eMedicine Specialties > Rheumatology > Introduction

The Approach to the Painful Joint

Author: Alan Baer, MD, Associate Professor of Medicine, Department of Medicine, Johns Hopkins University; Clinical Director, Johns Hopkins Rheumatology Practice at Good Samaritan Hospital; Chief of Rheumatology, Good Samaritan Hospital
Coauthor(s): Vinod Patel, MD, Medical Director, Jefferson Family Medicine Center; Clinical Assistant Professor, Department of Family Medicine, State University of New York at Buffalo; Robert McCormack, MD, Associate Professor of Clinical Emergency Medicine, University at Buffalo School of Medicine and Biomedical Sciences
Contributor Information and Disclosures

Updated: Jan 2, 2009

Introduction

Background

Joint pain can be caused by diverse processes, including inflammation, cartilage degeneration, crystal deposition, infection, and trauma. The differential diagnoses of joint pain are generated in large part from the history and physical examination.¹ Screening laboratory test results serve primarily to confirm clinical impressions and can be misleading if used indiscriminately. The initial aim of the evaluation is to localize the source of the joint symptoms and to determine the type of pathophysiologic process responsible for their presence.

Pathophysiology

Joint pain may arise from structures within or adjacent to the joint or may be referred from more distant sites. Sources of pain within the joint include the joint capsule, periosteum, ligaments, subchondral bone, and synovium, but not the articular cartilage, which lacks nerve endings. Determination of the anatomic part responsible for joint pain is often a difficult yet critical task, since it guides the approach to diagnosis and therapy. Knowledge of the anatomy of complex joints, such as the knee, shoulder, and ankle, aids in this assessment.

The evaluation of joint pain, both in terms of the history and the physical examination findings, is best achieved through an understanding of the basic pathophysiologic types of joint disease. These include synovitis, enthesopathy, crystal deposition, infection, and structural or mechanical derangements. These types of joint disease are not mutually exclusive. Examples of pathologic processes that commonly coexist include crystal deposition in osteoarthritis, synovitis in enthesopathies, and cartilage destruction in chronic synovitis.

Synovitis

The synovial membrane is the principal site of inflammation in persons with rheumatoid arthritis (RA) and many other inflammatory arthritides.² Synovitis is characterized pathologically by neovascularization; infiltration of the synovium with lymphocytes, plasma cells, and macrophages; and synovial lining cell hyperplasia. These cause synovial proliferation, recognized clinically by warmth, tenderness, and a boggy consistency of the soft tissues overlying the involved joint. The inflamed synovium may infiltrate and erode intra-articular bone and cartilage.

Enthesitis

The enthesis is the transitional zone where collagenous structures such as tendons and ligaments are interwoven into bone.³ Other examples of entheses include the interface between cortical bone and the periosteum and between vertebral bodies and the annulus fibrosus. It is the principal site of pathology in the seronegative spondyloarthropathies. As a result of inflammation at these interfaces, the radially oriented collagen fibers undergo metaplasia, forming fibrous bone. These metaplastic transformations result in new bone formation (periostitis), gradual ossification of syndesmoses (eg, the sacroiliac joints), and syndesmophyte formation along the outer fibers of the vertebral discs. When enthesitis occurs in a diarthrodial joint, a secondary synovitis may develop.

Crystal deposition

The deposition of crystals in articular structures may lead to symptomatic joint disease. The responsible crystals include monosodium urate, calcium pyrophosphate dihydrate, basic calcium phosphate (including hydroxyapatite), and calcium oxalate.

Monosodium urate crystal deposition occurs on the surface of hyaline cartilage, within the synovium and in periarticular structures, including tendon sheaths and bursae. As a result, inflammation related to urate crystal deposits may be localized to a bursa or tendon sheath adjacent to the joint or may be widespread, involving multiple joint structures. Clinically, an acute gouty joint is inflamed, with overlying erythema, warmth, or both.⁴ Prominent periarticular inflammation may resemble cellulitis.

Calcium pyrophosphate crystal deposition is confined to hyaline cartilage, fibrocartilage, and areas of chondroid metaplasia (ie, degenerated areas of tendons, ligaments, and joint capsule) within the joint.⁵ Shedding of these crystals into the joint space may trigger an acute inflammatory arthritis, known as pseudogout.

Infectious arthritis

The synovium may become the seat of acute or chronic infections related to bacterial, fungal, or viral organisms.⁶ These infections almost always arise from blood-borne organisms and may be part of a systemic infection. The infection is based in the synovium. The cardinal pathologic findings include intense infiltration by neutrophils with resultant necrosis of the synovium and subsequent formation of granulation and scar tissue. A dense mass of fibrin, infiltrated by neutrophils, forms over the surface of the synovium. Bacterial products released within the joint are capable of producing rapid cartilage destruction.

Structural or mechanical joint derangement

Degeneration of the articular cartilage is the principal pathologic feature of osteoarthritis.⁷ It occurs in response to both local and host factors. Local factors include previous joint trauma (eg, meniscal tears), congenital or developmental joint alterations (eg, congenital hip dysplasia, slipped capital femoral epiphysis), alterations of the subchondral bone (eg, osteopetrosis, avascular necrosis, Paget disease), alterations of supporting structures (eg, hypermobility), and cartilage derangements (eg, ochronosis, crystal deposition). Host factors include genetic traits, obesity, and occupation. Damage to the articular cartilage is associated with subchondral bone sclerosis and marginal osteophyte formation. Patients with osteoarthritis may have an associated synovitis, with the formation of bland synovial effusions.

Clinical

History

Two determinations serve to focus the history and physical examination of a patient with joint pain.¹

The first determination is whether the pain stems from the joint or an adjacent bursa, tendon, ligament, bone, or muscle or whether it is referred from a visceral organ or nerve root. This is generally more difficult with pain in proximal, larger joints. Thus, hip pain can arise from degenerative disc disease or stenosis of the lumbar spine⁸ , aortoiliac occlusive disease, hip arthritis, or trochanteric bursitis.

If the pain is stemming from the joint, three broad categories of joint disease must be differentiated.⁹

The first category is inflammatory arthritis.¹⁰ It is characterized by inflammation affecting joint structures, such as the synovium, synovial cavity, and entheses. The second category is noninflammatory arthritis.⁷ This is joint disease resulting primarily from alterations in the structure or mechanics of the joint. The joint disease may occur as a result of (1) cartilage or meniscal damage with or without concomitant alterations in the structure of the subchondral bone or (2) alterations in joint anatomy as a result of congenital, developmental, metabolic, or past inflammatory diseases. The third category is arthralgia.¹¹ Apart from joint tenderness, abnormalities of the joint cannot be identified. Such patients may have a syndrome of altered pain sensation (eg, fibromyalgia) or an early rheumatic syndrome whose clinical signs are not yet apparent or too subtle for detection (eg, arthralgias of systemic lupus erythematosus [SLE]).

These types of joint disorders may occur together in the same joint. Inflammatory joint disorders often lead to structural derangement of the joint, and, similarly, structural joint problems (eg, traumatic arthritis, osteoarthritis) often have an associated, albeit minor, inflammatory component. Finally, reports of joint pain and tenderness in any type of joint disease are influenced by the patient's emotional state and pain threshold.

• Symptoms of joint disease
  • Pain
    • With inflammatory joint disease, the pain is present both at rest and with motion. It is worse at the beginning than at the end of usage.
    • With noninflammatory (ie, degenerative, traumatic, or mechanical) joint disease, the pain occurs mainly or only during motion and improves quickly with rest. Patients with advanced degenerative disease of the hips, spine, or knees may also have pain at rest and at night.
    • Pain that arises from small peripheral joints tends to be more accurately localized than pain arising from larger proximal joints. For example, pain arising from the hip joint may be felt in the groin or buttocks, in the anterior portion of the thigh, or in the knee.
  • Stiffness
    • Stiffness is a perceived sensation of tightness when attempting to move joints after a period of inactivity. It typically subsides over time. Its duration may serve to distinguish inflammatory from noninflammatory forms of joint disease.
    • With inflammatory arthritis, the stiffness is present upon waking and typically lasts 30-60 minutes or longer.
    • With noninflammatory arthritis, stiffness is experienced briefly (eg, 15 min) upon waking in the morning or following periods of inactivity.
  • Swelling
    • With inflammatory arthritis, joint swelling is related to synovial hypertrophy, synovial effusion, and/or inflammation of periarticular structures. The degree of swelling often varies over time.
    • With noninflammatory arthritis, the formation of osteophytes leads to bony swelling. Patients may report gnarled fingers or knobby knees. Mild degrees of soft tissue swelling do occur and are related to synovial cysts, thickening, or effusions.
  • Limitation of motion
    • Loss of joint motion may be due to structural damage, inflammation, or contracture of surrounding soft tissues.
    • Patients may report restrictions on their activities of daily living, such as fastening a bra, cutting toenails, climbing stairs, or combing hair.
  • Weakness
    • Muscle strength is often diminished around an arthritic joint as a result of disuse atrophy.
    • Weakness with pain suggests a musculoskeletal cause (eg, arthritis, tendonitis) rather than a pure myopathic or neurogenic cause.
    • Manifestations include decreased grip strength, difficulty rising from a chair or climbing stairs, and the sensation that a leg is "giving way."
  • Fatigue
    • Fatigue is usually synonymous with exhaustion and depletion of energy in patients with arthritis.
    • With inflammatory polyarthritis, the fatigue is usually noted in the afternoon or early evening.
    • With psychogenic disorders, the fatigue is often noted upon arising in the morning and is related to anxiety, muscle tension, and poor sleep.
• Historical features important to the differential diagnoses
  • Temporal pattern of arthritis
    • The onset of symptoms can be abrupt or insidious. With an abrupt onset, joint symptoms develop over minutes to hours. This may occur in the setting of trauma, crystalline synovitis, or infection. With an insidious pattern, joint symptoms develop over weeks to months. This onset is typical of most forms of arthritis, including rheumatoid arthritis (RA) and osteoarthritis.
    • Duration of symptoms is considered either acute or chronic. Acute is less than 6 weeks in duration; chronic is 6 or more weeks in duration.
    • The temporal patterns of joint involvement are migratory, additive or simultaneous, and intermittent. With a migratory pattern, inflammation persists for only a few days in each joint (eg, acute rheumatic fever, disseminated gonococcal infection). With an additive or simultaneous pattern, inflammation persists in involved joints as new ones become affected. With an intermittent pattern, episodic involvement occurs, with intervening periods free of joint symptoms (eg, gout, pseudogout, Lyme arthritis).
  • Number of involved joints
    • Monoarthritis is the involvement of one joint.
    • Oligoarthritis is the involvement of 2-4 joints.
    • Polyarthritis is the involvement of 5 or more joints.
  • Symmetry of joint involvement
    • Symmetric arthritis is characterized by involvement of the same joints on each side of the body. This symmetry is typical of RA and SLE.
    • Asymmetric arthritis is characteristic of psoriatic arthritis, reactive arthritis (Reiter syndrome), and Lyme arthritis.
  • Distribution of affected joints
    • The distal interphalangeal joints of the fingers are usually involved in psoriatic arthritis, gout, or osteoarthritis but are usually spared in RA.
    • Joints of the lumbar spine are typically involved in ankylosing spondylitis but are spared in RA.
  • Distinctive types of musculoskeletal involvement
    • Spondyloarthropathy involves entheses, leading to heel pain (inflammation at the insertions of the Achilles tendon and/or plantar fascia), dactylitis (sausage digits), tendonitis, and back pain (sacroiliitis and vertebral disc insertions).
    • Gout commonly involves tendon sheaths and bursae, resulting in superficial inflammation.
  • Extra-articular manifestations
    • Constitutional symptoms suggest an underlying systemic disorder and are not expected in patients with degenerative joint disease. These may include fatigue, malaise, and weight loss.
    • Skin lesions may be present. Physical examination of the skin, but not the joints, may indicate the specific diagnosis of a number of rheumatic diseases. Examples include SLE, dermatomyositis, scleroderma, Lyme disease, psoriasis, Henoch-Schönlein purpura, and erythema nodosum.
    • Ocular symptoms or signs are also possible. Episcleritis and scleritis may be associated with RA or Wegener granulomatosis, anterior uveitis with ankylosing spondylitis, and iridocyclitis with juvenile RA. Conjunctivitis may be caused by reactive arthritis.

Physical

The musculoskeletal examination helps distinguish joint inflammation (eg, RA) from joint damage (eg, degenerative joint disease). It can also help elucidate the site of musculoskeletal involvement (eg, synovitis, enthesitis, tenosynovitis, bursitis) and the distribution of joint involvement.

• Signs of inflammatory joint disease
  • Synovial hypertrophy
    • This is the most reliable sign of an inflammatory arthritis.
    • The synovial membrane is normally too thin to palpate. In a person with chronic inflammatory arthritis, the synovial membrane has a doughy or boggy consistency, a feature best appreciated at the joint line or margin.
  • Joint effusions
    • Effusions develop in response to synovial inflammation, trauma, anasarca, intra-articular hemorrhage (hemarthrosis), or an adjacent focus of acute inflammation (sympathetic effusion).
    • These are detected by performing fluid ballottement or cross-fluctuation through the synovial cavity.
  • Pain with motion, particularly at the extremes of joint motion
    • Pain throughout the whole range of motion is observed in a person with an acutely inflamed joint.
    • Pain experienced as the joint is gently forced (ie, stressed) towards its limitation of range is suggestive of synovitis.
    • Pain not present throughout the entire range of motion may indicate an extra-articular source, such as tendinitis.
  • Erythema and warmth
    • Erythema of the joint is restricted to acute inflammatory forms of arthritis, such as gout, septic arthritis, or acute rheumatic fever. It is rare in persons with RA but may occasionally occur in those with psoriatic arthritis.
    • Warmth of the joint is a sensitive sign of inflammatory arthritis and can be detected by passing the hand back and forth from the joint to a neutral area distal or proximal. Differences in warmth can also be detected by comparing the same joint on each side of the body.
  • Limited range of motion: In a person with inflammatory joint disease, limitation of motion results from the presence of a tense effusion, markedly thickened synovium, adhesions, capsular fibrosis, or pain.
  • Joint tenderness
    • This is a sensitive sign of joint disease, but it is not specific for inflammatory arthritides.
    • In an acutely inflamed joint, tenderness can be elicited over the entire synovial reflection.
    • Focal tenderness may indicate a focus of inflammation outside the joint, such as tendinitis, osteomyelitis, or fracture.
    • The presence of joint tenderness in the absence of other joint abnormalities must be interpreted in the context of the patient's emotional state.
• Signs of degenerative or mechanical joint disease
  • Bony overgrowth of the joints (osteophytes): Those located at the distal interphalangeal joints are called Heberden nodes, while those located at the proximal interphalangeal joints are called Bouchard nodes.
  • Limited range of motion: In persons with degenerative/traumatic joint disease, the limitation of motion results from intra-articular loose bodies, osteophyte formation, or subluxation.
  • Crepitus during active or passive range of motion
    • A palpable or audible grating sensation is produced during motion of the joint.
    • Soft, fine crepitus may be felt (or heard with a stethoscope) in a rheumatoid joint when the cartilage surface is no longer smooth.
    • Coarse crepitus or grating may be felt in joints severely damaged by long-standing rheumatoid or degenerative arthritis.
  • Joint deformity: Several types must be distinguished.
    • Restriction in the normal range of motion, such as a lack of full joint extension that results in a flexion deformity, is one type.
    • Another is malalignment of the articulating bones, such as ulnar deviation of the fingers or valgus deformity of the knee.
    • The third type is an alteration in the relationship of the two articulating surfaces, such as subluxation (ie, some contact between the two articulating surfaces) and dislocation (ie, complete loss of contact between the two articulating surfaces).
• Techniques of the musculoskeletal examination
  • Inspection
    • Each joint has a characteristic or normal appearance, and each assumes a characteristic resting position.
    • Compare one side of the body with the other in order to detect joint abnormalities, including swelling, deformity, overlying erythema, or wasting of the periarticular musculature.
    • With a sagittal view of the patient, take note of joint deformities that result from the lack of full extension of a joint (eg, flexion deformities).
    • With a coronal view of the patient, take note of joint malalignment, which may result in valgus or varus deformities.
  • Palpation
    • Palpation of the joints is used to assess for signs of inflammation (eg, warmth, synovial hypertrophy, joint effusion, tenderness) and for signs of joint damage (eg, bony swelling, crepitus).
    • The examiner should palpate with enough pressure to blanch his or her thumbnail. This ensures that the assessment of joint tenderness is uniform. The application of this amount of force during palpation should not cause pain in a normal joint.
  • Assessment of range of motion
    • Assess limitation of passive motion by comparing it with the expected range of motion observed in healthy individuals and with the range of motion in the contralateral joint.
    • Active range of motion can be used to assess the presence of pathology in juxta-articular structures, such as tendons and bursae.
    • Pain occurring during only a portion of the range of motion may be related to an extra-articular structure, such as a tendon or bursa.
    • Assess pain with joint motion; observe the patient's face for wincing.
    • Assess crepitus by palpating the joint with one hand while moving the joint passively with the other. In the lower extremities, crepitus of the hip or knee can sometimes be heard as the patient arises from a chair, climbs a step, or pivots on the affected joint.
    • Assess instability or abnormal mobility by applying forces to the relaxed joint in planes of motion normally associated with little or no motion. Instability of a lower extremity joint (eg, knee, ankle) should also be assessed by observing the joint during weight-bearing and walking. Instability of the joint may be due to laxity of ligaments or destruction of the articular surface.
• Examination techniques useful for detection of arthritis in specific joints
  • Hands
    • To detect synovial effusions in interphalangeal joints, gently squeeze the superolateral joint lines with the thumb and index finger while palpating the volar and dorsal sides with the opposite thumb and finger. Use the fingers to detect a ballooning effect as pressure is applied to the joint.
    • To detect metacarpophalangeal (MCP) joint synovitis, gently squeeze the dorsal aspects of the fully extended MCP joint distally with the thumb and index finger of one hand while screening for a ballooning effect with the same fingers of the opposite hand placed over the proximal aspects of the joint.
    • To assess grip strength, the patient is asked to squeeze two adjacent fingers of the examiner with maximum force.
  • Wrists
    • For wrist assessment, support the wrist in 15° flexion. Palpate the dorsal aspect of the radiocarpal and ulnocarpal joints for a spongy consistency, which is indicative of synovial hypertrophy.
    • Percuss over the volar aspect of the wrist; elicitation of paresthesias in the median nerve distribution is indicative of carpal tunnel syndrome.
  • Elbows
    • Assess for flexion deformity (ie, inability to fully extend); this may be an early sign of an inflammatory arthritis.
    • Palpate for soft tissue swelling of synovitis in fossae between the olecranon and lateral or medial epicondyles.
    • Assess for subcutaneous nodules in olecranon bursae and over the extensor surfaces of the elbow and forearm; these may represent rheumatoid nodules or tophi.
  • Shoulders
    • Evaluate the function of the entire shoulder complex. Observe the patient abduct both arms from 0° along side the body to 180° straight up. Assess external rotation by noting the position behind the neck or head to which the patient's hands can reach from above. Assess internal rotation by noting the highest level the dorsum of the patient's hands can reach in the back from below. A limitation of active shoulder motion should prompt an evaluation of passive motion.
    • Isolate and assess the motion of the glenohumeral joint. Abduction is checked with the patient's scapula fixed in place and the elbow flexed. The examiner uses one hand to prevent the spine or tip of the scapula from moving and then uses the other hand to abduct the patient's flexed arm. Normal glenohumeral abduction is 90°. External rotation is a movement mediated solely by the glenohumeral joint. It can be assessed by externally rotating the arm, flexed to 90° at the elbow and positioned either with the arm at the patient's side or in 90° of abduction. Limitation of glenohumeral motion is an indication of glenohumeral joint arthritis or capsular fibrosis.
    • Assess rotator cuff function. Observe the patient actively abduct the arm. Pain experienced at 60-100° of active abduction is an indication of supraspinatus tendonitis and/or subacromial bursitis.¹²
  • Spine: Assess the range of motion of the entire spine (ie, cervical, thoracic, lumbar).
    • For the cervical spine, ask the patient to touch the chin to the chest (flexion) and then look up at the ceiling (extension). For lateral flexion, ask the patients to touch an ear to their shoulder. For lateral rotation, ask patients to touch their chin to a shoulder. During lateral rotation and flexion, pain that occurs on the ipsilateral side of the neck is bony in origin (eg, apophyseal joint disease), while pain on the contralateral side is muscular or ligamentous in origin.
    • With the thoracic spine, restriction of chest expansion is a sign of ankylosing spondylitis. The circumference of the chest should be measured at the level of the nipples. A difference of less than 2.5 cm with inspiration is clearly abnormal.
    • For the lumbar spine, assess flexion, extension, and lateral flexion.¹³ Pain upon extension suggests pathology in the posterior elements of the spine (eg, facet joints or neurogenic compression seen with spinal stenosis). Pain upon flexion suggests disc disease. Lateral flexion is restricted early in the course of ankylosing spondylitis. Lumbar spine flexion is measured reproducibly with the Schober test. With the patient erect, make a horizontal mark at the level of the sacral dimples and make a second mark over the spine at a distance 10 cm above the first mark. Have the patient bend forward in an attempt to touch the floor. The distance between the 2 marks is measured in flexion. Normally, the distance should increase from 10 cm to more than 15 cm. Restriction of lumbar spine flexion can be seen with muscle spasm and ankylosing spondylitis. More severe restriction of motion (eg, result <2 cm) without acute lumbar pain is a reliable sign of ankylosing spondylitis.
  • Hips
    • Perform the log-rolling test. With the patient's leg in extension, the examiner gently rolls the entire limb back and forth. Limitation of internal or external rotation (particularly when compared to the contralateral hip) or groin pain is suggestive of true hip pathology.
    • The Thomas test helps assess for hip flexion deformity. The opposite hip is fully flexed as a means to flatten the lumbar lordosis and fix the pelvis. If the knee of the involved side is observed to elevate off the examining table, then an ipsilateral hip flexion deformity is present. This may be an indication of hip arthritis or tight hip flexor muscles.
    • For the Trendelenburg test, the patient is asked to stand and bear weight on only the involved leg. If the contralateral pelvis drops below level, then weakness of the hip abductors (ie, gluteus medius) is present on the affected side. Weakness of the hip abductors is a sign of hip arthritis. It can also have a neurogenic (eg, L5 root disease) or myogenic cause.
  • Knees¹⁴
    • Assess for synovitis. Visually inspect the knee for swelling and erythema; compare the affected knee with the contralateral knee. Palpate for warmth. Compare the temperature of the affected knee with that of the contralateral knee. The examiner should gently pass his or her hand from the patient's mid thigh or mid calf to the knee, assessing for a warmer temperature over the knee.
    • Assess for synovial effusion by eliciting the bulge sign and performing ballottement. The bulge sign test is performed with the patient supine, quadriceps relaxed, and knee fully extended. A small effusion, if present, is displaced from the medial side of the knee by stroking with the examiner's thumb. Its return is facilitated by quickly tapping the lateral side with the ends of the examiner's fingers and is observed as a gradual filling out of the recess created by stroking. Repeat the process several times in quick succession to be confident of the result. Ballottement is useful for detecting large knee effusions. With the patient's knee relaxed and fully extended, cup both hands around the knee, bringing the knee effusion into the central portion of the synovial cavity. Using the right index finger, push the patella straight down and release it quickly. The presence of a patellar tap, felt as the patella knocks against the underlying femoral condyles, is indicative of an effusion.
    • Assess range of motion. Synovitis with or without a synovial effusion may result in a decrease in the range of motion, including a loss of full extension (flexion deformity) and/or a reduction in flexion.
    • Assess for joint damage. Palpate the knee for crepitus with passive movement. Palpate the patella for crepitus as the patient actively extends the knee from a flexed position.
    • Assess for joint laxity. Test for lateral instability by attempting to adduct and abduct the lower leg with the knee held in 15° of flexion. Test for anteroposterior instability by attempting to push and pull the lower leg backward and forward with the knee held in 30° of flexion (Lachman test). Observe the alignment of the knee with the patient standing and bearing weight on both knees. Observe the back of the knee for popliteal or Baker cysts.
  • Ankles
    • Palpate for tenderness and soft tissue swelling over talar, subtalar, and midtarsal joints.
    • Assess range of motion of the talar (ie, with dorsiflexion, plantar flexion) and subtalar (ie, with inversion, eversion) joints.
  • Feet
    • Squeeze the row of metatarsophalangeal joints, assessing for the presence of pain or tenderness.
    • Palpate the small joints of the feet, assessing for the presence of tenderness, bony or soft tissue swelling, or joint effusion.

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