This browser is too old to run Achievable.

Update it, or open this page in a current version of Chrome, Safari, Firefox or Edge. On an iPhone or iPad, update iOS: every browser there runs on the version of Safari that comes with it.

Achievable logoAchievable logo
NPTE-PTA
Sign in
Sign up
Purchase
Textbook
Practice exams
Support
How it works
Resources
Exam catalog
Mountain with a flag at the peak
Textbook
Introduction
1. Cardiovascular system
2. Pulmonary system
3. Neuromuscular system
4. Pediatrics
5. Musculoskeletal system
5.1 Anatomy of musculoskeletal system
5.2 Anatomical terminology and exercise training principles
5.3 Joint mechanics and phases of healing
5.4 Upper extremity anatomy
5.5 Special tests of upper extremity
5.6 Comparing clinical presentation and interventions for upper extremity
5.7 Lower extremity anatomy
5.8 Special tests of lower extremity
5.9 Comparing clinical presentation and interventions for lower extremity
5.10 Spine and pelvis anatomy
5.11 Special tests of the spine, pelvis, and temporomandibular joint
5.12 Comparing clinical presentation and interventions for the spine, pelvis, and temporomandibular joint
5.13 Other musculoskeletal conditions
5.13.1 Arthritic and inflammatory joint conditions
5.13.2 Muscle, bone, and pain conditions
5.14 Gait
5.15 Prosthetics
5.16 Orthotics
5.17 Medications, imaging, and fractures
5.18 Surgical protocols
6. Other systems
7. Non-systems
Wrapping up
Achievable logoAchievable logo
5.13.1 Arthritic and inflammatory joint conditions
Achievable NPTE-PTA
5. Musculoskeletal system
5.13. Other musculoskeletal conditions
Our NPTE-PTA course is now in "early access" - get 50% off for a limited time.

Arthritic and inflammatory joint conditions

9 min read
Font
Discuss
Share
Feedback

Osteoarthritis (OA) or degenerative joint disease (DJD)

  • Chronic degenerative joint disease that causes the breakdown of cartilage, the protective tissue that cushions the ends of bones in joints

    • Characterized by degeneration of articular cartilage with subchondral bone hypertrophy (sclerosis, osteophytes) and capsular thickening of weight-bearing joints
    • Most common form of arthritis
    • Most common joints are cervical spine, lumbar spine, hips, knees, and great toe (weight-bearing joints), plus the hands (DIP and PIP joints and the thumb CMC joint)
  • Symptoms

    • Early: intermittent pain brought on by specific activities and relieved by rest; morning stiffness under 30 minutes
      • Progressing to chronic pain present with weight-bearing activities (including ambulation, standing, stair climbing)
    • Swelling in joints
    • Loss of range of motion of joints
    • Bony deformities can occur
    • First CMC joint OA causes pain at the base of the thumb, especially with gripping and pinching; the CMC grind test, which presses through the thumb while rotating it, reproduces the pain and crunching in the joint
  • Diagnosis

    • Clinical presentation
    • X-ray
  • Medical management

    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs)
    • Intra-articular corticosteroid injections into the joint space
  • Physical therapy management

    • Joint mobility
    • Joint strengthening
    • Aquatic therapy
    • Aerobic/conditioning activities

Rheumatoid conditions

Rheumatoid arthritis (RA)

  • Chronic autoimmune disease that causes inflammation and damage to the joints due to the overproduction of antibodies

    • Etiology is unknown, but it is thought to have genetic links
  • Disease is characterized by times of exacerbation and remission

  • Most common areas are hands, feet, cervical spine

  • Symptoms (bilateral, symmetrical)

    • Joint pain, especially in the hands, feet, wrists, and knees
    • Swelling and stiffness in the joints; morning stiffness usually lasts more than 1 hour
    • Fatigue
    • Fever
    • Deformities in the joints
  • Diagnosis

    • Clinical presentation
    • X-ray imaging
    • Lab values
      • Erythrocyte sedimentation rate, rheumatoid factor, anti-CCP antibody
  • Medical management

    • Antirheumatic medications/immunosuppressive agents (disease-modifying antirheumatic drugs, DMARDs), e.g., synthetic methotrexate and biologic adalimumab (Humira)
    • Corticosteroid medications
  • Physical therapy management

    • Management of pain and inflammation (during exacerbation phase)
    • Improve joint mobility and mechanics (during remission phase)
    • Progressive resistance training during the remission phase; during an exacerbation, avoid heavy resistive exercise and limit exercise to gentle AROM and low-intensity isometrics

OA vs. RA at a glance

Feature Osteoarthritis Rheumatoid arthritis
Onset pattern Slow, progressive, mechanical (worse with use) Autoimmune; marked by exacerbation and remission
Joint symmetry Often asymmetrical Bilateral, symmetrical
Morning stiffness Under 30 minutes Usually more than 1 hour
Common joints Weight-bearing joints (hips, knees, spine, great toe) Hands, feet, wrists, cervical spine
Systemic features None (localized to joint) Fatigue, fever, systemic inflammation
PT management Progressive strengthening throughout Progressive resistance training during remission; only gentle AROM and low-intensity isometrics during an exacerbation

PTA insight: During an RA exacerbation, the PTA’s role is to collect data on the patient’s response (increased pain, swelling, fatigue), recognize signs of an exacerbation or an excessive response to treatment (e.g., pain lasting more than 1-2 hours after exercise, increased joint swelling or warmth), and communicate those findings to the supervising PT rather than independently modifying the plan of care.

Psoriatic arthritis

  • Chronic, inflammatory arthritis that often, but not always, occurs in people with the skin condition psoriasis

    • Autoimmune disorder
  • Typically occurring in the axial skeleton and joints of the digits

  • Symptoms

    • Joint pain
    • Swelling
    • Stiffness
    • Fatigue
    • Skin psoriasis
    • Changes in fingernails and toenails (discoloration)
    • Inflammation where tendons and ligaments attach to bone
  • Diagnosis

    • Clinical presentation
    • Lab tests only to rule out rheumatoid arthritis
  • Medical management

    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs)
    • Antirheumatic medications
    • Biological response modifier medications
  • Physical therapy management

    • Improve joint mobility and mechanics
    • Joint protection strategies
    • Aquatic therapy
    • Aerobic/conditioning activities

Reactive arthritis

  • Reactive arthritis (formerly Reiter’s syndrome) is an acute spondyloarthropathy that follows a genitourinary infection, most often Chlamydia, or an enteric infection such as Shigella, Salmonella or Yersinia, and classically brings urethritis and conjunctivitis with the arthritis; the joint itself is not infected

Ankylosing spondylitis

  • An autoimmune disease that causes inflammation and stiffness, primarily in the spine, and is notably more common in men. Men typically develop AS in early adulthood. It causes inflammation of the joints (vertebrae) and ligaments in the spine, leading to stiffness, pain, eventual fusion of the bones, and development of osteoporosis

  • Symptoms

    • Mid and low back pain
    • Morning stiffness of the spine
    • Back pain is inflammatory, with prolonged stiffness that worsens with rest or inactivity and improves with movement and exercise, unlike mechanical back pain from SI, facet or disc problems, which is provoked by movement or position
    • Increased thoracic kyphosis with loss or reversal of cervical lordosis
    • Flattening (decreased lordosis) of the lumbar spine
    • Degeneration of peripheral and costovertebral joints
  • Diagnosis

    • Clinical presentation
    • Bone scan shows increased uptake in the vertebrae/sacroiliac joints
      • Lab test for the HLA-B27 antigen
  • Medical management

    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs)
    • Local corticosteroid injections for peripheral joints or entheses (long-term systemic corticosteroids are not recommended for spinal disease)
    • Biologic agents (TNF inhibitors, e.g., adalimumab)
  • Physical therapy management

    • Improve joint mobility and mechanics
    • Emphasis on spinal extension
    • Joint protection strategies
    • Freestyle swimming
    • Aerobic/conditioning activities
    • Activities to maintain respiratory function
    • Strengthening, especially of the spinal and hip extensors; avoid high-impact or contact sports and repetitive or forced spinal flexion

Gout

  • Gout is characterized by elevated serum uric acid (hyperuricemia), because the body makes too much uric acid or has trouble getting rid of it; the uric acid crystals that form inflame the joint

  • Primary gout is an inherited disorder of purine metabolism in which uric acid changes into crystals and deposits in the peripheral joints; it is far more common in men and in women after menopause

  • Secondary gout affects all ages and genders with elevated uric acid in the blood secondary to other disease processes, primarily of the kidneys.

  • Most often affects the first metatarsophalangeal joint (great toe); also the ankle, midfoot, and knee

  • Symptoms

    • Sudden onset of severe, intense pain in one or more joints, typically the big toe.
      • Pain may feel like burning, throbbing, or crushing
    • Significant swelling and redness in the affected joint
    • The joint may feel hot to the touch and tender to the slightest touch
  • Diagnosis

    • Clinical presentation
    • Lab tests
      • Identify uric acid levels
  • Medical management

    • Non-steroidal anti-inflammatory drugs (NSAIDs)
    • Colchicine medications
    • Corticosteroid medications
    • Allopurinol medications
    • COX-2 inhibitor medications
    • Glucocorticoids are used to treat acute gout flares, whereas allopurinol is the most commonly prescribed and preferred initial urate-lowering therapy
  • Physical therapy management

    • Gait training with an assistive device per the PT’s plan of care to unload the affected joint during a flare
    • Education on diet restrictions limiting consumption of red and organ meats, shellfish, alcohol (especially beer), and fructose-sweetened drinks, and medication adherence

Tendinopathy (tendinitis vs. tendinosis)

  • Tendinopathy is an umbrella term for tendon dysfunction caused by overuse or repetitive motions that put excessive stress on the tendon
    • Can also be caused by sudden trauma or age-related degeneration
Definitions
Tendinitis
An acute inflammatory response in a tendon, with pain, swelling, and warmth.
Tendinosis
A chronic, degenerative change in tendon tissue (collagen disorganization) without inflammation; the main treatment is progressive tendon loading (e.g., eccentric training) rather than anti-inflammatory measures.
  • Symptoms
    • Pain is typically located over the affected tendon, often worse with activity
    • Stiffness at the affected joint
    • Weakness in the joint
    • Swelling and warmth suggest an acute (tendinitis) presentation; a thickened, tender tendon with chronic, activity-related pain but little warmth or swelling suggests tendinosis
  • Diagnosis
    • Clinical presentation and special tests specific to the joint
    • MRI
  • Medical management
    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs), primarily for acute tendinitis
    • Corticosteroid medications
  • Physical therapy management
    • Flexibility; joint mobilization (performed by the PT)
    • Soft tissue techniques
      • Deep friction massage, a technique described by Cyriax that reaches the deep structures of the body, is used to produce traumatic hyperemia in chronic lesions and to relieve pain, although its effectiveness has not been clearly documented
    • Progressive resistance training, including eccentric loading for tendinosis
    • Modalities for managing pain (for acute tendinitis)
    • Functional mobility training

Bursitis

  • Inflammation of bursae due to overuse, trauma, gout, or infection

  • Symptoms

    • Pain at rest
    • PROM and AROM presenting an empty end feel limited by pain before tissue resistance, not in the joint’s capsular pattern, which suggests a non-capsular (bursal) lesion
    • Swelling of the joint area
    • Redness over the inflamed bursa
    • Warmth to the affected area may feel hot to the touch
    • Tenderness over the affected area when pressed
  • Diagnosis: clinical presentation

  • Medical management

    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs)
  • Physical therapy management

    • Same conservative approach as tendinopathy above: flexibility, joint mobilization (performed by the PT), soft tissue techniques, progressive resistance training, modalities for pain and inflammation, and functional mobility training.

Medications and safety across these conditions

Medication implications for the PTA

Medication class PT implications
NSAIDs/acetaminophen Mask pain, so monitor exercise intensity and post-session soreness; watch for GI bleeding and renal effects
Systemic corticosteroids Osteoporosis/fracture risk, skin fragility, delayed healing, hyperglycemia, muscle wasting
Corticosteroid injections Can weaken tendon tissue; avoid aggressive loading of the injected area for 1-2 weeks after injection
DMARDs/biologics (methotrexate, adalimumab) Infection risk, so follow infection-control practice; fatigue is common
Colchicine/allopurinol GI upset (colchicine); starting allopurinol can trigger a gout flare

Safety: recognizing when to modify or stop treatment

  • RA cervical involvement: avoid end-range cervical flexion and manipulation (atlantoaxial instability risk); report new neurologic signs immediately
  • AS with spinal osteoporosis: avoid spinal flexion loading and manipulation; report new spinal pain after minor trauma (fracture risk)
  • Possible septic bursitis: fever or spreading redness - stop treatment and report to the PT immediately
  • Acute gout flare: avoid direct pressure or aggressive loading over the affected joint

Osteoarthritis (OA)

  • Degenerative cartilage breakdown with subchondral sclerosis/osteophytes; most common arthritis
  • Affects weight-bearing joints (spine, hips, knees, great toe) plus hand DIP/PIP/thumb CMC
  • Early intermittent activity pain → chronic weight-bearing pain; morning stiffness <30 min
  • Managed with acetaminophen/NSAIDs and intra-articular corticosteroid injections
  • PT: joint mobility, strengthening, aquatic/aerobic therapy (progressive throughout)

Rheumatoid arthritis (RA) vs. OA

  • RA: autoimmune, bilateral/symmetrical, cycles of exacerbation/remission; affects hands, feet, cervical spine
  • Symptoms: pain/swelling/stiffness (morning stiffness usually >1 hr, vs. <30 min in OA), fatigue, fever, deformities; diagnosed via ESR, rheumatoid factor, anti-CCP
  • Managed with DMARDs (methotrexate, adalimumab) and corticosteroids
  • PT: manage pain/inflammation during flares (gentle AROM/isometrics only); joint mobility work and resistance training in remission
  • Cervical involvement: avoid end-range flexion/manipulation (atlantoaxial instability risk)
  • Key contrast: OA is mechanical/asymmetrical with progressive strengthening; RA is autoimmune/symmetrical with systemic symptoms and flare-limited loading

Psoriatic arthritis & Ankylosing spondylitis (AS)

  • Psoriatic arthritis: autoimmune, linked to psoriasis; affects axial skeleton/digits; skin/nail changes, enthesitis; PT emphasizes mobility, joint protection, aquatic/aerobic work
  • AS: autoimmune spinal inflammation, more common in men; causes kyphosis, loss of lordosis, spinal fusion, osteoporosis
  • Diagnosis: HLA-B27 antigen, bone scan uptake at spine/SI joints
  • PT: emphasize spinal extension, strengthen spinal/hip extensors, freestyle swimming, respiratory maintenance; avoid high-impact/contact sports and forced or loaded spinal flexion (fracture risk)

Gout

  • Elevated serum uric acid (hyperuricemia) causing uric acid crystal deposits; primary (inherited purine metabolism disorder, men/postmenopausal women) vs. secondary (kidney-related, any age)
  • Sudden severe pain/swelling/redness, often first MTP joint; diagnosed via serum uric acid
  • Medications: NSAIDs, colchicine, corticosteroids, allopurinol, COX-2 inhibitors
  • PT: gait training with assistive device during flare; dietary education (limit red/organ meats, shellfish, alcohol, fructose)
  • Avoid pressure/loading on joint during flare; starting allopurinol may trigger flare

Tendinopathy & Bursitis

  • Tendinitis = acute inflammation (pain, swelling, warmth); tendinosis = chronic degeneration (no inflammation) → treat with progressive/eccentric loading, not anti-inflammatories
  • Bursitis: inflammation of bursae (overuse, trauma, gout, infection); empty end-feel, pain before resistance, non-capsular pattern
  • Both managed with acetaminophen/NSAIDs (corticosteroids also listed for tendinopathy) and PT: flexibility, joint mobilization (by the PT), soft tissue work, progressive resistance, modalities, functional training
  • Watch for septic bursitis (fever, spreading redness) — stop and notify PT

Medication implications & Safety for PTA

  • NSAIDs/acetaminophen mask pain—monitor exercise intensity/soreness; GI/renal risks
  • Systemic corticosteroids: osteoporosis, fragile skin, delayed healing, hyperglycemia, muscle wasting
  • Corticosteroid injections: avoid aggressive loading of area for 1-2 weeks
  • DMARDs/biologics: infection risk, fatigue common
  • Report RA flare signs (pain >1-2 hrs post-exercise, swelling/warmth), new neuro signs, new spinal pain after trauma, or septic bursitis signs immediately to supervising PT

Sign up for free to take 29 quiz questions on this topic

Previous
Next  | 5.13.2 Muscle, bone, and pain conditions
All rights reserved ©2016 - 2026 Achievable, Inc.

Arthritic and inflammatory joint conditions

Osteoarthritis (OA) or degenerative joint disease (DJD)

  • Chronic degenerative joint disease that causes the breakdown of cartilage, the protective tissue that cushions the ends of bones in joints

    • Characterized by degeneration of articular cartilage with subchondral bone hypertrophy (sclerosis, osteophytes) and capsular thickening of weight-bearing joints
    • Most common form of arthritis
    • Most common joints are cervical spine, lumbar spine, hips, knees, and great toe (weight-bearing joints), plus the hands (DIP and PIP joints and the thumb CMC joint)
  • Symptoms

    • Early: intermittent pain brought on by specific activities and relieved by rest; morning stiffness under 30 minutes
      • Progressing to chronic pain present with weight-bearing activities (including ambulation, standing, stair climbing)
    • Swelling in joints
    • Loss of range of motion of joints
    • Bony deformities can occur
    • First CMC joint OA causes pain at the base of the thumb, especially with gripping and pinching; the CMC grind test, which presses through the thumb while rotating it, reproduces the pain and crunching in the joint
  • Diagnosis

    • Clinical presentation
    • X-ray
  • Medical management

    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs)
    • Intra-articular corticosteroid injections into the joint space
  • Physical therapy management

    • Joint mobility
    • Joint strengthening
    • Aquatic therapy
    • Aerobic/conditioning activities

Rheumatoid conditions

Rheumatoid arthritis (RA)

  • Chronic autoimmune disease that causes inflammation and damage to the joints due to the overproduction of antibodies

    • Etiology is unknown, but it is thought to have genetic links
  • Disease is characterized by times of exacerbation and remission

  • Most common areas are hands, feet, cervical spine

  • Symptoms (bilateral, symmetrical)

    • Joint pain, especially in the hands, feet, wrists, and knees
    • Swelling and stiffness in the joints; morning stiffness usually lasts more than 1 hour
    • Fatigue
    • Fever
    • Deformities in the joints
  • Diagnosis

    • Clinical presentation
    • X-ray imaging
    • Lab values
      • Erythrocyte sedimentation rate, rheumatoid factor, anti-CCP antibody
  • Medical management

    • Antirheumatic medications/immunosuppressive agents (disease-modifying antirheumatic drugs, DMARDs), e.g., synthetic methotrexate and biologic adalimumab (Humira)
    • Corticosteroid medications
  • Physical therapy management

    • Management of pain and inflammation (during exacerbation phase)
    • Improve joint mobility and mechanics (during remission phase)
    • Progressive resistance training during the remission phase; during an exacerbation, avoid heavy resistive exercise and limit exercise to gentle AROM and low-intensity isometrics

OA vs. RA at a glance

Feature Osteoarthritis Rheumatoid arthritis
Onset pattern Slow, progressive, mechanical (worse with use) Autoimmune; marked by exacerbation and remission
Joint symmetry Often asymmetrical Bilateral, symmetrical
Morning stiffness Under 30 minutes Usually more than 1 hour
Common joints Weight-bearing joints (hips, knees, spine, great toe) Hands, feet, wrists, cervical spine
Systemic features None (localized to joint) Fatigue, fever, systemic inflammation
PT management Progressive strengthening throughout Progressive resistance training during remission; only gentle AROM and low-intensity isometrics during an exacerbation

PTA insight: During an RA exacerbation, the PTA’s role is to collect data on the patient’s response (increased pain, swelling, fatigue), recognize signs of an exacerbation or an excessive response to treatment (e.g., pain lasting more than 1-2 hours after exercise, increased joint swelling or warmth), and communicate those findings to the supervising PT rather than independently modifying the plan of care.

Psoriatic arthritis

  • Chronic, inflammatory arthritis that often, but not always, occurs in people with the skin condition psoriasis

    • Autoimmune disorder
  • Typically occurring in the axial skeleton and joints of the digits

  • Symptoms

    • Joint pain
    • Swelling
    • Stiffness
    • Fatigue
    • Skin psoriasis
    • Changes in fingernails and toenails (discoloration)
    • Inflammation where tendons and ligaments attach to bone
  • Diagnosis

    • Clinical presentation
    • Lab tests only to rule out rheumatoid arthritis
  • Medical management

    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs)
    • Antirheumatic medications
    • Biological response modifier medications
  • Physical therapy management

    • Improve joint mobility and mechanics
    • Joint protection strategies
    • Aquatic therapy
    • Aerobic/conditioning activities

Reactive arthritis

  • Reactive arthritis (formerly Reiter’s syndrome) is an acute spondyloarthropathy that follows a genitourinary infection, most often Chlamydia, or an enteric infection such as Shigella, Salmonella or Yersinia, and classically brings urethritis and conjunctivitis with the arthritis; the joint itself is not infected

Ankylosing spondylitis

  • An autoimmune disease that causes inflammation and stiffness, primarily in the spine, and is notably more common in men. Men typically develop AS in early adulthood. It causes inflammation of the joints (vertebrae) and ligaments in the spine, leading to stiffness, pain, eventual fusion of the bones, and development of osteoporosis

  • Symptoms

    • Mid and low back pain
    • Morning stiffness of the spine
    • Back pain is inflammatory, with prolonged stiffness that worsens with rest or inactivity and improves with movement and exercise, unlike mechanical back pain from SI, facet or disc problems, which is provoked by movement or position
    • Increased thoracic kyphosis with loss or reversal of cervical lordosis
    • Flattening (decreased lordosis) of the lumbar spine
    • Degeneration of peripheral and costovertebral joints
  • Diagnosis

    • Clinical presentation
    • Bone scan shows increased uptake in the vertebrae/sacroiliac joints
      • Lab test for the HLA-B27 antigen
  • Medical management

    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs)
    • Local corticosteroid injections for peripheral joints or entheses (long-term systemic corticosteroids are not recommended for spinal disease)
    • Biologic agents (TNF inhibitors, e.g., adalimumab)
  • Physical therapy management

    • Improve joint mobility and mechanics
    • Emphasis on spinal extension
    • Joint protection strategies
    • Freestyle swimming
    • Aerobic/conditioning activities
    • Activities to maintain respiratory function
    • Strengthening, especially of the spinal and hip extensors; avoid high-impact or contact sports and repetitive or forced spinal flexion

Gout

  • Gout is characterized by elevated serum uric acid (hyperuricemia), because the body makes too much uric acid or has trouble getting rid of it; the uric acid crystals that form inflame the joint

  • Primary gout is an inherited disorder of purine metabolism in which uric acid changes into crystals and deposits in the peripheral joints; it is far more common in men and in women after menopause

  • Secondary gout affects all ages and genders with elevated uric acid in the blood secondary to other disease processes, primarily of the kidneys.

  • Most often affects the first metatarsophalangeal joint (great toe); also the ankle, midfoot, and knee

  • Symptoms

    • Sudden onset of severe, intense pain in one or more joints, typically the big toe.
      • Pain may feel like burning, throbbing, or crushing
    • Significant swelling and redness in the affected joint
    • The joint may feel hot to the touch and tender to the slightest touch
  • Diagnosis

    • Clinical presentation
    • Lab tests
      • Identify uric acid levels
  • Medical management

    • Non-steroidal anti-inflammatory drugs (NSAIDs)
    • Colchicine medications
    • Corticosteroid medications
    • Allopurinol medications
    • COX-2 inhibitor medications
    • Glucocorticoids are used to treat acute gout flares, whereas allopurinol is the most commonly prescribed and preferred initial urate-lowering therapy
  • Physical therapy management

    • Gait training with an assistive device per the PT’s plan of care to unload the affected joint during a flare
    • Education on diet restrictions limiting consumption of red and organ meats, shellfish, alcohol (especially beer), and fructose-sweetened drinks, and medication adherence

Tendinopathy (tendinitis vs. tendinosis)

  • Tendinopathy is an umbrella term for tendon dysfunction caused by overuse or repetitive motions that put excessive stress on the tendon
    • Can also be caused by sudden trauma or age-related degeneration
Definitions
Tendinitis
An acute inflammatory response in a tendon, with pain, swelling, and warmth.
Tendinosis
A chronic, degenerative change in tendon tissue (collagen disorganization) without inflammation; the main treatment is progressive tendon loading (e.g., eccentric training) rather than anti-inflammatory measures.
  • Symptoms
    • Pain is typically located over the affected tendon, often worse with activity
    • Stiffness at the affected joint
    • Weakness in the joint
    • Swelling and warmth suggest an acute (tendinitis) presentation; a thickened, tender tendon with chronic, activity-related pain but little warmth or swelling suggests tendinosis
  • Diagnosis
    • Clinical presentation and special tests specific to the joint
    • MRI
  • Medical management
    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs), primarily for acute tendinitis
    • Corticosteroid medications
  • Physical therapy management
    • Flexibility; joint mobilization (performed by the PT)
    • Soft tissue techniques
      • Deep friction massage, a technique described by Cyriax that reaches the deep structures of the body, is used to produce traumatic hyperemia in chronic lesions and to relieve pain, although its effectiveness has not been clearly documented
    • Progressive resistance training, including eccentric loading for tendinosis
    • Modalities for managing pain (for acute tendinitis)
    • Functional mobility training

Bursitis

  • Inflammation of bursae due to overuse, trauma, gout, or infection

  • Symptoms

    • Pain at rest
    • PROM and AROM presenting an empty end feel limited by pain before tissue resistance, not in the joint’s capsular pattern, which suggests a non-capsular (bursal) lesion
    • Swelling of the joint area
    • Redness over the inflamed bursa
    • Warmth to the affected area may feel hot to the touch
    • Tenderness over the affected area when pressed
  • Diagnosis: clinical presentation

  • Medical management

    • Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs)
  • Physical therapy management

    • Same conservative approach as tendinopathy above: flexibility, joint mobilization (performed by the PT), soft tissue techniques, progressive resistance training, modalities for pain and inflammation, and functional mobility training.

Medications and safety across these conditions

Medication implications for the PTA

Medication class PT implications
NSAIDs/acetaminophen Mask pain, so monitor exercise intensity and post-session soreness; watch for GI bleeding and renal effects
Systemic corticosteroids Osteoporosis/fracture risk, skin fragility, delayed healing, hyperglycemia, muscle wasting
Corticosteroid injections Can weaken tendon tissue; avoid aggressive loading of the injected area for 1-2 weeks after injection
DMARDs/biologics (methotrexate, adalimumab) Infection risk, so follow infection-control practice; fatigue is common
Colchicine/allopurinol GI upset (colchicine); starting allopurinol can trigger a gout flare

Safety: recognizing when to modify or stop treatment

  • RA cervical involvement: avoid end-range cervical flexion and manipulation (atlantoaxial instability risk); report new neurologic signs immediately
  • AS with spinal osteoporosis: avoid spinal flexion loading and manipulation; report new spinal pain after minor trauma (fracture risk)
  • Possible septic bursitis: fever or spreading redness - stop treatment and report to the PT immediately
  • Acute gout flare: avoid direct pressure or aggressive loading over the affected joint
Key points

Osteoarthritis (OA)

  • Degenerative cartilage breakdown with subchondral sclerosis/osteophytes; most common arthritis
  • Affects weight-bearing joints (spine, hips, knees, great toe) plus hand DIP/PIP/thumb CMC
  • Early intermittent activity pain → chronic weight-bearing pain; morning stiffness <30 min
  • Managed with acetaminophen/NSAIDs and intra-articular corticosteroid injections
  • PT: joint mobility, strengthening, aquatic/aerobic therapy (progressive throughout)

Rheumatoid arthritis (RA) vs. OA

  • RA: autoimmune, bilateral/symmetrical, cycles of exacerbation/remission; affects hands, feet, cervical spine
  • Symptoms: pain/swelling/stiffness (morning stiffness usually >1 hr, vs. <30 min in OA), fatigue, fever, deformities; diagnosed via ESR, rheumatoid factor, anti-CCP
  • Managed with DMARDs (methotrexate, adalimumab) and corticosteroids
  • PT: manage pain/inflammation during flares (gentle AROM/isometrics only); joint mobility work and resistance training in remission
  • Cervical involvement: avoid end-range flexion/manipulation (atlantoaxial instability risk)
  • Key contrast: OA is mechanical/asymmetrical with progressive strengthening; RA is autoimmune/symmetrical with systemic symptoms and flare-limited loading

Psoriatic arthritis & Ankylosing spondylitis (AS)

  • Psoriatic arthritis: autoimmune, linked to psoriasis; affects axial skeleton/digits; skin/nail changes, enthesitis; PT emphasizes mobility, joint protection, aquatic/aerobic work
  • AS: autoimmune spinal inflammation, more common in men; causes kyphosis, loss of lordosis, spinal fusion, osteoporosis
  • Diagnosis: HLA-B27 antigen, bone scan uptake at spine/SI joints
  • PT: emphasize spinal extension, strengthen spinal/hip extensors, freestyle swimming, respiratory maintenance; avoid high-impact/contact sports and forced or loaded spinal flexion (fracture risk)

Gout

  • Elevated serum uric acid (hyperuricemia) causing uric acid crystal deposits; primary (inherited purine metabolism disorder, men/postmenopausal women) vs. secondary (kidney-related, any age)
  • Sudden severe pain/swelling/redness, often first MTP joint; diagnosed via serum uric acid
  • Medications: NSAIDs, colchicine, corticosteroids, allopurinol, COX-2 inhibitors
  • PT: gait training with assistive device during flare; dietary education (limit red/organ meats, shellfish, alcohol, fructose)
  • Avoid pressure/loading on joint during flare; starting allopurinol may trigger flare

Tendinopathy & Bursitis

  • Tendinitis = acute inflammation (pain, swelling, warmth); tendinosis = chronic degeneration (no inflammation) → treat with progressive/eccentric loading, not anti-inflammatories
  • Bursitis: inflammation of bursae (overuse, trauma, gout, infection); empty end-feel, pain before resistance, non-capsular pattern
  • Both managed with acetaminophen/NSAIDs (corticosteroids also listed for tendinopathy) and PT: flexibility, joint mobilization (by the PT), soft tissue work, progressive resistance, modalities, functional training
  • Watch for septic bursitis (fever, spreading redness) — stop and notify PT

Medication implications & Safety for PTA

  • NSAIDs/acetaminophen mask pain—monitor exercise intensity/soreness; GI/renal risks
  • Systemic corticosteroids: osteoporosis, fragile skin, delayed healing, hyperglycemia, muscle wasting
  • Corticosteroid injections: avoid aggressive loading of area for 1-2 weeks
  • DMARDs/biologics: infection risk, fatigue common
  • Report RA flare signs (pain >1-2 hrs post-exercise, swelling/warmth), new neuro signs, new spinal pain after trauma, or septic bursitis signs immediately to supervising PT

More from Other musculoskeletal conditions

  • Muscle, bone, and pain conditions