot be changed.

One unchangeable risk factor for osteoarthritis is having a family history. For example, if your mother, father, brother or sister has had osteoarthritis, you are more likely than someone without a family history to get osteoarthritis. *Increasing age is another known risk factor for osteoarthritis that cannot be changed. As you age, your risk of developing osteoarthritis increases. Only 7% of adults aged 18 through 44 have arthritis, while this disease affects half (51%) of adults aged 75 and over.*Women are more likely to develop osteoarthritis than men.1 in 2 older women have arthritis (53%), while about 4 out of 10 older men (37%) have this disease.*Other risk factors for osteoarthritis can be changed.

In many cases you can lower your risk for developing osteoarthritis by avoiding or making improvements in these factors.

One risk factor that can be changed is overuse of the joint. Constant, repetitive use of the joints can increase the chances of developing osteoarthritis. For example, certain work environments can lead to an increased chance of having osteoarthritis. Construction workers have been found to have increased chances of developing osteoarthritis of the knee or the hip.Also, repeated heavy lifting can lead to the development of osteoarthritis.

With awareness, you can change the way you do things to prevent overuse of your joints.*Significant injury to the body, such as torn ligaments or fracture, can put affected joints at risk of osteoarthritis. This is especially true for injuries involving the knee or the hip.

*Being overweight or obese places extra stress on the weight-bearing joints of the body. Aside from placing extra stress on the joints, obesity strains the heart, increases blood pressure and cholesterol, and increases the risk of developing diabetes.This is quickly becoming a major health problem in the United States and it is not an age-specific issue.

If you are overweight, especially during the middle or later years of life, the risk of developing osteoarthritis of the knee is increased.

Also, the extra stress on the joints may cause increased pain in the affected joint, limiting your ability to exercise, and resulting in weaker muscles and more weight gain.

By working with your healthcare provider, you can establish a diet and exercise program to lose weight, if necessary. This may help to prevent osteoarthritis before it develops or to reduce some of the symptoms of osteoarthritis.

*Osteoarthritis of the knee is likely to develop, and more likely to progress, if the large muscles in the thigh, also known as the quadriceps, are weak. By working with your healthcare provider, you can establish an exercise program to keep your muscles strong and your joints stable.

In the upcoming slides, we will discuss different types of exercise and how strong muscles and stable joints prevent osteoarthritis and minimize its progression.

*Synovial joints have several features that enable effective movement. The bone surfaces, e.g. the femur and tibia at the knee joint, are smooth and covered with articular (hyaline) cartilage to prevent friction. The joint is enclosed by a capsule of fibrous tissue. A synovial membrane, situated inside the joint capsule, contains blood vessels supplying the intra-articular structure and secretes synovial fluid. Synovial fluid protects the joint against friction and nourishes the cartilage. Ligaments and tendons around the periphery reinforce the capsule and stabilize the joint. References Dieppe P. Osteoarthritis and related disorders. Introduction and history. In: Klippel J, Dieppe P, editors. Rheumatology. London: Mosby, 1998;1.11.2.Grays anatomy online. Available at: http://education.yahoo.com/reference/gray. Accessed 29 April 2004.

*Articular cartilage is composed of cells known as chondrocytes (90% of total volume). The ECM contains collagen and proteoglycan aggregates, which provide strength, elasticity and recoil. In normal adult cartilage, the ECM is constantly degraded and repaired, a process that is regulated by the chondrocytes through the synthesis of enzymes which degrade collagen and proteoglycan (e.g. matrix metalloproteinase) and their inhibitors (e.g. tissue inhibitor of metalloproteinase).

ReferencesGrays anatomy online. Available at: http://education.yahoo.com/reference/gray. Accessed 29 April 2004.Kuettner K, Thonar E. Rheumatology. In: Klippel J, Dieppe P, editors. Rheumatology. London: Mosby, 1998;6.16.16.

*A combination of articular cartilage and synovial fluid allows joints to move without friction and absorbs the shock as weight loads are transmitted to the underlying bone during joint use. When weight is loaded onto the joint through movement, the cartilage layer compresses; the greater the weight the more the cartilage compresses. When weight is removed from the joint, the cartilage rebounds to its original dimensions. Cartilage is a resilient substance and little deformation of the cartilage is visible during loading and unloading.

ReferenceHerfindal E, Gourley D. Textbook of therapeutics: drug and disease management. 6th ed. Baltimore: Williams and Wilkins, 1996.

*OA is a progressive irreversible disease characterized by the degradation of articular cartilage. Cartilage becomes pitted and frayed at the surface and becomes increasingly inelastic. As OA progresses, loss of cartilage increases and may wear away completely leaving the bone ends exposed and able to rub together. Pieces of cartilage and/or bone may break off into the synovial fluid. The bone ends thicken in an attempt to increase the surface area available for load bearing and as a result, bony outgrowths known as osteophytes form. In addition, there is hypertrophy (thickening) of all the soft tissues including the synovium, capsule and ligaments.

ReferencesDieppe P. Osteoarthritis and related disorders. Introduction and history. In: Klippel J, Dieppe P, editors. Rheumatology. London: Mosby, 1998;1.11.2.Herfindal E, Gourley D. Textbook of therapeutics: drug and disease management. 6th ed. Baltimore: Williams and Wilkins, 1996.

*In OA, there is an alteration in collagen structure and a decrease in the number and quality of proteoglycan aggregates. More chondrocytes are produced and they exhibit a state of hypermetabolism, upregulating the synthesis of collagen and proteoglycan aggregates. However, the collagen and proteoglycan properties are altered and the extracellular matrix becomes weakened. The cartilage surface first cracks, then fragments of cartilage break off in the synovial fluid. Over time, cartilage may wear away completely leaving the bone exposed.

ReferencesGrays anatomy online. Available at: http://education.yahoo.com/reference/gray. Accessed 29 April 2004.Kuettner K, Thonar E. Rheumatology. In: Klippel J, Dieppe P, editors. Rheumatology. London: Mosby, 1998;6.16.16.****Joints in the body are made up of several components: BonesThe 2 bones are lined up end to end. CartilageAt the end of each bone is a smooth, firm material known as cartilage. This cushion covers the ends of the bones and keeps them from rubbing together. This provides a smooth surface for the joints movement. Joint capsule This surrounds the entire structure, and is lined with a tissue known as the synovium. The synovium makes synovial fluid that fills in the space between the bone ends and also helps to keep smooth movement of the joint. Muscles and tendons The joint is supported by the muscles and the tendons which are attached to the bones and help it to move.

When the joint is healthy: The cartilage provides a cushion for the the bones to glide smoothly against each other.Movement and bending occur without any problem.**Primary OA has no single specific cause but is generally associated with aging, normal mechanical stresses and genetic factors. It usually occurs in weight-bearing joints that have undergone abnormal stresses (e.g. from obesity or overuse), and is frequently linked with increased age. Common sites of involvement include the hands, hips, knees and feet. Primary OA is the most common form of OA. In contrast, secondary OA may occur in any joint at any age and has an identifiable underlying cause (e.g. inflammatory or metabolic disease). Secondary OA develops following any process that damages the joint such as fractures, dislocations, sports injuries, joint surgery or repetitive trauma (occupational trauma).

ReferenceSolomon L. Clinical features of osteoarthritis. Textbook Rheum 1997;2:13831393.*OA is characterized by cartilage degradation, which results in a loss of joint space and bony outgrowths (osteophytes) which are visible by X-ray. Joint grinding/grating is also a result of cartilage loss. Patients with OA have characteristic joint deformities such as bony lumps on the finger joints (Heberdens nodes). Symptoms of OA include use-related joint pain, joint stiffness after periods of inactivity, loss of movement/difficulty performing certain tasks, joint locking/giving way, feelings of instability and restricted/painful movements.

ReferencesHope R, Longmore J, McManus S, et al. Oxford Handbook Clinical Medicine. 4th ed. Oxford: Oxford University Press, 1998.Dieppe P, Lim K. Osteoarthritis and related disorders. Clinical features and diagnostic problems. In: Klippel J, Dieppe P, editors. Rheumatology. London: Mosby, 1998; 3.13.16.

**The hand joints most commonly affected are the distal interphalangeal (DIP; joint closest to the fingertips) and the proximal interphalangeal (PIP; middle joint on fingers, and the joint closet the tip of the thumb). The hallmarks of OA are Heberdens nodules (which occur at the DIP) and Bouchards nodes (which occur at the PIP). These firm swellings are often tender and sometimes red.The knuckles (metacarpophalangeal; MCP) are rarely affected in OA.

ReferenceDieppe P, Lim K. Osteoarthritis and related disorders. Clinical features and diagnostic problems. In: Klippel J, Dieppe P, editors. Rheumatology. London: Mosby, 1998;3.13.16.***Stretching or range-of-motion exercises, such as yoga or tai chi, can help prevent joint stiffness as well as improve flexibility, increase muscle strength, and promote relaxation.

Again, before starting to exercise, speak with your healthcare provider about which of these would fit your needs and which type of program would be best suited for you.******