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- Diffuse Idiopathic Skeletal Hyperostosis
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- Calcification and ossification of ligaments, spine and peripheral entheses
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- Decreased ROM, Stiffness,dysphagia
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- ALL mainly affected , PLL can be affected and can cause spinal stenosis
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- Vertebral motion unaffected
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- Tx spine most affected (T7-T11) on the right - aortic pulsation
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- Rare in <50 years old patients
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- More males than females
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- Usually 3rd and 5th decade of life
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- White people affected more than any other race
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- Associated with Diabetes, obesity, gout, hyperlipidemia, HLA-B8 & hypertension
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- No association with HLA-B27
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- Pain due to nerve impingement and/or bony growths
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- Decreased in ROM
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- Dysphagia, hoarseness, sleep apnea if in the cx
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- Spinal/extremity pain
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- CRP, ESR, RF, ANA normal
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- AP and lateral X-rays gold standard
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- CT and MRI for occult f#
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- AS
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- Spondylosis Deformans (no tx ALL ossification)
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- Seronegative spondyloarthropathies
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- Charcot Spine
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- Acromegaly
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- Psoriasis
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- Reactive arthritis
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- Pseudogout
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- Hypoparathyroidism
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- Mobilisation and NSAIDs
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- Hip and Knee ossification may require surgery if severely affecting ADL
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- Exercise (ROM exercises, stretching of muscles, strengthening of muscles)
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- Bisphosphonates
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- Activity modification
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- Surgery if: F#, Cx myelopathy, lx stenosis, neurological deficits, infection, painful deformity
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Myelopathy
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Cx Radiculopathy
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Dysphagia
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VB f#
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Instability
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Heterotopic ossification
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- Most Common cause of chronic inflammatory arthritis
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- Build up of uric acid - after breaking down purines
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- Sodium urate builds up in joints
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- Hyperurcemia
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- Male (>40yo)
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- Obesity/ Hyperlipidaemia
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- Purine diet (fish, meats)
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- Alcohol/soft drinks
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- Medication (diuretics, low dose aspirin, ethambutol, pyrazinamide, cyclosporine)
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- Genetics (SLC2A9, ABCG2, SLC22A12, GCKR, PDZK1)
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- Kidney disease
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- Heart failure
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- Metabolic syndromes
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- Stress (surgery, trauma, starvation), diet, drugs can trigger a flare up
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- Usually 1st MTP joint, talar, subtalar, ankle and knee can be affected
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- Check tendons and bursas
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- Acute onset of joint pain
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- Wakes patient up/develops gradually over few hours (reaches max intensity within 24 hours)
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- Severe pain - sometimes tender to touch
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- Swollen, red, warm joint
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- Can also have systemic signs- fever, malaise, fatigue
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- Tophi on joints, ears, finger pads, tendons, bursae
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- CPPD
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- Septic Arthritis
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- OA
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- RA
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- Psoriatic arthritis
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- Cellulitis
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- Synovial fluid (yellow and cloudy, crystals and white blood cells)
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- Synovial fluid in septic arthritis will be more opaque with yellow-green appearance, higher WBC count and positive gram stain
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- Polarising microscopy (needle-shaped, negative birefringent crystals)
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- Arthrocentesis (confirms diagnosis and rules out septic arthritis, lyme disease or pseudogout)
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- ESR, CRP, serum urate can be elevated
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- Urine uric acid
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- US (hyperechoic enhancement on the cartilage), DECT
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- Reducing inflammation + suppresion of serum urate levels
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- Acute
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- Rx should be started within 24 hours of first flare up
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- Ice packs, NSAIDs, colchicine, systemic glucocorticoids for 7-10 days
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Non-acute:
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Urate-lowering therapy (ULT)
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Guidelines for ULT:
- Frequent Flares (>2/year) - CKD stage 2 or more - Tophus diagnosis on physical exam or imaging - Past urolithiasis |
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- Medications including Xanthine Oxidase Inhibitors (XOI) - stops synthesis of uric acid (Allopurinol, febuxostat)
Uricosuric: increases renal urate clearance (Probenecid, Lesinurad) Interleukin-1 inhibitor: Blocks interleukin-1 (anakinra, canakinumab) |
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- Modification of lifestyle: limiting alcohol, meats,seafood, sugar, weight loss, drinking more water
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- Depends on comorbidity
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- Mortality higher in people with cardiovascular problems
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- Most patients live normal life
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- Younger patients have gout more severelyr
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- Tophi
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- Joint deformity
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- OA
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- Bone loss
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- Urate nephropathy and nephrolithiasis
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- Conjunctivitis
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- Uveitis
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- Scleritis
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- Hydroxyapatite Deposition Disease
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- AKA calcific tendinitis
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- Common in shoulder, elbow, wrist, hip, knee, ankle, spine
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- Metaplastic transformation of tenocytes to chrondrocytes
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- Women 4th and 5th decade of life
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- Some can be bilateral
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- Critical area of suprapinatus tendon is most commonly affected then lower side of infraspinatous and preinsertional area of the subscapularis tendon
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- Precalcific stage: Tendon transforms into fibrocartilaginous tissue
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- Calcific stage: Calcium deposits
Consists of formative and resorptive phase Formative: Calcium crystals deposit into the tendon by chondrocytes Resorptive: Vascular weaving + Macrophages phagocytose calcium, oedema and increased pressure in the tendon, calcium crystals may move into the bursa - Most painful phase |
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- Postcalcific: Tendon remodelled by fibroblasts - lasts several months , complete healing occurs
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- Low grade pain
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- Acute/gradual restricted ROM
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- Can resolve spontaneously
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- +ve shoulder impingement signs
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- Can be severe and wake patient up at night
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- Toothpaste- Like
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- Low signal on both T1 & T2
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- Outside articulating surfaces
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- Type A: Sharply defined, homogenous, dense calcification
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- Type B: Sharply defined, dense in appearance, multiple fragments
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- Type C: Heterogenous calcification in appearance with dawny deposit
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- Type D: Dystrophic calcification in the tendon insertion
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- C and D = resorptive phase
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- Rest
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- Physical therapy (Shoulder ROM, scapular strengthening)
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- SMT
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- NSAIDs
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- Corticosteroid injections
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- Shockwave therapy
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- US therapy
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- Surgery if no better within 6 months (last resort)
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- Damage of the nerves, injured extremity due to lack of sensation
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- Decreased Pain sensation and proprioception
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- Joint is swollen + unstable
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- Thought to be
Neurotraumatic: Neuropathy + repeated microtrauma = joint destruction Neurovascular: Increased peripheral blood flow= osteolysis + demineralisation |
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- Dysfunction between Calcatonin gene related peptide (CGRP), nuclear factor-kB ligand (RANKL) and osteoprotegerin (OPG)
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Eichenholtz:
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- Stage 0: Red, hot, swollen foot with no deformity with normal radiographs
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Stage I: Erythema, foot oedema, elevated temperature, no pain
Boney debris, fragmenation of subchrondral bone, joint subluxation/f#/dislocation on X-ray |
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Stage II: Decreased signs of inflammation
Absorption of boney debris + new bone formation, merging of large fragments with sclerosis of bone ends, stability slowly increases, however x-ray looks worse than stage I |
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Stage III: Inflammation resolves, changes in foot architecture due to bone remodelling - risk of ulceration due to new pressure points
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- Diabetic Neuropathy
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- Spinal Cord injuries
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- Poliomyelitis
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- Leprosy
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- Syphilis
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- Syringomyelia
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- Chronic alcoholism
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- Charcot Marie Tooth Disease
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- Steroids
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- Erythematous Foot with oedema and calor
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- Unilateral, sudden onset after trauma/repetitive microtrauma
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- Inflammation
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- Gait and biomechanical altercations
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- Osteomyelitis (can trigger Charcot disease)
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- Cellulitis
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- Septic Arthritis
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- Gout/pseudogout
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- Foot/ankle sprain
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- F#
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- DVT
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The 6 Ds
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Distended Joint
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Density Increase
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Debris
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Dislocation
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Disorganisation
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Destruction
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- In early stages, immbolise foot and restrict weight bearing (crutches, wheelchairs)
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- Fractures may heal on their own in a stable position if not stressed
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- Bisphosphonates (to inhibit osteoclastic reabsorption)
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- Calcitonin supplements
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- Pamidronate, Zoledronic acid
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- Surgery (although controversial in acute stages)
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- Stopping smoking if relevant
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- 8 months recovery time
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- Majority develop ulcerations
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- Foot deformities (flatfoot, rocker bottom foot, hammer toes, ankle equinus contracture)
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- Boney prominences - ulcerations, infection, possible amputation
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- Condition can reoccur again
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- 5 year mortality = 13%
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- Calcium Pyrophosphate Dihydrate Disease
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- Involves synovial and periarticular tissues
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- Can cause acute inflammatory reaction (pseudogout)
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- Chondrocalcinosis = deposition of crystals in cartilage
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- Can also be mistaken for RA
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- Affects large, weight -bearing joints
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- Imbalance between production of pyrophosphate and pyrophosphatases in the cartilage
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- Hyperparathyroidism
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- Gout
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- OA
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- RA
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- Haemochromatosis
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- Osteoporosis
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- Hypomagnesaemia
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- Chronic kidney disease
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- Calcium supplements
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- >65 years old, male
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- Symptoms caused by the crystals causing an inflammatory response from the immune system
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- Joint Oedema
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- Erythma
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- Tenderness
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- Some can have a low grade fever
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- Waxing and waning of non-synchronous inflammatory arthritis in the non-weight bearing joints
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- Gout
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- RA
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- AS
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- Erosive OA
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- Haemochromatosis
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- Hyperparathyroidism
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- Wilson's disease
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- Decrease inflammation and stabilising the underlying disease
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- Joint aspiration and intraarticular glucocorticoid if acute and 1-2 joints affected
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- >3 joints affected - NSAIDs if contraindicated, colchicine/systemic glucocorticoids
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- Rule out septic arthritis (synovial fluid cultures)
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- Ice packs and joint rest
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- If younger patient, screen for metabolic conditions (Hyperparathyroidism, haemochromatosis and family hx)
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- Self limiting usually involves within days-weeks
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- Complications:
- Degradation of menisci and synovial tissue - Gout Tophi - Spinal involvement (Mistaken for AS, DISH) |
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- Unclear aetiology with hyperuricemia
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- Unclear aetiology with normal serum urate levels
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- Patients with renal impairment
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- Failed trial of XOI
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- Multiple side effects from medications
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- Refractory gout (Level 1)
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