Osteoarthritis slideshare

Dr Ajay Shah IOM, Nepal
knee osteoarthritis

1. Osteoarthritis Moderator: Assoc Prof Dr Suresh Uprety Presenter: Dr Ajay shah MS orthopedics 1 st year Resident

2. C ontent Anatomy Introduction Aetiology and risk factors Pathogenesis Pathology Symptoms and Signs Investigations Management

3. ANATOMY Usually a condition of synovial joints Components Articular cartilage Synovial membrane S ynoviocytes Produce lubricants, hyaluronic acid, cytokines and growth factors

4. Fibrous capsule Lined by synovial membrane Continuous with the periosteum Provide stability throughout the ROM of joints Synovial Fluid Viscous slippery fluid rich in albumin and hyaluronic acid Intra articular discs of fibrocartilage Hip joint- labrum-deepens the articulation Knee joint- mensci - improve congruency Protect from both compressive and shear forces

5. Introduction Osteoarthritis, non-inflammatory degenerative joint disorder characterized by degeneration of cartilage that results in structural and functional failure of synovial joints. Most common type of joint disorder Intrinsic disease of cartilage in which chondrocytes respond to biochemical and mechanical stresses resulting in breakdown of matrix.

6. Joints involvement Knee joint MC joint to involve MC sites: anteromedial compartment- Tibiofemoral joint lateral facet- Patellofemoral joint Hip joint Superolateral aspect of joint Hand Distal interphalangeal joints, PIP joints Feet - 1 ST MTP Spine Facet joints of cervical and lumbosacral spine

7. Prevalence Internationally, OA is the most common articular disease On the basis of the radiographic criteria for osteoarthritis more than 50% of adults older than 65 years are affected by the disease In individual older than 55 years, the prevalence of OA is higher among women than among men Leading cause of chronic disability in those older than 70 years, costing US greater than $100 billion annually

8. Types of OA 1 Primary/Idiopathic When there is no obvious predisposing factors Common form of OA Its mainly due to wear and tear changes occurring in old ages mainly in weight bearing joints 2 Secondary OA When degenerative joint changes occur in response to recognizable local or systemic factors

9. Causes of secondary OA Developmental Developmental dysplasia of hip Legg-calves perthe’s disease Epiphyseal dysplasia Mechanical Hypermobility syndromes Leg length discrepancy Mal-alignment Trauma (acute or chronic) Sports injury Iatrogenic Occupational Accidental Metabolic Hemochromatosis Gout Pseudogout Calcium crystal deposition

10. Endocrine Acromegaly Hyperparathyroidism Hypothyroidism Inflammatory Any systemic rheumatic disease Septic arthritis Miscellaneous Hemophilia Osteonecrosis Paget’s disease Neuropathic arthropathy

11. OA Variants Atrophic destructive OA including rapidly progressive hip OA and Milwaukee shoulder Rapid period with joint damage progresses to extensive bone loss Whole head of femur and humerus may disappear

12. Hypertrophic OA Particularly common at hip and knee joints Characterized by massive osteophyte formation It may be associated with calcium pyrophosphate dehydrate crystal deposition diffuse idiopathic skeletal hyperstosis (DISH)

13. Erosive inflammatory OA of interphalangeal joints Involves terminal interphalangeal joints of hands Associated with signs of inflammation and development of joint erosions. Radiograph shows erosion of joint ( sea gull appearance)

14. Kashin Beck disease Rare polyarticular form of OA Joint pain, polyarticular swelling and deformity from childhood Adults have short stature Radiographs reveal distorted epiphyses and tubular long bones

15. Risk factors Systemic predisposition Genetics Age Gender Diet and obesity Local biomechanical factors Abnormal joint shape and size Previous injury Neuromuscular problems Obesity Loading/occupational factors Bone mineral density

16. Pathogenesis

17. Pathological Changes Focal areas of loss of articular cartilage Bone growth at the joint margins Sclerosis of underlying bone Cyst formation in underlying bone Loss of bone Varying degrees of synovial inflammation Fibrosis and thickening of joint capsule

18. Gross Appearance

19. Microscopic Features

20. Symptoms and signs at different joint sites Knee Joint MC site medial patellofemoral joint Pain: globally over knee and proximal tibia In isolated patellofemoral OA, pain is anteriorly over knee and is often worst during ascending and descending stairs Symptoms of instability Swelling and stiffness

21. Antalgic gait Weakness/Wasting of quadriceps muscles Varus deformity Restricted extension and flexion Audible crepitus

22. Hip joint Pain usually felt in groin, radiates down anterolateral aspect of thigh Pain is worse on exercise and walking distance is reduced Morning and rest stiffness Antalgic gait Weakness of hip abductors Restricted internal rotation with flexion

23. Hand joint MC affected joints are DIPs and thumb base ( radiocarpal and radiotrapezoid joints) Strongly associated with knee OA and genetic predisposition, suggesting as feature of generalized OA More common in women and often start around the time of menopause( sometimes called as menopausal OA)

24. Bouchard's nodes are a classic sign of   OA of the hand . Named after the French pathologist Charles-Joseph Bouchard, who studied arthritis patients in the 19th century . Bouchard nodes are bony enlargements of the proximal interphalangeal (PIP) joints. Heberden’s nodes are similar bony swellings that develop at the distal interphalangeal (DIP) joint. Bouchard's nodes are less common than Heberden's nodes .

25. FOOT Hallux rigidus : 1 st MTP joint OA Pain and tenderness over dorsum of joint Limited dorsiflexon secondary to large osteophytes Stiffness of 1 st MTP joint and compensatory hyperextension of IP joint Grind test

26. Investigations Plain Radiographhs Four cardinal signs Joint space narrowing Osteophytes formation Subchondral bone cysts Sclerosis of underlying bone

27. Kellgren and lawrence

28. Grade 0 : Normal Grade 1: Minimal osteophyte, doubtful significance Grade 2: Definite osteophyte, no loss of joint space Grade 3: Some diminution of joint space Grade 4: Advanced joint space loss and sclerosis of bone

29. X-rays

30. Blood Tests Raised CRP ( in some cases) Normal ESR Rheumatoid factor and Antinuclear antibodies are negative MRI Early cartilage and subchondral bone changes, although it is not routinely used due to cost Arthroscopy Reveal early fissuring and surface erosions Synovial Fluid Analysis Viscous with low turbidity Can be used to exclude gout, CPPD or septic arthritis if diagnosis is in doubt

31. Outerbridge classification Grade 0 : Normal cartilage Grade I : Softening and swelling of cartilage Grade II : Fragmentation and fissuring of the cartilage in an area less than ½ inch in diameter Grade III : Fragmentation and fissuring of the cartilage in an area more than ½ inch in diameter Grade IV : Exposure of underlying bone

32. Modified Outerbridge Classification Grade 0 : Intact cartilage Grade I : Chondral softening or blistering with intact surface Grade II : Superficial ulceration,fibrillation , or fissuring less than 50% of depth of cartilage Grade III : Deep ulceration, fibrillation, fissuring, or chondral flap more than 50% of cartilage without exposed bone Grade IV : Full thickness wear with exposed subchondral bone

33. Secondary OA: Special Tests Ochronosis : Presence of homogenistic acid in urine which turns black in exposure to air Wilson’s disease : Reduced serum ceruloplasmin , increased urinary excretion of copper Hemochromatosis : Raised serum iron and ferritin Gout : Raised serum urate Hypothyroidism : Low T3 ,T4 and raised TSH Hyperparathyroidism : Raised PTH,calcium and low phosphate Tabes dorsalis : Positive VDRL DM : Abnormal glucose tolerance test

34. Management Basic principles of symptomatic management of OA Pyramid of treatment for symptomatic OA ( From Dieppe and Lohmander,2005)

35. Based on the UK National Institute for Health and Care Excellence (NICE) 2014 guideline. Step 1: Take a holistic approach and encourage self-management Assessing the impact of OA on the individual’s quality of life, function, mood , relationships and activities Self-management strategies include Alterations of diet (lose weight) Alteration in activities Changing footwear

36. Step 2: Introduce the “core treatments” appropriate for most people with OA These includes Provision of information about the condition and its management To increase their exercise level Footwear advice To do specific exercises to strengthen muscles around affected joints

37. Step 3: Introduce specific non-surgical interventions These may be pharmacological or non-pharmacological Non-pharmacological Supervised courses of physical therapy Use of aids and devices Braces and splints Walking aids such as sticks or crutches Electrotherapy such as TENS

38. PHYSIOTHERAPY Hamstring stretching exercises

39. Quadriceps strengthening exercises

40. Calf muscle strengthening

41. Knee Brace Advantages Enhanced stability Reduced swelling Reduced pressure Increased confidence

42. Knee adduction moment (KAM) during gait is known to indicate disease severity and prognosis of varus knee Thus, to reduce KAM is a key strategy in treatment of knee OA. KAM is primarily calculated as the product of the resultant ground reaction force (GRF) in the frontal plane and the perpendicular distance from the GRF to the knee joint center (frontal plane lever arm).

43. Pharmacological NSAIDs Non-selective NSAID COX-2 selective Tramadol, opioids Intra-articular injection Local anaesthetic Corticosteroids Supplements Glucosamine Chondroitin sulfate etc

44. Step 4: Consider surgical options Arthroscopic procedures Joint debridement Removal of mechanical obstructions Joint lavage Drilling of sclerotic lesions Abrasion chondroplasty Autologous chondrocyte transplantation

45. Proximal T ibial Osteotomy Indications for proximal tibial osteotomy are P ain and disability resulting from osteoarthritis that significantly interfere with high-demand employment or recreation E vidence on weight-bearing radiographs of degenerative arthritis that is confined to one compartment with a corresponding varus or valgus deformity

46. Contraindications to a proximal tibial osteotomy N arrowing of lateral compartment cartilage space Lateral tibial subluxation of more than 1 cm M edial compartment tibial bone loss of more than 2 or 3 mm Flexion contracture of more than 15 degrees Knee flexion of less than 90 degrees More than 20 degrees of correction needed Inflammatory arthritis S ignificant peripheral vascular disease .

47. LATERAL CLOSING WEDGE OSTEOTOMY A dvantages I t is made near the deformity, that is, the knee joint M ade through cancellous bone, which heals rapidly P ermits the fragments to be held firmly in position by staples or a rigid fixation device, such as a plate-and-screw construct P ermits exploration of the knee through the same incision.

48. Disadvantages Fibular osteotomy or release of proximal TF joint Peroneal nerve injury Shortening of leg Muscle detachment Difficult to correct in 2 plans

49. MEDIAL OPENING WEDGE OSTEOTOMY

50. Proximal Fibular O steotomy Proximal fibular osteotomy is an alternative treatment to high tibial osteotomy. It is a surgical procedure for medial compartment knee osteoarthritis  

51. Total Knee Arthroplasty After PTO At 10 to 15 years after proximal tibial osteotomy, 40% of patients require conversion to total knee arthroplasty Studies have shown that the outcome of total knee arthroplasty in patients with previous high tibial osteotomies was not significantly different from outcomes after primary total knee arthroplasty Although total knee arthroplasty after high tibial osteotomy is technically demanding and is a longer operative procedure . Unicompartmental arthroplasty has poor results after high tibial osteotomy (28% failure at 5 years).

52. Indications of TKA Relieve pain caused by severe arthritis, with or without deformity Failed high tibial osteotomy Kellgren and Lawrence grade IV

53. Arthrodesis Of Knee Most frequent indication for knee arthrodesis is failed total knee arthrodesis, secondary to infection Salvage procedure after failed TKA, expected to have some inferior results compared with primary knee arthrodesis including Lower fusion rates Higher infection rates Shortening of leg

54. Techniques Compression arthrodesis with external fixation Arthrodesis with intramedullary rod fixation Arthrodesis with plate fixation

55. Hip Joint : Total Hip Arthroplasty I ndication A lleviation of incapacitating arthritic pain in patients older than age 65 years whose pain could not be relieved sufficiently by non surgical means and for whom the only surgical alternative was resection of hip joint or arthrodesis

56. Ankle joint Surgical Treatment Arthroscopic debridement Arthrodesis Total ankle replacement

57. Foot Arthrodesis Subtalar arthrodesis Calcaneocuboid arthrodesis Talonavicular arthrodesis Double arthrodesis Triple arthrodesis

58. First MTP Joint OA Surgical Treatment Cheilectomy Osteotomy -Dorsiflexion phalangeal osteotomy -Metatarsal osteotomy Arthrodesis Arthroplasty - Hemiarthroplasty -Total joint arthroplasty

59. References Apley’s system of orthopedics and fractures, 9 th edition Robbins and cotran pathologic basis of disease,9 th edition Campbell’s operative orthopedics, 13 th edition