DEGENERATIVE DISORDER OF BONE AND JOINT NYOMAN KERTIA Section of Rheumatology, Internal Medicine Department Faculty of Medicine GMU / Dr. Sardjito General Hospital

LUMBOSACRAL SPONDYLOSIS

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

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)

OSTEOARTHRITIS

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)

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

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

INFLAMMATORY ARTHROPATY

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.

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

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

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

DIFFERENTIAL DIAGNOSIS INFLAMMATORY VS DEGENERATIVE ARTHROPATY OSTEOARTHRITIS RHEUMATOID ARTHRITIS

RHEUMATOID ARTHRITIS This shows stage 4 or “burnt-out” RA , with the classical chronic hand deformities including joint subluxation. ACRFP

SOFT TISSUE RHEUMATISM

CHEIROARTHROPATHY

TENDINITIS

BURSITIS

ANKYLOSING SPONDYLITIS

NON-BACTERIAL INFLAMASI NORMAL NON-BACTERIAL INFLAMASI PURULENT HEMORAGIK

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. 92-0032. 1992.

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

Synthesis: Synoviocyte, chondrocyte Hyaluronic acid Bone Cartilage HA Capsule Chondrocytes HA • • • • • Synovial lining •   •   Osteoclast Osteoblast Bone Synthesis: Synoviocyte, chondrocyte

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

Standing wrong Right Right wrong Sitting Right Sleeping Wrong

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