penyakit degeneratif muskuloskeletal

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  • Penyakit Degeneratif Muskuloskeletal

  • DefinisiDegeneratif SendiKelainan daripada sendi (satul/lebih) yang dimulainya dengan kerusakan tulang rawan sendi, diikuti dengan progresivitas kerusakan, penebalan & remodelling tulang subchondral, dan disertai dengan peradangan sekunder membran sinovial.Degeneratif Jaringan lunakNekrosis lokal dp. tendon/kapsel sendi peradangan

  • Penyakit degeneratif sendi (Osteoarthritis) Macam :Primer / idiopatik (aging, genetik)Sekunder (trauma, deformitas, gout, dll.)Patologi :Perubahan sifat biokimiawi & fisik tlg. RawanSinovitisPenebalan kapsulOsteofit, sklerosis, pembentukan kista subchondral.

  • DIAGNOSA OA KLINIS RADIOLOGIK SCINTIGRAFI MRI TES LABORATORIUM ANALISA CAIRAN SENDI ARTHROSKOPI MARKERBIOKOMIAWI (COMP,CS,KS,coll chain etc.)

  • Gambaran klinis OAGejalaNyeri resting painKaku sendiTandaPembengkakanAtrofi ototKrepitusROM Lain2 : Bouchard nodes, kelainan X-ray

  • CLINICAL FEATURESSYMPTOMSPainStiffnessAlteration in shapeFunctional impairmentanxiety,depression SIGNSCrepitusRestricted movementTendernessBony swellingDeformityMuscle wasting/weaknessEffusion, increased warmthInstability

  • DERAJAT KLINIS

    INDEKS LEQUESNE

    INDEKS WOMAC (WEST ONTARIO & MAC MASTER)

  • RADIOLOGIKTUJUANDiagnosisPenentuan derajat perubahan strukturalIdentifikasi chondrocalcinosis

    4 GAMBARAN UTAMA RADIOLOGIKPenyempitan celah sendiSklerosis subchondralPembentukan kista subchondralOsteofit

  • DERAJAT RADIOLOGIKKELLGREN & LAWRENCE (1957)

    KALLMAN (1989)

    CROFT (1990)

    AMERICAN COLLEGE OF RHEUMATOLOGY (1991)

  • TES LABORATORIUMNON SPESIFIKDIAGNOSA BANDING PENYAKIT LAIN a.l.c reactive proteinasam uratrematoid faktordll.

  • ARTHROSKOPIDIAGNOSTIK

    DERAJAT KERUSAKAN KARTILAGO

    RESPON SMOAD/DMOAD

    TERAPI DEBRIDEMEN & LAVAGE

  • ANALISA CAIRAN SENDI TIDAK SPESIFIK

    IDENTIFIKASI KRISTAL CPPD IDENTIFIKASI KRISTAL URAT SEPSIS

  • Non FarmakologikPenyuluhan Pendidikan Kontrol Berat BadanFisioterapi & Terapi KerjaFarmakologikSistemikLokalPembedahan PENATALAKSANAAN OA MASA KINI

  • BedahInjeksi Intra artikuler Lavage sendiNSAIDAnalgesik (Acetaminophen)Pendidikan PenderitaTerapi Fisik & Terapi KerjaKontrol BB, Olah raga, Penggunaan OrtotikAnalgesik Topikal

  • Non NSAID

    Analgesik- Asetaminofen- Tramadol

    Narkotik

  • NSAIDNon selektif cox-1 & cox-2 inhibitorSelektifCOX-2 inhibitorGangguan sintesis matriksKelompok I >>>Kelompok II >>Kelompok III >

  • SMOAD (STRUCTURAL MODIFYING OSTEOARTHRITIS DRUG)/ DMOAD GAG-peptideGAGPSPENTOSANCHONDROITIN SULFATEGLUCOSAMINE SULFATELOCAL CORTICOSTEROIDHYALURONIC ACIDETIDRONATECALCITONINDOXYCYLINEAVOCADO/SOYBEAN UNSAPONIFIABLESSEVERAL NSAIDDIACEREIN

  • LOKALTopikal- NSAID- CapsaicinIntra artikuler- Kortikosteroid- Hyaluronic acid (HA)- Glycosaminoglycan polysulfate (GAGPS)- Orgotenin, yttrium-90, silicon, somastotin & tenoksikam

  • PEMBEDAHAN

    PENCEGAHAN PROGRESIVITAS OA

    DEFINITIP PENGGANTIAN LAPISAN TULANG RAWAN

  • OPERASI PENCEGAHAN

    Lavage & DebridementDrillingAllo/Autografting Osteo chondralPeriosteal & Perichondral ResurfacingTransplantasi selOsteotomi

  • OPERASI DEFINITIP

    Resection & Interpositional arthroplastyArtificial joint arthroplasty- Hemi/Partial- TotalArthrodesis

  • PENGOBATAN OA MASA DEPANBiologic agent- Growth factor- Anti cytokineGene therapyCytokine inhibitors- IL-1 inhibitors- TNF- inhibitorsNitric oxide synthase inhibitorsMetallo protease inhibitors

  • Degeneratif Tlg. Belakang (spondylosis deformans)ManifestasiBack pain, ishialgia, paraparese.Degeneratif diskus, sendi facet, spinal stenosis, segmental instabilitas, HNPTerapiKonservatifMedikamentosa, Fisioterapi, Spinal support dllOperatipDekompresi (laminektomi), stabilisasi

  • Degeneratif Jaringan LunakMyofascial pain syndrome (Fibrositis)KapselSubacromial bursitisBicipital tendinitisAdhesive capsulitis (Frozen Shoulder) dll.TendonDe Quervains diseaseGanglionTrigger finger (snapping finger)Tennis elbow (lateral epicondylitis)

  • Terapi non artikular degeneratif KonservatifMedikamentosaFisioterapiOperatifTendon releaseEksisiRepair dll.

  • RINGKASANOA MULTIFAKTORIAL DIAGNOSA TIDAK SULITDERAJAT PERUBAHAN STRUKTUR TIDAK SESUAI DENGAN GAMBARAN KLINISPROGRESIVITAS ?STRES BIOMEKANIK PERANAN PENTINGSMOAD CEGAH PROGRESIVITAS MENINGKATKAN DAYA PERBAIKANPENCEGAHAN HINDARI FAKTOR RESIKO

  • Osteoporosis is a systemic skeletal disease characterised by low bone mass and micro-architectural deterioration of bone tissue with a consequent increase in bone fragility & susceptibility to fracture

    Definition of Osteoporosis

  • NIH (National Institutes of Health) Consensus Development Panel on Osteoporosis Prevention,Diagnosis, and Therapy. JAMA. 2001;285:785-795.OSTEOPOROSIS:NEW DEFINITIONA skeletal disorder characterized bycompromised bone strength predisposing aperson to an increased risk of fracture

  • BoneQuality

    BoneStrengthandArchitectureTurnover rateDamage AccumulationDegree of MineralizationProperties of the collagen/ mineral matrix Shifting the Osteoporosis Paradigm Bone Strength NIH Consensus Statement 2000Adapted from NIH Consensus Development Panel on Osteoporosis. JAMA 285:785-95; 2001

    BoneQuantityBone sizeBone density

  • BONE QUALITY VS QUANTITYBone TurnoverDamage StateOrganic MatrixMineralizationArchitectureBMD

  • Silva MJ, Gibson LJ. Bone 1997:21;1919Parfitt AM. Am J Med 1991; 91 (Suppl5B):42S-46S.

    The importance of architectural integrity10% decrease in BMD due to loss in trabecular number equals70% reduction in bone strength10% decrease in BMD due to loss in trabecular thickness equals20% reduction in bone strength

  • WHO, Guidelines for Preclinical Evaluation and Clinical Trials in Osteoporosis, 1998.T-ScoreWorld Health Organization (WHO) Osteoporosis Guidelines

  • Osteoporosis and Peak Bone MassPeak bone mass is achieved by men and women in the middle of the third decade of life.After a plateau period, there begins a period of net bone loss (about 0.3% to 0.5% a year).With menopause, women may lose bone at the rate of 3% to 5% a year.Adapted from Scientific American Online, April 2002

  • Established Risk Factors for Osteoporosis Genetic Female White or Asian races Thin or low peak bone mass Family history of fractures Medical Menopause Menstrual dysfunction or early menopause Glucocorticoid, thyroid, use Lifestyle Smoking Excessive alcohol use Lack of exercise

    Nutritional Low calcium Vitamin D deficiency Vitamin A excess

  • Pathogenesis of Osteoporosis:

    Genetic factors play an important role in the development of osteoporosis.Abnormal receptors for vit.DGenetic abnormalities for an expression osteoporosis phenotypeHormonal factorsEstrogen & testosteron deficiency IL-6 Osteoclast Other factorsPhysical stressObesityLate menarche/early menopause, smoking, alcohol use, insufficiency dietRace

  • B. L. Riggs: J Clin Invest 106:12031204, 2000 (73 ).

  • The Aim of Osteoporosis TreatmentIts not to reduce bone resorptionIts not to increase bone densitybut Its a fracture reduction

  • Bone Measurement TechniquesTechniquePrecision (%)Significantchange (%)Spine DEXAHip DEXAQ-CTp-DEXAUltrasound11.5324348511

  • Yates AA, et al. J Am Diet Assoc. 1998;9:699-706.NIH Consensus Conference. JAMA 1994; 272: 1942-8.Nonpharmacological Management for Prevention and Tx of OsteoporosisCalcium (1200 mg-1500 mg/day in divided doses)Vitamin D 400-800 IU/dayWeight bearing exerciseFall-prevention techniques

  • Nutrition and OsteoporosisBone mass is determined by endogenous (genetic, hormonal) and exogenous (nutritional, physical activity) factors.Nutrition plays a role in the pathogenesis, prevention, and treatment of osteoporosis.Calcium, vitamin D, protein, and calories are important nutrients in osteoporosis.

  • Yates AA, et al. J Am Diet Assoc. 1998;9:699-706.NIH Consensus Conference. JAMA 1994; 272: 1942-8.Preventing Osteoporosis:outcomes of the Australian Fracture Prevention Summit MJA, April 2002;176:3-15Nonpharmacological Management for Prevention and Tx of OsteoporosisCalcium (1200 mg-1500 mg/day in divided doses)Vitamin D 400-800 IU/dayAvoid risk factorsWeight bearing exercise, Fall-prevention techniquesPhysiotherapy/other physical modalities, (TENS etc.)Cognitive behaviourNerve blockadeVertebroplasty, Kyphoplasty

  • Pharmacology-Medical TreatmentAntiresorptive drugsInhibit osteoclast-mediated bone lossAnabolic AgentsDirectly stimulate bone formationCombination therapy ?Additional / other drugsPhytoestrogen, nandroloneanalgesics

  • Antiresorptive drugsEstrogenBiphosphonatesSelective Estrogen Receptor Modulators (SERMs)Calcitonin

  • POSTMENOPAUSE: estrogen deficiencyLifespan OsteoblastOsteoblastogenesisLifespan OsteocyteOsteoclastogenesisLifespan Osteoclast

  • Summary & Conclusions1.Osteoporosis is a preventable disease not a condition of aging.2.Persons at risk can be identified.3.Technology for accurate bone density measurement exists.(contd)

  • Summary & Conclusions (contd)4.Estrogen is the agent of choice for prevention and treatment of postmenopausal osteoporosis but with their side effects.5.Alternatives for women who cannot take estrogen include:a.Raloxifene and other SERMsb. Alendronate and other bisphosphonates c.Calcitonin

    ***The importance of architectural integrity

    A reduction of 10% in BMD that is due to a reduction in trabecular thickness will result in a 20% reduction in bone strengthA reduction of 10% in BMD that is due to a reduction in trabecular number will result in a 70% reduction in bone strengthHigh turnover rates increase the number of resorptive sites. In a trabecular network that is already compromised by bone loss, a high turnover state may weaken crucial, but unsupported trabeculae to the point of failure without causing a significant decrease in bone mass.In high turnover stages, the probability of trabecular plates being perforated is also increased. Loss of vital trabeculae in this manner could dramatically reduce bone strength, again with relatively little effect on bone mass

    Silva MJ, Gibson LJ. Bone 1997:21;1919Parfitt AM. Am J Med 1991; 91 (Suppl5B):42S-46S.*It should be noted that these guidelines are based on data from postmenopausal Caucasian women; they may not be applicable to other races or ethnic groups.Patients with osteopenia may still be at risk for fracture.There are patients with osteopenia who have fractures already. Many physicians are confused about this phenomenon. For example, a patient having a T-score 2.2 is at significant risk for fracture even though osteopenic.**While a number of factors contribute to a predisposition to developing osteoporosis, a few are key. In general, genetics play a major role. Those women who approach menopause with low peak bone mass may lose additional bone mass as a result of menopause and have bone mass below the threshold of fracture more rapidly than women who enter menopause with high peak bone mass. Some women may have high peak bone mass but lose bone mass very rapidly. Menopause is a paramount factor. Other risk factors include white or Asian races. Positive family history, cigarette smoking , which alters estrogen metabolism, and sedentary lifestyle are frequently cited as factors that increase risk. Certainly, women with any of these genetic, medical, nutritional or lifestyle factors may be at increased risk of bone loss.Medical conditions that can affect risk include menstrual dysfunctions sufficiently severe to lead to hypo-estrogen, endocrinopathies, hyperprolactinemia, hyperparathyroidism, hyperthyroidism, or Cushing's syndrome.Other medical conditions that relate to calcium excretion and absorption also are considered risk factors for osteoporosis.

    **The National Academy of Sciences Guidelines of 1997 emphasized the need for adequate calcium through diet or supplementation in excess of 1200 mg daily for postmenopausal women.Extra doses of vitamin D are particularly important for the institutionalized elderly. Weight-bearing exercise has been shown to maintain or increase bone mineral density in pre- and postmenopausal women.There are a variety of fall-prevention techniques that are beyond the scope of this presentation.**The National Academy of Sciences Guidelines of 1997 emphasized the need for adequate calcium through diet or supplementation in excess of 1200 mg daily for postmenopausal women.Extra doses of vitamin D are particularly important for the institutionalized elderly. Weight-bearing exercise has been shown to maintain or increase bone mineral density in pre- and postmenopausal women.There are a variety of fall-prevention techniques that are beyond the scope of this presentation.