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Arthropathies Cheat Sheet by



- Diffuse Idiopathic Skeletal Hypero­stosis
- Calcif­ication and ossifi­cation of ligaments, spine and peripheral entheses
- Decreased ROM, Stiffn­ess­,dy­sphagia
- ALL mainly affected , PLL can be affected and can cause spinal stenosis
- Vertebral motion unaffected
- Tx spine most affected (T7-T11) on the right - aortic pulsation

DISH Demogr­aphics

- Rare in <50 years old patients
- More males than females
- Usually 3rd and 5th decade of life
- White people affected more than any other race
- Associated with Diabetes, obesity, gout, hyperl­ipi­demia, HLA-B8 & hypert­ension
- No associ­ation with HLA-B27

DISH Presen­tation

- Pain due to nerve imping­ement and/or bony growths
- Decreased in ROM
- Dysphagia, hoarse­ness, sleep apnea if in the cx
- Spinal­/ex­tremity pain

DISH Invest­iga­tions

- CRP, ESR, RF, ANA normal
- AP and lateral X-rays gold standard
- CT and MRI for occult f#

DISH on x-ray

Ossifi­cation of the Anterior Longit­udinal Ligament (ALL)
- Radiol­­ucent horizontal cleft
- Disc height preserved (OA)
- Bony bars
- No sacroi­lii­tis­/facet joint involv­ement (AS)
- Hypero­­stosis ends from mid-an­­terior portion of the VB (out and up) on 4 or more contiguous vertebrae
- Looks like flowing candle wax
- Can affect costot­­ra­n­s­verse, costo-­­ve­r­t­ebral and other joints

DISH in other areas

Most commonly in the pelvis, patella, calcaneus, and elbow - can affect any place where there is a ligame­nto­us/­ten­dinous insertion
"­Whi­ske­rin­g" of the bone and ossifi­cation of ligame­nt/­tendon


- AS
- Spondy­losis Deformans (no tx ALL ossifi­cation)
- Serone­gative spondy­loa­rth­rop­athies
- Charcot Spine
- Acromegaly
- Psoriasis
- Reactive arthritis
- Pseudogout
- Hypopa­rat­hyr­oidism


- Mobili­sation and NSAIDs
- Hip and Knee ossifi­cation may require surgery if severely affecting ADL
- Exercise (ROM exercises, stretching of muscles, streng­thening of muscles)
- Bispho­sph­onates
- Activity modifi­cation
- Surgery if: F#, Cx myelop­athy, lx stenosis, neurol­ogical deficits, infection, painful deformity


Cx Radicu­lopathy
VB f#
Hetero­topic ossifi­cation


- Most Common cause of chronic inflam­matory arthritis
- Build up of uric acid - after breaking down purines
- Sodium urate builds up in joints

Gout Causes­/Risk Factors

- Hyperu­rcemia
- Male (>40yo)
- Obesity/ Hyperl­ipi­daemia
- Purine diet (fish, meats)
- Alcoho­l/soft drinks
- Medication (diure­tics, low dose aspirin, ethamb­utol, pyrazi­namide, cyclos­porine)
- Genetics (SLC2A9, ABCG2, SLC22A12, GCKR, PDZK1)
- Kidney disease
- Heart failure
- Metabolic syndromes
- Stress (surgery, trauma, starva­tion), diet, drugs can trigger a flare up

Gout Presen­tation

- Usually 1st MTP joint, talar, subtalar, ankle and knee can be affected
- Check tendons and bursas
- Acute onset of joint pain
- Wakes patient up/dev­elops gradually over few hours (reaches max intensity within 24 hours)
- Severe pain - sometimes tender to touch
- Swollen, red, warm joint
- Can also have systemic signs- fever, malaise, fatigue
- Tophi on joints, ears, finger pads, tendons, bursae

Gout DDx

- Septic Arthritis
- OA
- RA
- Psoriatic arthritis
- Cellulitis

Gout Invest­iga­tions

- Synovial fluid (yellow and cloudy, crystals and white blood cells)
- Synovial fluid in septic arthritis will be more opaque with yellow­-green appear­ance, higher WBC count and positive gram stain
- Polarising microscopy (needl­e-s­haped, negative birefr­ingent crystals)
- Arthro­cen­tesis (confirms diagnosis and rules out septic arthritis, lyme disease or pseudo­gout)
- ESR, CRP, serum urate can be elevated
- Urine uric acid
- US (hyper­echoic enhanc­ement on the cartil­age), DECT

Gout vs CPPD crystals

Above is Gout and CPPD crystals under polarising light microscopy

Gout on imaging

Yellow Arrow = Over hanging margin sign
Red Arrow = Marginal Erosions
Green Arrow = Peri-a­rti­cular Erosion
- Tophi around joints
- Paraar­ticular erosion + sclerosis and overha­nging margin sign
- Feet, hands, elbow mainly affected
- Can destroy the joint if chronic
- "­­lumpy and bumpy"

Gout Management

- Reducing inflam­mation + suppresion of serum urate levels
- Acute
- Rx should be started within 24 hours of first flare up
- Ice packs, NSAIDs, colchi­cine, systemic glucoc­ort­icoids for 7-10 days
Urate-­low­ering therapy (ULT)
Guidelines for ULT:
- Frequent Flares (>2­/year)
- CKD stage 2 or more
- Tophus diagnosis on physical exam or imaging
- Past urolit­hiasis
- 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)
- Modifi­cation of lifestyle: limiting alcohol, meats,­sea­food, sugar, weight loss, drinking more water
Colchicine Contra­ind­ica­tions: Older popula­tions, patients with chronic kidney and liver problems, taking other medica­tions that affect cytochrome P450 and P-glyc­opr­otein should stop/m­odify medica­tion.
Glucoc­ort­icoids can be offered instead to the above patients
Colchine side effects: Vomiting, nausea, diarrheoa, myotox­icity, myelos­upp­ression

Gout Prognosis

- Depends on comorb­idity
- Mortality higher in people with cardio­vas­cular problems
- Most patients live normal life
- Younger patients have gout more severelyr

Gout Compli­cations

- Tophi
- Joint deformity
- OA
- Bone loss
- Urate nephro­pathy and nephro­lit­hiasis
- Conjun­cti­vitis
- Uveitis
- Scleritis


- Hydrox­yap­atite Deposition Disease
- AKA calcific tendinitis
- Common in shoulder, elbow, wrist, hip, knee, ankle, spine
- Metapl­astic transf­orm­ation of tenocytes to chrond­rocytes
- Women 4th and 5th decade of life
- Some can be bilateral
- Critical area of suprap­inatus tendon is most commonly affected then lower side of infras­pin­atous and preins­ert­ional area of the subsca­pularis tendon

HADD Stages

- Precal­cific stage: Tendon transforms into fibroc­art­ila­ginous tissue
- 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
- Postca­lcific: Tendon remodelled by fibrob­lasts - lasts several months , complete healing occurs

HADD Presen­tation

- Low grade pain
- Acute/­gradual restricted ROM
- Can resolve sponta­neously
- +ve shoulder imping­ement signs
- Can be severe and wake patient up at night

HADD on imaging


- Toothp­aste- Like
- Low signal on both T1 & T2
- Outside articu­lating surfaces

HADD radiograph appearance

- Type A: Sharply defined, homoge­nous, dense calcif­ication
- Type B: Sharply defined, dense in appear­ance, multiple fragments
- Type C: Hetero­genous calcif­ication in appearance with dawny deposit
- Type D: Dystrophic calcif­ication in the tendon insertion
- C and D = resorptive phase

HADD Management

- Rest
- Physical therapy (Shoulder ROM, scapular streng­the­ning)
- Cortic­ost­eroid injections
- Shockwave therapy
- US therapy
- Surgery if no better within 6 months (last resort)

Charcot Joint

- Damage of the nerves, injured extremity due to lack of sensation
- Decreased Pain sensation and propri­oce­ption
- Joint is swollen + unstable
- Thought to be
Neurot­rau­matic: Neuropathy + repeated microt­rauma = joint destru­ction
Neurov­asc­ular: Increased peripheral blood flow= osteolysis + demine­ral­isation
- Dysfun­ction between Calcatonin gene related peptide (CGRP), nuclear factor-kB ligand (RANKL) and osteop­rot­egerin (OPG)

Charcot Stages

- Stage 0: Red, hot, swollen foot with no deformity with normal radiog­raphs
Stage I: Erythema, foot oedema, elevated temper­ature, no pain
Boney debris, fragme­nation of subchr­ondral bone, joint sublux­ati­on/­f#/­dis­loc­ation on X-ray
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
Stage III: Inflam­mation resolves, changes in foot archit­ecture due to bone remode­lling - risk of ulceration due to new pressure points

Charcot Causes

- Diabetic Neuropathy
- Spinal Cord injuries
- Poliom­yelitis
- Leprosy
- Syphilis
- Syring­omyelia
- Chronic alcoholism
- Charcot Marie Tooth Disease
- Steroids
Knee Involv­ement: Tabes Dorsalis
Talona­vic­ular/ Tarsom­eta­tarsal: Diabetes

Charcot Presen­tation

- Erythe­matous Foot with oedema and calor
- Unilat­eral, sudden onset after trauma­/re­pet­itive microt­rauma
- Inflam­mation
- Gait and biomec­hanical alterc­ations

Charcot DDx

- Osteom­yelitis (can trigger Charcot disease)
- Cellulitis
- Septic Arthritis
- Gout/p­seu­dogout
- Foot/ankle sprain
- F#

Charcot in Imaging

- Disloc­ation + displa­cement of the joint rules out infection.
- Can present similar to DJD (ghost chrond­roc­ytes, subcho­ndral cysts, sclerotic bone, fragmented and irregular cartilage thinning) and Osteom­yelitis
- Bone biopsy and histology to determine charcot joint vs osteom­yelitis (OM has plasma cells, lympho­cytes, neutro­phills + reactive new bone formation + necrosis + capillary fibrosis and prolif­eration
- CT can also be prescribed - labeled white blood cell nuclear imaging


The 6 Ds
Distended Joint
Density Increase

Charcot Management

- In early stages, immbolise foot and restrict weight bearing (crutches, wheelc­hairs)
- Fractures may heal on their own in a stable position if not stressed
- Bispho­sph­onates (to inhibit osteoc­lastic reabso­rption)
- Calcitonin supple­ments
- Pamidr­onate, Zoledronic acid
- Surgery (although contro­versial in acute stages)
- Stopping smoking if relevant

Charcot Prognosis

- 8 months recovery time
- Majority develop ulcera­tions

Charcot Compli­cations

- Foot deform­ities (flatfoot, rocker bottom foot, hammer toes, ankle equinus contra­cture)
- Boney promin­ences - ulcera­tions, infection, possible amputation
- Condition can reoccur again
- 5 year mortality = 13%


- Calcium Pyroph­osphate Dihydrate Disease
- Involves synovial and periar­ticular tissues
- Can cause acute inflam­matory reaction (pseud­ogout)
- Chondr­oca­lci­nosis = deposition of crystals in cartilage
- Can also be mistaken for RA
- Affects large, weight -bearing joints

CPPD Causes

- Imbalance between production of pyroph­osphate and pyroph­osp­hatases in the cartilage
- Hyperp­ara­thy­roidism
- Gout
- OA
- RA
- Haemoc­hro­matosis
- Osteop­orosis
- Hypoma­gne­saemia
- Chronic kidney disease
- Calcium supple­ments
- >65 years old, male

CPPD Presen­tation

- Symptoms caused by the crystals causing an inflam­matory response from the immune system
- Joint Oedema
- Erythma
- Tenderness
- Some can have a low grade fever
- Waxing and waning of non-sy­nch­ronous inflam­matory arthritis in the non-weight bearing joints


- Gout
- RA
- AS
- Erosive OA
- Haemoc­hro­matosis
- Hyperp­ara­thy­roidism
- Wilson's disease

CPPD Imaging

CPPD of the Knee
- Calcif­­ic­ation in joint compar­­tments
DJD presen­­tation in an unusual location = CPPD
- In scapho - lunate ligament , causes a wide
scapho­­-l­unate joint + collapse of wrist
- Arthro­cen­tesis for synovial fluid analysis (rhomboid crystals) + radiog­raphy
- US for cartilage abnorm­alities

CPPD Management

- Decrease inflam­mation and stabil­ising the underlying disease
- Joint aspiration and intraa­rti­cular glucoc­ort­icoid if acute and 1-2 joints affected
- >3 joints affected - NSAIDs if contra­ind­icated, colchi­cin­e/s­ystemic glucoc­ort­icoids
- Rule out septic arthritis (synovial fluid cultures)
- Ice packs and joint rest
- If younger patient, screen for metabolic conditions (Hyper­par­ath­yro­idism, haemoc­hro­matosis and family hx)

CPPD Prognosis

- Self limiting usually involves within days-weeks
- Compli­cat­ions:
- Degrad­ation of menisci and synovial tissue
- Gout Tophi
- Spinal involv­ement (Mistaken for AS, DISH)

Refer if

- Unclear aetiology with hyperu­ricemia
- Unclear aetiology with normal serum urate levels
- Patients with renal impairment
- Failed trial of XOI
- Multiple side effects from medica­tions
- Refractory gout (Level 1)


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