Download - Knee Osteoarthritis
OSTEOARTHRITIS OF THE KNEE
OA = JOINT FAILURE
The pathologic sine qua non - hyaline articular cartilage loss, present in a focal and, initially, non-uniform manner.
Accompanied by increasing thickness and sclerosis of the subchondral bony plate, by outgrowth of osteophytes at the joint margin, by stretching of the articular capsule, by mild synovitis in many affected joints, and by weakness of muscles bridging the joint.
JOINT PROTECTIVE MECHANISMS AND THEIR FAILURE
Synovial fluid
Joint capsule and ligaments
Muscles and tendons
Sensory afferents
Cartilage
By providing a limit to excursion, thereby fixing the ROM
Reduces friction between articular surfaces
The ligaments, overlying skin and tendons have mechanoreceptor sensory afferent nerves which fire at different frequencies throughout a joint's ROM, providing feedback by way of the spinal cord to muscles and tendons to anticipate joint loading
Focal stress across the joint is minimized by muscle contraction that decelerates the joint before impact and assures that when joint impact arrives, it is distributed broadly across the joint surface.
CARTILAGE AND ITS ROLE IN JOINT FAILURE
Two major macromolecules in cartilage Type 2 collagen (tensile strength) Aggrecan (proteoglycan
macromolecule linked with hyaluronic acid, which consists of highly negatively charged glycosaminoglycans)
CARTILAGE AND ITS ROLE IN JOINT FAILURE
Mechanical and osmotic stress on chondrocytes induces these cells to alter gene expression and increase production of inflammatory cytokines and matrix-degrading enzymes Type 2 cartilage is degraded
primarily by MMP-13 (collagenase 3) Aggrecan degradation is by two
aggrecanases (ADAMTS-4 and ADAMTS-5) and perhaps of MMPs
CARTILAGE AND ITS ROLE IN JOINT FAILURE
Both collagenase and aggrecanases act primarily in the territorial matrix surrounding chondrocytes normally
However, as the osteoarthritic process develops, their activities and effects spread throughout the matrix, especially in the superficial layers of cartilage
CARTILAGE AND ITS ROLE IN JOINT FAILURE
The synovium and chondrocytes synthesize numerous growth factors and cytokinesChief among them is interleukin (IL) 1
Transcriptional effects on chondrocytes
Stimulates proteinases Suppresses cartilage matrix synthesis
Tumor necrosis factor (TNF) may play a similar role
CARTILAGE AND ITS ROLE IN JOINT FAILURE
These cytokines also induce chondrocytes to synthesize - Prostaglandin E2 Nitric oxide (inhibits aggrecan
synthesis and enhances proteinase activity)
Bone morphogenic protein 2 (BMP-2) -stimulates anabolic activity
Healthy cartilage is metabolically sluggish, with slow matrix turnover and synthesis and degradation in balance, cartilage in early OA or after an injury is highly metabolically active.
It is characterized by gradual depletion of aggrecan, an unfurling of the tightly woven collagen matrix, and loss of type 2 collagen.
Loses its compressive stiffness
Increasing vulnerability of cartilage
DERANGED BIOCHEMICAL PROCESSES AND STRUCTURE MODIFYING TREATMENTS
RISK FACTORS
Most potent risk factor for OA Aged cartilage is less responsive to dynamic
loading (i.e. less matrix synthesized) Joint protectors fail more with age
Muscles that bridge become weaker Sensory nerve input slows with age, retarding
the feedback loop of mechanoreceptors Ligaments stretch with age
Systemic factors
• Increased age
• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increasing bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORS
Hormone loss with menopause may contribute to this risk, there is little understanding to this.
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increasing bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORS
Highly heritable disease, but varies by joint. 50% percent of the hand and hip OA is attributable
to inheritance However, this is 30% in knee OAEmerging evidence has identified high risk genetic mutations e.g. polymorphism within Growth Differentiation Factor 5 gene Decreases GDF5 (normally has anabolic effects on the synthesis of cartilage matrix)
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increasing bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORS
Fracture through the joint surface Avascular necrosis Tears of ligamentous and fibrocartilaginous
structures, such as the ACL and meniscus (knee) and labrum (hip)
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increasing bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORS
Weakness in the quadriceps muscles bridging the knee
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weak
• Increasing bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORS
The role of bone in serving as a shock absorber for impact load is not well understood, but persons with increased bone density are at high risk of OASuggests that resistance of bone to impact during joint use may play a role in disease development
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increased bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORSMalalignment increases stress on a focal area of cartilage, which then breaks down
Varus knees - exceedingly high risk of cartilage loss in the medial or inner compartment
Valgus malalignment predisposes to rapid cartilage loss in the lateral compartment.
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increasing bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORS
Patients have impaired proprioception across their knees, and this may predispose them to further disease progression
Several studies have shown that proprioceptive acuity in OA knee may be improved with interventions as simple as an elastic bandage, neoprene sleeve, bracing, or exercise
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increasing bone density
• Mal-alignment• Proprioceptive
deficit
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORS
It is a stronger risk factor for disease in women than in men, Not only is obesity a risk factor for OA in weight-bearing joints, but obese persons have more severe symptoms from the disease
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increasing bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious
physical activities
RISK FACTORS
Workers performing repetitive tasks as part of their occupations for many years are at high risk of OA in those joints
One reason why workers may get disease is that during long days at work, their muscles may gradually become exhausted, no longer serving as effective joint protectors
In a study, compared to non runners, professional runners in Olympics had high risks of both knee and hip OA
Systemic factors
• Increased age• Female• Genetics
Local factors
• Previous damage
• Bridging muscle weakness
• Increasing bone density
• Mal-alignment• Proprioceptive
deficiencies
Loading factors
• Obesity• Injurious phys.
activity
SOURCES OF PAIN
Cartilage is aneural. Its loss in a joint is not accompanied by pain. Thus, pain in OA likely arises from innervated structures in the joint
Synovium, Ligaments Joint capsule Muscles Subchondral bone.
Most of these are not visualized by the x-ray, and the severity of x-ray changes in OA correlates poorly with pain severity.
SOURCES OF PAIN
Based on MRI studies in OA knees comparing those with and without pain likely sources of pain include Synovial inflammation Joint effusions - Capsular stretching from fluid in the joint stimulates
nociceptive fibres Bone marrow edema – it signals the presence of microcracks and scar,
which are the consequences of trauma. May stimulate bone nociceptive fibers
Osteophytes - When they grow, neurovascular innervation penetrates through the base of the bone and into the developing osteophyte
Outside the joint also, including bursae - Common sources of pain near the knee are anserine bursitis and iliotibial band syndrome.
CLINICAL FEATURES
Joint pain - activity-related. Pain comes on either during or just after joint use and then gradually resolves. Examples include
knee or hip pain with going up or down stairs, pain in weight-bearing joints when walking, and, for hand OA, pain when cooking.
Early in disease, pain is episodic, triggered often by a day or two of overactive use of a diseased joint
As disease progresses, the pain becomes continuous and even begins to be bothersome at night. Stiffness of the affected joint may be prominent, but morning stiffness is usually brief (<30 min). In knees, buckling may occur, in part, due to weakness of Quads
CLINICAL FEATURES
No blood tests are routinely indicated for workup of patients with OA unless symptoms and signs suggest inflammatory arthritis.
Examination of the synovial fluid is often more helpful diagnostically than an x-ray. If the synovial fluid white count is >1000 per L, inflammatory arthritis or gout or pseudogout are likely, the latter two being also identified by the presence of crystals.
ACR RADIOLOGIC AND CLINICAL CRITERIA FOR OA
THE WOMAC (WESTERN ONTARIO AND MCMASTER UNIVERSITIES) INDEXTO MONITOR THE COURSE OF THE DISEASE OR EFFECTIVENESS OF MEDICATIONS
Pain: (1) walking (2) stair climbing (3) nocturnal (4) rest (5) weight bearing
(7) getting in or out of car (8) going shopping (9) putting on socks (10) rising from bed (11) taking off socks (12) lying in bed (13) Getting in and out of bath (14) sitting (15) getting on or off toilet (16) heavy domestic duties (17) light domestic duties
Stiffness: (1) morning stiffness (2) stiffness occurring later in the dayPhysical function: (1) descending stairs (2) ascending stairs (3) rising from sitting (4) standing (5) bending to floor (6) walking on flat surface
Interpretation: • minimum total score: 0 • maximum total score: 96 • minimum pain subscore: 0 • maximum pain subscore: 20 • minimum stiffness subscore: 0 • maximum stiffness subscore: 8 • minimum physical function subscore: 0 • maximum physical function subscore: 68
Scoring and Interpretation -Response Points none 0 slight 1 moderate 2 severe 3 extreme 4
THE WOMAC (WESTERN ONTARIO AND MCMASTER UNIVERSITIES) INDEXTO MONITOR THE COURSE OF THE DISEASE OR EFFECTIVENESS OF MEDICATIONS
RADIOGRAPHS AND OTHER MODALITIES Knee joint using the extended-knee radiograph,
which is a bilateral AP image acquired while the patient is weight-bearing
Kellgren-Lawrence Grading Scale Grade 1: doubtful narrowing of joint space and
possible osteophytic lipping Grade 2: definite osteophytes, definite
narrowing of joint space Grade 3: moderate multiple osteophytes,
definite narrowing of joints space, some sclerosis and possible deformity of bone contour
Grade 4: large osteophytes, marked narrowing of joint space, severe sclerosis and definite deformity of bone contour
OTHERS MRI useful to exclude AVN, stress fractures,
occult fractures, inflammatory arthropathy Ultrasound is gaining popularity and is finding
increasing role in detecting small effusions, earl cartilage changes. It also is an adjunct for accurate aspiration and intraarticular injections
MANAGEMENT
NON-PHARMACOLOGIC RECOMMENDATIONS FOR THE MANAGEMENT OF KNEE OA - ACR
Strongly recommended- Participate in cardiovascular (aerobic) and/or resistance land-based exercise Participate in aquatic exercise Lose weight (for persons who are overweight)
NON-PHARMACOLOGIC RECOMMENDATIONS FOR THE MANAGEMENT OF KNEE OA - ACRConditionally recommended - Receive physical therapy with supervised exercise Psychosocial interventions Use medially directed patellar taping Wear medially wedged insoles if they have lateral compartment OA Wear laterally wedged insoles if they have medial compartment OA Use of thermal agents Walking aids Be treated with traditional Chinese acupuncture* Be instructed in the use of transcutaneous electrical stimulation*
NON-PHARMACOLOGIC RECOMMENDATIONS FOR THE MANAGEMENT OF KNEE OA
No recommendations regarding: Participation in balance exercises, either alone or in combination with strengthening
exercises Wearing knee braces Using laterally directed patellar taping
PHARMACOLOGIC RECOMMENDATIONS FOR KNEE OA - ACR
Conditionally recommend Acetaminophen Oral NSAIDs and Topical NSAIDs Tramadol Intraarticular corticosteroid injectionsConditionally recommend that patients with knee OA should not use the following: Chondroitin sulfate Glucosamine Topical capsaicinNo recommendations regarding the use of Intraarticular hyaluronates, and duloxetine
Acetaminophen Up to 1 g qidOral NSAIDs and COX-2 inhibitorsa
Naproxen 375–500 mg bid Salsalate 1500 mg bid Ibuprofen 600–800 mg 3–4 times a day
Topical NSAIDs Diclofenac Na 1% gel 4gm qid (for knees) Capsaicin 0.025–0.075% cream qid Opiates Various
Intraarticular injections Hyaluronans
Steroids
Varies from 3–5 weekly injections depending on preparation
NEUTRACEUTICALS
Two nutritional supplements – Glucosamines and chondroitin sulphate Some studies have shown that they stimulate glycosamines and proteoglycan synthesis They might also inhibit IL-1 and TNF medicated NO production
PLATELET RICH PLASMA INJECTIONS
Wang-Saegusa et al investigated 312 patients with knee OA. The patients were given 3 injections of plasma-rich plasma at 2-week intervals. At 6 months, the patients reported a significant improvement in pain, stiffness, function.
Theories to explain the mechanism - Proliferation of autologous chondrocytes and mesenchymal stem cells were demonstrated after
platelet-rich plasma exposure in an ovine model Increased hyaluronic acid secretion has also been noted in the presence of platelet-rich rather
than platelet-poor preparation Human osteoarthritic chondrocytes exposed to platelet-rich plasma demonstrated less interleukin-
1β-induced inhibition of collagen 2 and aggrecan gene expression, and diminished nuclear factor-B activation, which are pathways involved in osteoarthritis pathogenesis.
Thus studies suggest that platelet-rich plasma may play a role in improving clinical outcomes in patients with early onset osteoarthritis at both 6 months and 1 year
SURGICAL PROCEDURES
Débridement, Osteochondral or chondrocyte transplantation High tibial osteotomy Distal femoral osteotomy Arthroplasty Arthrodesis
Because of the progressive nature of the disease, many patients eventually require operative treatment
DÉBRIDEMENT
Open ArthroscopicLess postop pain Shorter rehab
Symptoms recurPainfulOften 6 months of postop rehab
Rarely used
Osteophytes excision
Loose bodies removal
Chondroplasty
Damaged menisci removal
DÉBRIDEMENT
Osteophytes excision
Loose bodies removal
Chondroplasty
Damaged menisci removal
Simple smoothing chondroplasty
Abrasion chondroplasty
surgery of the articular cartilage
• Loose fragments removed• Area and edges smoothed over using mechanized
shaver
Articular surface damaged such that underlying bone is exposed
Superficial abrasion of the bone surface by a rotatory 4.5mm burr. bleeding surface over the next 6 weeks forms scar tissue substitute for the original articular cartilage
6 week period using crutches for the recovery and healing
DÉBRIDEMENT
Osteophytes excision
Loose bodies removal
Chondroplasty
Damaged menisci removal
The abrasion chondroplasty has largely been replaced by the micro-fracture technique
Pierce exposed bone with a pick Bleeding of the underlying bone but preserves the structure of the bone surface
6 weeks on crutches is still necessary to allow proper healing of the defect after surgery
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
Osteochondral cylinder of a non-weight-bearing part of the femur condyle harvested transplanted in the defective portion of a weight-bearing partSingle large bone plug or multiple small plugs (mosaicplasty)
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
For larger lesions (2 to 3.5 cm)Allografts from a fresh osteoarticular size-matched hemicondyle Disadvantage - patients must be “on call” for immediate surgery when a suitable graft becomes available
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
For larger lesions (2 to 3.5 cm)Allografts from a fresh osteoarticular size-matched hemicondyle Disadvantage - patients must be “on call” for immediate surgery when a suitable graft becomes available
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
For larger lesions (2 to 3.5 cm)Allografts from a fresh osteoarticular size-matched hemicondyle Disadvantage - patients must be “on call” for immediate surgery when a suitable graft becomes available
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
For larger lesions (2 to 3.5 cm)Allografts from a fresh osteoarticular size-matched hemicondyle Disadvantage - patients must be “on call” for immediate surgery when a suitable graft becomes available
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
• Lesions up to 10 cm or for multiple lesions. • Small amount of articular cartilage removed for
growing of the autologous chondrocytes cells cultured 3 to 6 weeks implant the cells in the chondral defect under periosteal graft
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
• Lesions up to 10 cm or for multiple lesions. • Small amount of articular cartilage removed for
growing of the autologous chondrocytes cells cultured 3 to 6 weeks implant the cells in the chondral defect under periosteal graft
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
• Lesions up to 10 cm or for multiple lesions. • Small amount of articular cartilage removed for
growing of the autologous chondrocytes cells cultured 3 to 6 weeks implant the cells in the chondral defect under periosteal graft
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
• Lesions up to 10 cm or for multiple lesions. • Small amount of articular cartilage removed for
growing of the autologous chondrocytes cells cultured 3 to 6 weeks implant the cells in the chondral defect under periosteal graft
OSTEOCHONDRAL OR CHONDROCYTE TRANSPLANTATION
Osteochondral Autograft Transplant System (OATS)
Osteochondral allografting
Autologous chondrocyte implantation (ACI)
Satisfactory short-term results have been reported• However data are insufficient
• Indications are limited and include isolated, full-thickness, grade IV femoral defect.
• Patients must be willing to restrict activity for 12 months to allow the new cartilage to mature
PROXIMAL TIBIAL OSTEOTOMY
Well-established procedure for unicompartmental OA knee Varus or valgus deformities cause an abnormal distribution of the weight-bearing
stresses Most common is varus position degenerative changes in the medial part Biomechanical rationale in unicompartmental OA is “unloading”
PROXIMAL TIBIAL OSTEOTOMY
Indications - Pain and disability resulting from OA that significantly interfere with high-demand
employment or recreation Evidence on weight-bearing X-ray of degenerative arthritis that is confined to one
compartment (corresponding varus or valgus deformity) Able to use crutches/walker and have sufficient muscle strength and motivation to carry
out a rehab program
PROXIMAL TIBIAL OSTEOTOMY
Contraindications - Narrowing of lateral compartment cartilage space Lateral tibial subluxation of more than 1 cm Medial 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 Significant peripheral vascular disease.
TOTAL KNEE ARTHROPLASTY AFTER PROXIMAL TIBIAL OSTEOTOMY At 10 to 15 years after proximal tibial osteotomy, 40% of patients require conversion
to total knee arthroplasty. Most series of total knee arthroplasties after proximal tibial osteotomies report slightly lower rates of good and excellent clinical results than those reported for primary total knee arthroplasty.
DISTAL FEMORAL OSTEOTOMY If the valgus deformity at the knee is more than 12 to 15 degrees, or the plane of
the knee joint deviates from the horizontal by more than 10 degrees, Coventry recommended a distal femoral varus osteotomy rather than a proximal tibial
varus osteotomy.
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