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)


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


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


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


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




deficiencies

Loading factors


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


Local factors

• Previous damage




deficiencies

Loading factors


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


Local factors

• Previous damage




deficiencies

Loading factors


physical activities

RISK FACTORS

Weakness in the quadriceps muscles bridging the knee

Systemic factors


Local factors

• Previous damage

• Bridging muscle weak



deficiencies

Loading factors


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


Local factors

• Previous damage


• Increased bone density


deficiencies

Loading factors


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


Local factors

• Previous damage




deficiencies

Loading factors


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


Local factors

• Previous damage




deficit

Loading factors


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


Local factors

• Previous damage




deficiencies

Loading factors


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


Local factors

• Previous damage




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



Chondroplasty


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



Chondroplasty


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)





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





• 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





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”


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


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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Knee Osteoarthritis

Health & Medicine

Transcript of Knee Osteoarthritis