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DEGENERATIVE DISORDER
OF BONE AND JOINT NYOMAN KERTIA Section of Rheumatology, Internal Medicine Department Faculty of Medicine GMU / Dr. Sardjito General Hospital
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LUMBOSACRAL SPONDYLOSIS
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LUMBOSACRAL SPONDYLOSIS
MAY CAUSE LOCALIZED LOW BACK PAIN LBP INCREASES ET THE END OF THE DAY AND RADIATES ACROSS THE LOW BACK NARROWING OF THE SPINAL CANAL SPINAL STENOSIS & COMPRESSION OF NEURAL ELEMENTS PAIN WORSENS WITH SPINAL EXTENSION AND IPSILATERAL BENDING RO: OSTEOPHYTE, FACET JOINT NAROWING, PERIARTICULAR SCLEROSIS
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SOME SOURCES OF LOW BACK PAIN
Posterior Longitudinale Ligament Discus Corpus vertebrae Procesus spinosus Nucleus Flavum Ligament Annulus Joint capsul Nerve Spinal cordae and capsule (dura)
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OSTEOARTHRITIS
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Prevalence of Radiographic Evidence of OA in the Population
10 20 30 40 50 60 70 Knee, man DIP, man Knee, women DIP, women Prevalence (%) Age (years)
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PATHOGENESIS CHANGES IN ARTICULAR CARTILAGE & SUBCHONDRAL BONE
FAILURE OF CHONDROCYTES TO MAINTAIN THE BALANCE BETWEEN DEGRADATION AND SYNTHESIS OF EXTRACELLULAR MATRIX PROTEINASES AND PROINFLAMMATORY CYTOKINES HAVE AN IMPORTANT ROLE MECHANICAL STRESS CONTRIBUTES SIGNIFICANTLY TO DISEASE INITIATION & PROGRESSION
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OSTEOARTHRITIS The typical stance of a patient with knee OA: elderly female, often overweight, with genu varum deformity. They usually complain of a “mechanical” knee pain, characteristically felt on initial standing from a prolonged sitting position. Unlike patients with RA, those with OA do not have any systemic manifestations. ACRFP
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INFLAMMATORY ARTHROPATY
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The pathologic features readily correlate with the radiographic features of knee OA, i.e. loss of joint space, subchondral cysts, and attempts at repair or regeneration such as sclerosis and osteophytes.
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NORMAL versus OSTEOARTHRITIS
Normal Joint OA Joint Thickness of Capsul Capsul Bone Cyst Cartilage Subchondral Sclerosis Sinovium OA primarily starts as a cartilage problem, later involving other structures. Once these are affected, the patient starts to develop the pain characteristic of this condition. Cartilage Fibrillation Sinovium Hypertrophy Bone Osteophyte Formation
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CLINICAL FEATURES THE MOST COMMONLY AFFECTED ARE: CERVICAL & LUMBAR SPINE, DIP, KNEE, HIP STRONGLY AGED RELATED; ADDITIONAL RISK: FEMALE, OBESITY, TRAUMA, FAMILY HISTORY SIGNS& SYMPTOMS: PAIN, SHORT-LASTING STIFFNESS, CRACKING & CREPITUS, MILD SWELLING, FUNCTIONAL LIMITATION RADIOGRAPHS IS IMPORTANT IN MAKING THE DIAGNOSIS
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Drug Therapy Options in Osteoarthritis (Weight loss / exercise)
ACR Guidlines Drug Therapy Options in Osteoarthritis Baseline program (Weight loss / exercise) Mild or moderate pain Moderate or severe pain / inflammation / inflammation Acetaminophen Steroids COX-2 selective intra articular Inhibitors NSAIDs NSAIDs Hyaluronans Traditional NSAIDs Tramadol intra articular ( plus gastroprotection) Propoxyphene Opioids Surgery
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DIFFERENTIAL DIAGNOSIS
INFLAMMATORY VS DEGENERATIVE ARTHROPATY OSTEOARTHRITIS RHEUMATOID ARTHRITIS
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RHEUMATOID ARTHRITIS This shows stage 4 or “burnt-out” RA , with the classical chronic hand deformities including joint subluxation. ACRFP
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SOFT TISSUE RHEUMATISM
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CHEIROARTHROPATHY
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TENDINITIS
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BURSITIS
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ANKYLOSING SPONDYLITIS
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NON-BACTERIAL INFLAMASI
NORMAL NON-BACTERIAL INFLAMASI PURULENT HEMORAGIK
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Non-pharmacologic Treatment Options for Pain
Cognitive-Behavioral Relaxation Preparatory information Imagery Hypnosis Physical Agents Application of superficial heat and cold Massage Exercise Immobilization Electro-analgesia (eg, TENS) Acupuncture Carr DB, et al. AHCPR Pub. No
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Pharmacologic Treatment Options for Pain
Nonopioid analgesics paracetamol tramadol anti-inflammatory agents Opioid analgesics Local anesthetics, nerve block Co-analgesic such B-vitamin, anti-epilepticum (carbamazephin, gabaphentin, pregabalin) & tricyclic antidepressan DMOADs (Disease Modifying Osteoarthritis Drugs) SURGERY
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Synthesis: Synoviocyte, chondrocyte
Hyaluronic acid Bone Cartilage HA Capsule Chondrocytes HA • • • • • Synovial lining • • Osteoclast Osteoblast Bone Synthesis: Synoviocyte, chondrocyte
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Hyaluronan works on cells that was involved in joint destruction
Inflammatory cells synoviocytes Chondrocytes Decreases cell’s activity viscoinduction Improves cells metabolism Neosynthesis of endogenous HA JOINT CARTILAGE Decreased inflammatory process Reconstruction on supervicial level Matrix synthesis Improves tissue integration Pharmacologic activities of HA
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Standing wrong Right Right wrong Sitting Right Sleeping Wrong
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DIFFERENTIAL DIAGNOSIS OF ARTHRITIS
INFLAMMATION NO/MILD INFLAMMATION MONO/ OLYGO POLY ARTICULAR ARTICULAR DEGENERATIVE RECURRENCE SYMETRICAL NON-SYMETRICAL GOUT, CPPD RA, SLE AS, Ps. A, REITER NON- RECURRENCE SEPTIC REMEMBER THE OTHER CLINICAL SIGNS, SYMPTOMS AND LABORATORY RESULTS
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