OSTEOARTHRITIS

OSTEOARTHRITIS

MODERATORDr Manjit SinghDr Sanjeev SreenDr Deepak VashishtDr R K Banga

Presented By- Kuldeep Rathi

• The term Osteoarthritis / osteoarthrosis / chondromalacic

arthrosis / degenerative arthritis / hypertrophic arthritis /

arthritis deformans is currently used to define an idiopathic ,

slowly progressive disease of diarthrodial ( synovial) joints.

• Characterized by degeneration of articular cartilage

• Leads to fibrillation, fissures, gross ulceration and finally

disappearance of the full thickness of articular cartilage

• Osteoarthritis (OA), the most common joint disease, is age related, affecting more than 80% of people over the age of 55.

• It is more common in women, especially after menopause.

• OA in weight-bearing joints is strongly linked to body mass index.

• OA has a predilection for finger joints, knees, hips, shoulders, and the spine.

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CLASSIFICATION

• Commonly Occurs• Without any type of injury or obvious

causePRIMARY OA

• Cause is Known• Due to another disease or conditionSECONDARY OA

Risk factors for osteoarthritis

Age Obesity Trauma Genetics (significant family history) Reduced levels of sex hormones Muscle weakness Repetitive use (ie, jobs requiring heavy labor and bending) Infection Crystal deposition Acromegaly

Previous inflammatory arthritis (eg, burnt-out rheumatoid arthritis)

Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, and Wilson disease)

Hemoglobinopathies (eg, sickle cell disease and thalassemia)

Neuropathic disorders leading to a Charcot joint (eg, syringomyelia, tabes dorsalis, and diabetes)

• Underlying morphologic risk factors (eg, congenital hip dislocation and slipped femoral capital epiphysis)

• Disorders of bone (eg, Paget disease and avascular necrosis)

• Previous surgical procedures (eg, meniscectomy)

Advancing age

• With advancing age there is reductions in cartilage volume, proteoglycan content, cartilage vascularization, and cartilage perfusion.

• These changes may result in certain characteristic radiologic features, including a narrowed joint space and marginal osteophytes.

• However, biochemical and pathophysiologic findings support the notion that age alone is an insufficient cause of osteoarthritis.

Obesity

• Obesity increases the mechanical stress in a weight-bearing joint.

• It has been strongly linked to osteoarthritis of the knees and, to a lesser extent, of the hips.

• In addition to its mechanical effects, obesity may be an inflammatory risk factor for osteoarthritis.

• Obesity is associated with increased levels (both systemic and intra-articular) of adipokines (cytokines derived from adipose tissue), which may promote chronic, low-grade inflammation in joints.

Other causes

• Trauma or surgery (including surgical repair of traumatic injury) involving the articular cartilage, ligaments, or menisci can lead to abnormal biomechanics in the joints and accelerate osteoarthritis.

• Insults to the joints may occur even in the absence of obvious trauma. Microtrauma may also cause damage, especially in individuals whose occupation or lifestyle involves frequent squatting, stair-climbing, or kneeling.

• Muscle dysfunction compromises the body’s neuromuscular protective mechanisms, leading to increased joint motion and ultimately resulting in osteoarthritis. This effect underscores the need for continued muscle toning exercises as a means of preventing muscle dysfunction.

• Valgus malalignment at the knee has been shown to increase the incidence and risk of radiographic progression of knee osteoarthritis involving the lateral compartment

Genetics

• A hereditary component, particularly in osteoarthritis presentations involving multiple joints, has long been recognize

• Genetics inheritance – non-mendilian

• genes potentially linked to OA – vitamin D receptor– estrogen receptor 1– inflammatory cytokines

• IL-1 – leads to catabolic effect

• IL-4• matrilin-3• BMP-2, BMP-5

Pathologic lesions

• Primary lesion appears to occur in cartilage• That Leads to inflammation in synovium &• Changes in subchondral bone, ligaments,

capsule, synovial membrane and periarticular muscles

In a healthy joint, the ends of bones are encased in smooth cartilage. Together, they are protected by a joint capsule lined with a synovial membrane that produces synovial fluid. The capsule and fluid protect the cartilage, muscles, and connective tissues.

With osteoarthritis, the cartilage becomes worn away. Spurs grow out from the edge of the bone, and synovial fluid increases. Altogether, the joint feels stiff and sore

Normal Cartilage

• Avascular, alymphatic and aneural tissue• Smooth and resilient• Allows shearing and compressive forces to

be dissipated uniformly across the joint

Structure of Normal Cartilage

Structure of Normal Cartilage

• Chondrocytes are responsible for metabolism of ECM

• They are embedded in ECM and do not touch one another, unlike in other tissues in the body

• Chondrocytes depend on diffusion for nutrients and therefore the thickness of cartilage is limited

• Extracellular matrix is a highly hydrated combination of proteoglycans and non-collagenous proteins immobilized within a type II collagen network that is anchored to bone

Structure of Normal Cartilage• Divided into four morphologically distinct zones:Superficial: flattened chondrocytes • high collagen-to-proteoglycan ratio and high water

content. • Collagen fibrils form thin sheet parallel to articular

surface giving the superficial zone an extremely high tensile stiffness

• Restricts loss of interstitial fluid, encouraging pressurization of fluid.

Transitional zone: • Small spherical chondrocytes• Higher proteoglycan and lower water content than

superficial zone• Collagen fibrils bend to form arcades

Radial Zone:• Occupies 90% of the column of articular cartilage• Proteoglycan content highest in upper radial zone• Collagen oriented perpendicular to subchondral bone

providing anchorage to underlying calcified matrix• Chondrocytes are largest and most synthetically active

in this zone

Calcified zone:• Articular cartilage is attached to the

subchondral bone via a thin layer of calcified cartilage

• During injury and OA, the mineralization front advances causing cartilage to thin

Function of Normal Cartilage

• Critically dependent on composition of ECM• Type II collagen fibres provide 3D fibrous

network which immobilizes PG and limits the extent of their hydration

• When cartilage compresses the water and solutes are expressed until repulsive forces from PGs balance load applied

Function of Normal Cartilage

• On removing load, PGs rehydrate restoring shape of cartilage

• Loading and unloading important for the exchange of proteins in ECM and thus to chondrocytes

• Chondrocytes continually replace matrix macromolecules lost during normal turnover

OA cartilage

• The equilibrium between anabolism and catabolism is weighted in favor of degradation

• Disruption of the integrity of the collagen network as occurs early in OA allows hyperhydration and reduces stiffness of cartilage

Degenerative cartilage

Mechanisms responsible for degradation

• Catabolism of cartilage results in release of breakdown products into synovial fluid which then initiates an inflammatory response by synoviocytes

• These antigenic breakdown products include: chondrointon sulfate, keratan sulfate, PG fragments, type II collagen peptides and chondrocyte membranes

Mechanisms responsible for degradation

• Activated synovial macrophages then recruit PMNs establishing a synovitis

• They also release cytokines, proteinases and oxygen free radicals (superoxide and nitric oxide) into adjacent and synovial fluid

• These mediators act on chondrocytes and synoviocytes modifying synthesis of PGs, collagen, and hyaluronic acid as well as promoting release of catabolic mediators

Microscopic Synovial changes

Pathophysiology

• Primary and secondary osteoarthritis are not separable on a pathologic basis, though bilateral symmetry is often seen in cases of primary osteoarthritis, particularly when the hands are affected.

• Traditionally, osteoarthritis was thought to affect primarily the articular cartilage of synovial joints; however, pathophysiologic changes are also known to occur in the synovial fluid, as well as in the underlying (subchondral) bone, the overlying joint capsule, and other joint tissues .

• Although osteoarthritis has been classified as a noninflammatory arthritis, increasing evidence has shown that inflammation occurs as cytokines and metalloproteinases are released into the joint.

• These agents are involved in the excessive matrix degradation that characterizes cartilage degeneration in osteoarthritis.Therefore, it is no longer appropriate to use the term degenerative joint disease when referring to osteoarthritis.

• In early osteoarthritis, swelling of the cartilage usually occurs, because of the increased synthesis of proteoglycans; this reflects an effort by the chondrocytes to repair cartilage damage.

• This stage may last for years or decades and is characterized by hypertrophic repair of the articular cartilage.

• As osteoarthritis progresses, however, the level of proteoglycans eventually drops very low, causing the cartilage to soften and lose elasticity and thereby further compromising joint surface integrity.

• Microscopically, flaking and fibrillations (vertical clefts) develop along the normally smooth articular cartilage on the surface of an osteoarthritic joint.

• Over time, the loss of cartilage results in loss of joint space.

• In major weight-bearing joints of persons with osteoarthritis, a greater loss of joint space occurs at those areas experiencing the highest loads. This effect contrasts with that of inflammatory arthritides, in which uniform joint-space narrowing is the rule.

• Erosion of the damaged cartilage in an osteoarthritic joint progresses until the underlying bone is exposed.

• Bone denuded of its protective cartilage continues to articulate with the opposing surface.

• Eventually, the increasing stresses exceed the biomechanical strength of the bone.

• The subchondral bone responds with vascular invasion and increased cellularity, becoming thickened and dense (a process known as eburnation) at areas of pressure.

• The traumatized subchondral bone may also undergo cystic degeneration, which is attributable either to osseous necrosis secondary to chronic impaction or to the intrusion of synovial fluid.

• Osteoarthritic cysts are also referred to as subchondral cysts, pseudocysts, and may range from 2 to 20 mm in diameter.

• Osteoarthritic cysts in the acetabulum are termed Egger cysts.

This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the acetabulum. Subcondral cyst.

• At areas along the articular margin, vascularization of subchondral marrow, osseous metaplasia of synovial connective tissue, and ossifying cartilaginous protrusions lead to irregular outgrowth of new bone (osteophytes).

• Fragmentation of these osteophytes or of the articular cartilage itself results in the presence of intra-articular loose bodies (joint mice).

• Along with joint damage, osteoarthritis may also lead to pathophysiologic changes in associated ligaments and the neuromuscular apparatus.

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STAGES OF OA (Stage 1) At the earliest stages of OA, joints look like this:

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STAGES OF OA (Stage 2) As Osteoarthritis progresses, it looks like this:

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STAGES OF OA (Stage 3) Advancing Osteoarthritis looks like this:

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STAGES OF OA (Stage 4) Patients with this level of OA usually have pain most of the time:

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STAGES OF OA (Stage 5) This is the end stage of disease. Note that there is no cartilage left on the end of the bone:

Pain mechanisms in osteoarthritis

• Pain, the main presenting symptom of osteoarthritis, is presumed to arise from a combination of mechanisms, including the following:

• Osteophytic periosteal elevation • Vascular congestion of subchondral bone, leading to increased intraosseous

pressure • Synovitis• Fatigue in muscles that cross the joint • Overall joint contracture • Joint effusion and stretching of the joint capsule • Torn menisci • Inflammation of periarticular bursae • Periarticular muscle spasm • Psychological factors • Central pain sensitization

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Vicious Cycle of Pain in OA Damage to Cartilage triggers

inflammation as the tissue tries to repair itself.

This Inflammation causes Pain, which can lead to a decrease in exercise and, in turn, to a loss in muscle tone and strength.

Less Exercise combined with Muscle Loss can lead to Weight Problems or Obesity, which can increase stress on the damaged joint and more cartilage breakdown.

PAIN

Reduced Mobility and Activity and

thus WEIGHT GAIN

Increased Joint Stress

Cartilage Deterioration

Synovitis

History

• The progression of osteoarthritis is characteristically slow, occurring over several years or decades.

• Early in the disease process, the joints may appear normal.

• However, the patient’s gait may be antalgic if weight-bearing joints are involved.

• Pain is usually the initial source of morbidity in osteoarthritis, with the disease’s primary symptom being deep, achy joint pain exacerbated by extensive use.

• PAIN WITH CHANGES OF WEATHER – pain intensified by lowered barometric pressure , which permits greater synovial swelling.

• Stiffness during rest (gelling) may develop, with morning

joint stiffness usually lasting for less than 30 minutes. • Initially, pain can be relieved by rest and may respond to

simple analgesics. • However, joints may become unstable as the

osteoarthritis progresses; therefore, the pain may become more prominent (even during rest) and may not respond to medications.

Physical Examination

• Physical examination findings are mostly limited to the affected joints.

• Reduced range of motion and crepitus are frequently present. • Malalignment with a bony enlargement may occur. • a bland effusion may be present. • muscle atrophy around a more severely affected joint may occur. • Osteoarthritis of the hand most often affects the distal

interphalangeal (DIP) joints but also typically involves the proximal interphalangeal (PIP) joints and the joints at the base of the thumb.

• Heberden nodes, which represent palpable osteophytes in the DIP joints, are more characteristic in women than in men.

• Inflammatory changes are typically absent or at least not pronounced.

Diagnostic Considerations

• The initial diagnostic goal is to differentiate osteoarthritis from other arthritis, such as rheumatoid arthritis.

• The history and physical examination findings are usually sufficient to diagnose osteoarthritis.

• Radiographic findings confirm the initial impression , and laboratory values are typically within the reference range.

• In Rheumatoid arthritis • Rheumatoid arthritis predominantly affects the wrists, as well as the

metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints.

• It rarely, if ever, involves the distal interphalangeal (DIP) joints or the lumbosacral spine.

• Rheumatoid arthritis is associated with prominent, prolonged (>1 hour) morning stiffness and overtly swollen, warm joints.

• Radiographic findings include bone erosion (eg, periarticular osteopenia or marginal erosions of bone) rather than formation.

• Systemic inflammation (elevated erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP] level)

• Positive serologies (rheumatoid factor [RF] or anti–cyclic citrullinated peptide [anti-CCP] antibodies)

• Inflammatory joint fluid with a predominance of polymorphonuclear leukocytes (PMNs)

Secondary osteoarthritismust be considered in individuals with any of the

following:• Chondrocalcinosis • History of joint trauma • Metabolic bone disorders • Hypermobility syndromes • Neuropathic diseases • The following disorders should also be considered in

the differential diagnosis:• Crystalline arthropathies (ie, gout and pseudogout) • Inflammatory arthritis (eg, rheumatoid arthritis)

• Seronegative spondyloarthropathies (eg, psoriatic arthritis and reactive arthritis)

• Septic arthritis or postinfectious arthropathy • Fibromyalgia • Tendonitis

Differential Diagnoses

• Avascular Necrosis• Fibromyalgia• Gout and Pseudogout• Imaging in Ankylosing Spondylitis• Imaging in Neuropathic Arthropathy

(Charcot Joint)• Lyme Disease• Psoriatic Arthritis• Rheumatoid Arthritis

• Osteoarthritis is typically diagnosed on the basis of clinical and radiographic evidence.

• No specific laboratory abnormalities are associated with osteoarthritis.

• Levels of acute-phase reactants are typically within the reference range in patients with osteoarthritis.

• The erythrocyte sedimentation rate (ESR) is not usually elevated, though it may be slightly so in cases of erosive inflammatory arthritis.

• The synovial fluid analysis usually shows a white blood cell (WBC) count below 2000/µL, with a mononuclear predominance.

Plain Radiography

• Plain radiography is the imaging method of choice because it is more cost-effective than other modalities and because radiographs can be obtained more readily and quickly.

• One important characteristic of primary osteoarthritis is that the abnormalities found in the load-bearing (ie, highly stressed) areas of the affected joint differ from those found in the non–load-bearing areas.

• In the load-bearing areas, radiographs can depict joint-space loss, as well as subchondral bony sclerosis and cyst formation

• Radiographs recommended views – weight-bearing views of affected joint

• optional views – knee

• sunrise view • PA view in 30 degrees of flexion

• findings – joint space narrowing – osteophytes – eburnation of bone– subchondral sclerosis – subchondral cysts

Radiographic Classification of Degenerative Joint Disease

KNEES

• Grade 0 - Normal• 1 - Doubtful narrowing of joint space and

possible osteophytic lipping• 2 - Definite osteophytes and possible

narrowing of joint space• 3 - Moderate multiple osteophytes,

definite narrowing of joint space, some sclerosis, and possible deformity of bone ends

• 4 - Large osteophytes, marked narrowing of joint space, severe sclerosis, and definite deformity of bone ends. Subchondral cysts may be present.

HIPS

• Grade 0 - Normal• 1 - Possible narrowing of joint space

medially and possible osteophytes around the femoral head

• 2 - Definite narrowing of joint space inferiorly, definite osteophytes, and slight sclerosis

• 3 - Marked narrowing of joint space, slight osteophytes, some sclerosis and cyst formation, and deformity of femoral head and acetabulum

• 4 - Gross loss of joint space with sclerosis and cysts, marked deformity of femoral head and acetabulum, and large osteophytes

• Magnetic resonance imaging (MRI) can depict many of the same characteristics of osteoarthritis that plain radiography can, but it is not necessary in most patients with osteoarthritis, unless additional pathology amenable to surgical repair is suspected.

• Pathology that can be seen on MRI includes joint narrowing, subchondral osseous changes, and osteophytes. Unlike radiography, MRI can directly visualize articular cartilage and other joint tissues (eg, meniscus, tendon, muscle, or effusion).

• Computed tomography (CT) is rarely used in the diagnosis of primary osteoarthritis. However, it may be used in the diagnosis of malalignment of the patellofemoral joint or of the foot and ankle joints.

• Currently, ultrasonography has no role in the routine clinical assessment of the patient with osteoarthritis. However, it is being investigated as a tool for monitoring cartilage degeneration, and it can be used for guided injections of joints not easily accessed without imaging.

Arthrocentesis

• A diagnostic joint aspiration for synovial fluid analysis can help exclude inflammatory arthritis, infection, or crystal arthropathy.

• The presence of noninflammatory joint fluid helps distinguish osteoarthritis from other causes of joint pain.

• Other synovial fluid findings that aid in the differentiation of osteoarthritis from other conditions are negative Gram stains and cultures, as well as the absence of crystals when fluid is viewed under a polarized microscope

Treatment• The goals of osteoarthritis treatment include alleviation of pain and

improvement of functional status.• Optimally, patients should receive a combination of

nonpharmacologic and pharmacologic treatment.• Nonpharmacologic interventions, which are the cornerstones of

osteoarthritis therapy, include the following:• Patient education • REST – with joint placed in such position to relax capsule and

ligaments, thereby minimizing the compression of articular surfaces.• RANGE OF MOTION – excess motion carried to extreme should be

avoided.• WEIGHT BEARING- using crutches or awalker

• VERTICAL LOAD REDUCTION- by reduction of weight or use of a cane in the opposite hand to the involved joint.

• TRACTION - during acute – inflammatory phase• PHYSICAL THERAPY- isometric excercises to build

muscle power while minimizing joint stress• BODY MECHANICS- by eliminating faulty posture,

applying shoes support• GRADUATED EXCERCISES- to improve and balance

muscle power acting about the joint.• WRM DRY CLIMATE

Surgical treatment

• Operative arthroscopic debridement – indications

• degenerative meniscal tears

• high tibial osteotomy – indications

• younger patients with unicompartmental disease

• unicompartmental arthroplasty (knee) – indications

• isolated unicompartmental disease

• total joint replacement – indications

• indicated for advanced disease

American Academy of Orthopaedic Surgeons guidelines

The AAOS recommends the following pharmacologic treatments for symptomatic osteoarthritis of the knee

• Oral NSAIDs • Topical NSAIDs • Tramadol

The AAOS was unable to recommend for or against the use of the following for symptomatic knee osteoarthritis:

• Acetaminophen • Opioids • Pain patches • Intra-articular corticosteroid injections • Growth factor injections and/or platelet rich plasma

• The recommendation on acetaminophen is a downgrade from the previous AAOS guideline, and reflects the use of new criteria that resulted in the selection of only one study, which found no statistical significance or minimum clinically important improvement with acetaminophen compared with placebo.

The AAOS does not recommend treatment with any of the following:

• Intra-articular hyaluronic acid • Glucosamine and/or chondroitin sulfate or hydrochloride

Intra-articular injections

• Intra-articular pharmacologic therapy includes injection of a corticosteroid or sodium hyaluronate (ie, hyaluronic acid [HA] ), which may provide pain relief and have an anti-inflammatory effect on the affected joint.

• Ultrasound guidance can facilitate arthrocentesis and injection

Corticosteroid• After the introduction of the needle into the joint and before steroid

administration, aspiration of as much synovial fluid as possible should be attempted.

• Aspiration often provides symptomatic relief for the patient and allows laboratory evaluation of the fluid, if necessary.

• Infected joint fluid and bacteremia are contraindications to steroid injection.

• In patients with osteoarthritic knee pain, steroid injections generally result in clinically and statistically significant pain reduction as soon as 1 week after injection.

• The effect may last, on average, anywhere from 4 to 6 weeks per injection, but the benefit is unlikely to continue beyond that time frame.

• For hip osteoarthritis, a randomized, placebo-controlled study confirmed the effectiveness of corticosteroid injection, with benefits often lasting as long as 3 months.

• Some controversial evidence exists regarding frequent steroid injections and subsequent damage to cartilage (chondrodegeneration).

• Accordingly, it is usually recommended that no more than three injections per year be delivered to any individual osteoarthritic joint.

• Systemic glucocorticoids have no role in the management of osteoarthritis.

Sodium hyaluronate

• Intra-articular injection of sodium hyaluronate, also referred to as viscosupplementation, has been shown to be safe and possibly effective for symptomatic relief of knee osteoarthritis.

• Intra-articular HAs approved by the FDA for the treatment of osteoarthritic knee pain include the naturally extracted, non–cross-linked sodium hyaluronate products Hyalgan, Supartz, Orthovisc, and Euflexxa, as well as the cross-linked sodium hyaluronate product known as hylan G-F 20 (Synvisc).

• The exact mechanisms of action through which HAs provide symptomatic relief are unknown.

Possible mechanisms include direct binding to receptors (CD44 in particular) in the synovium and cartilage that can lead to several biologic activation pathways

• The HA class in general has demonstrated a very favorable safety profile for chronic pain management in knee osteoarthritis, with the most common adverse event being injection-site pain

Arthroscopy

• A procedure of low invasiveness and morbidity, arthroscopy will not interfere with future surgery.

• However, a randomized, controlled trial in patients with moderate-to-severe osteoarthritis found that arthroscopic surgery for osteoarthritis of the knee provided no additional benefit beyond that afforded by optimized physical and medical therapy.

• Arthroscopy is indicated for removal of meniscal tears and loose bodies; less predictable arthroscopic procedures include debridement of loose articular cartilage with a microfracture technique and cartilaginous implants in areas of eburnated subchondral bone .

• These treatments have varying success rates and should be performed only by surgeons experienced in arthroscopic surgical techniques.

• Overall, arthroscopy is not recommended for nonspecific “cleaning of the knee” in osteoarthritis.

OA Spine

• OA may affect any level of the spine, but most commonly occurs at C5, T8, and L3, the areas of greatest spinal flexibility.

• Joints of the spine include cartilaginous joints, nucleus pulposus of the intervertebral discs; synovial lined apophyseal joints; cervical pseudoarthroses called uncovertebral joints; and fibrous articulation, the annulus fibrosus of the intervertebral discs .

• OA will typically affect all spinal joints in the same area, but features of disease at each joint type are described separately for clarity.

• Intervertebral (osteo)chondrosis is primary degeneration of the nucleus pulposus of the intervertebral discs.

• Radiographs reveal progressive uniform or nonuniform narrowing of the disc space and reactive subchondral sclerosis at the vertebral endplate with osteophytes extending from the anterolateral vertebral margins.

• Progressive desiccation or rupture of the disc will sometimes allow gas to appear in the disc substance, which on radiographs will appear as a thin linear lucency within the disc (vacuum sign) seen on extension and often disappearing on flexion .

• The vacuum sign helps to exclude infection as a cause of disc space loss.

• Discogenic low back pain caused by ruptured discs is typically worsened by flexing the spine, which increases pressure on the disc, and likewise decreased by extension of the spine, or by lying supine.

vacuum sign

Schmorl's nodes in the lumbar spine

The degenerating disc may herniate into the adjacent vertebral body, producing a Schmorl node , or impinge on the spinal cord, causing spinal stenosis.

OA of the synovial apophyseal, or facet joints,

• is characterized by joint space narrowing, marginal osteophytes, and bony sclerosis.• Lumbar facet disease may produce central low back pain that worsens on extension,

which loads the facet joints and decreases with flexion.• Osteophytes and hypertrophy of the joint capsule may cause spinal stenosis by

encroaching onto the spinal cord or the nerve roots at the intervertebral foramina.• Pain due to stenosis may radiate below the knee, worsen with exertion and extension,

and resolve with rest or by bending forward, a pattern known as neurogenic claudication or pseudoclaudication.

• Concurrent intervertebral disc degeneration worsens intersegmental instability and increases the load on the lumbar facet joints, which can lead to subluxation of the joints, allowing the forward movement of one vertebral body over another (spondylolisthesis).

• In the cervical spine, the posterior margins of the vertebral bodies project slightly beyond the disc to form pseudoarthroses called uncovertebral joints.

• Osteophytes at both the uncovertebral and facet joints can cause cervical spinal stenosis.

• Spondylosis deformans refers to degenerative disease of the annulus fibrosus of the intervertebral disc and is characterized by formation of large osteophytes along the anterior and lateral aspects of the spine.

• Osteophytes of axial OA are oriented horizontal to their point of origin, which distinguishes them from the fine, vertically oriented syndesmophytes of the inflammatory spondyloarthropathies

• Axial osteophytes of OA also differ from the paravertebral hyperostoses of diffuse idiopathic skeletal hyperostosis or DISH.

• In DISH, there is ossification of the paravertebral ligaments, particularly at the anterolateral aspects of the vertebral bodies, producing upward or downward pointing hyperostoses, which are sometimes bridging, appearing to flow like candle wax from one vertebra to the next.

Spondyloarthropathy

AP radiograph of the thoracolumbar spine shows ossification of interspinous ligament (open arrow) and syndesmophytes (white arrow). Note the ossification of iliolumbar ligament (black arrow).

OA

Xray of the lumbar spine shows scoliosis and narrowing of the intervertebral spaces on the concave side where extensive osteophyte formation is present

• In general, anteroposterior (AP), lateral, and lumbosacral spot radiographs are adequate to diagnose OA of the spine, and oblique views of the lumbar spine to show the facet joints are not usually necessary.

• Magnetic resonance imaging (MRI), or alternatively, computed axial tomography (CT), are necessary to diagnose herniated vertebral discs and/or lumbar spinal stenosis.

• It is important to make a specific diagnosis when these problems are suspected, as physical therapy designed to alleviate one disorder may aggravate the other.

Sacroiliac Joints

• OA of the sacroiliac joint occurs frequently in older individuals and presents on radiographs as asymmetric joint space narrowing, osteophytes at the inferior aspect of the joint, and distinct sclerotic joint margins.

• The finding of pseudowidened joint spaces, indistinct joint margins, and erosions or fusion of the joint, particularly in a young person, suggests the presence or aftermath of an inflammatory sacroiliitis, rather than OA.

Management

PREVENTION• Direct trauma to spine whether or not fracture ,

require a period of rest inrecumbency untill hemorrhage ,edema are absorbed, ligament regain their strength and integrity of articular cartilage is restored.

• Change of occupation or reduction of work hours will prevent muscle fatigue

• A program of carefully graduated exercises • Maintainance of muscle strenth is the key to retarding

degeneration of spine

Conservative

• Bed rest – in position of greatest comfort• Heat• Massage• Traction• Excercises

pharmacotherapy

• Salicylates• Mainstay

• Oral corticosteroids • Rarely indicated for associated

rheumatoid disease

Surgical

• Spinal fusion • Specially for L-S arthritis/ traumatic

arthritis• Foraminotomy• Removal of osteophyte• Removal of raptured disc

OA Hip

ETIOLOGY• Incongruity of articular cartilage• After perthes ds / fracture

• Instability – causes abnormal mechanical stresses eg subluxation , dysplasia of hip

• Avascular necrosis of femoral head• Concentration of pressure load over small area - as in

coxa vara/ anteversion• Direct injury – infection• ideopathic

pathogenesis

• In normal mechanism of standing hip is stable in extension , slight abduction, and in slight int. rotation

• The anterior and inferior Capsule is taut in this position

• Progressive fibrosis thickens the synovium, sub-synovial tissue and overlyuing capsule

• With Thickening & shortening and loss of elasticity of INFERIOR capsule femur is pulled into opposite deformity of flexion, adduction and internal rotation

• Any attempt to attain standing position impososes sever stretching of inf capsule, which is supplied by obturater nerve causing pain

• obturater nerve also supplies the adducters, which undergo reflex spasm and increasing the deformity

Clinical picture

• Repeated attacks of slight pain• Protected limp• Tenderness• Muscle spasm• Flexion, Adduction, Internal Rotation

deformity• Limitation of motion• Fabere test may prove diagnostic

Clinical examination

• One should record• Limp, antalgic or trendelenburg• Position in which hip is least painful• Amt of apparent shortening or lengthening• Fixed adduction or abduction deformity• Degree of passive adduction or abduction• Amt of fixed flexion deformity• Degree of fixed rotation• Amt of passive int. & ext. rotation

treatment

• SURGICAL-• Aim is to relieve pain

• INTERTROCHANTERIC OSTEOTOMY• I/C• Relief of pain• Correction of deformity• Reversal of degenerative process

• When the joint motion is greatly restricted ( <70 degree flexion) osteotomy is of no value

Various osteotomies

• Varus osteotomy of pauwels• Valgus osteotomy• Displacement osteotomy alone• An INTERTROCHANTERIC OSTEOTOMY will effect

satisfactory reduction or complete relief of pain, will correct deformity and provide stability but will not increase the joint motion.

• For young and middle aged patients, regardless of the stage of disease, osteotomy that does not pose the risk of THR is preferred procedure.

HIP REPLACEMENT

• Implantating an artificial femoral head and socket to replace the degenerated joint will relieve pain while preserving the motion and stability.

Treatment of OA KNEE

Surgical debridement

• Surgical debridement of the osteoarthritic knee generally includes limited synovectomy, excision of osteophytes, removal of loose bodies, chondroplasty, and removal of damaged menisci.

• Satisfactory results have been reported after open debridement of an osteoarthritic knee

PROXIMAL TIBIAL OSTEOTOMY

• High tibial osteotomy is a well-established procedure for the treatment of unicompartmental osteoarthritis of the knee.

• The biomechanical rationale for proximal tibial osteotomy in patients with unicompartmental osteoarthritis of the knee is “unloading” of the involved joint compartment by correcting the malalignment and redistributingthe stresses on the knee joint

• The indications for proximal tibial osteotomy are• (1)pain and disability resulting from osteoarthritis that

significantly interfere with high-demand employment or recreation And

• (2) evidence on weight-bearing radiographs of degenerative arthritis that is confined to one compartment with a corresponding varus or valgus deformity.

• The patient must be able to use crutches or a walker and have sufficient muscle strength and motivation to carry out a rehabilitation program.

Contraindications to a proximal tibial osteotomy are• (1) narrowing of lateral compartment cartilage space, • (2) lateral tibial subluxation of more than 1 cm,• (3) medial compartment tibial bone loss of more than 2

or 3 mm, • (4) flexion contracture of more than 15 degrees, • (5) knee flexion of less than 90 degrees, • (6) more than 20 degrees of correction needed,• (7) inflammatory arthritis, and• (8) significant peripheralvascular disease

Various HTO

• LATERAL CLOSING WEDGE OSTEOTOMY• MEDIAL OPENING WEDGE TIBIAL OSTEOTOMY• DISTAL FEMORAL OSTEOTOMIES

LATERAL CLOSING WEDGE OSTEOTOMY

A, Medial joint collapse resultingin varus deformity and medial knee pain.B, After high tibial osteotomy

KNEE ARTHROPLASTY

• Surgery Indicated for PAIN, continuously disabling and refractory to

conservative measuresRepeated acute attacks of locking, pain and

effusion or hemarthrosisInstabilityDeformityProgressive limitation of motion.