Tibiofemoral Joint – formed between tibia and femur

A HINGE JOINTPatellofemoral joint – formed between the

patella and the femur A GLIDING JOINT

Femurproximal – head and neck of

femur, greater trochanter

distal – medial and lateral

condyles and epicondyles

Patella – largest sesamoid bone in body

Tibia – tibial plateau forms knee joint with femur

The fibula is not a part of the knee joint

The Quadriceps – Knee Extension

1. Vastus Medialis2. Vastus Lateralis3. Vastus Intermedius4. Rectus Femoris – 2 joint

muscle that also acts as a hip flexor

               

The Hamstrings- knee flexion

3 muscles:1. Biceps Femoris2. Semimembranosus3. Semitendinosus

The Adductors (Groin)Adduct the thigh

1. Adductor Longus2. Adductor Magnus3. Adductor Brevis4. Gracilis

The Sartorius: - flexes,

abducts, and laterally rotates thigh

- longest muscle in the body, “tailor’s muscle”

- Crosses hip and knee joint

The Iliotibial Tract(IT Band)

- neither a muscle or tendon, but a long, thick band of tissue that inserts into the lateral tibia (Gerdy’s Tubercle)

1. ACL – Anterior Cruciate Ligament2. PCL – Posterior Cruciate Ligament3. MCL – Medial Collateral Ligament4. LCL – Lateral Collateral Ligament

MCL:- Medial Collateral

Ligament- Runs from

medial femur to medial tibia

LCL:- Lateral Collateral

Ligament- Runs from lateral

femur to head of fibula

A “c”-shaped piece of fibrocartilage located in the knee joint between the femur and attached to the top of the tibia

Cartilage = meniscus

Medial

- larger and more C-shaped

- more firmly attached to tibia - has attachments to MCL

Lateral

- smaller and more round or O-shaped- not firmly attached to tibia and LCL

Mostly avascular – little or no blood supplyOnly the outer 20% has a blood supply* Does not have the ability to heal itself unless

there is a small tear in the outer 20%

1. Stability2. Shock absorption3. Lubrication and nutrition4. Allows adequate weight distribution

Normal Torn

TraumaFractures around kneeLigamentous sprainsMuscular strains

Degenerative conditionsOsteoarthritis of knee jointOsteochondritis dessicansTraumatic arthritis

Inflammatory conditionsRheumatoid arthritisJuvenile RheumatismNeuropathic jointHemophilic arthritisBursitisOther conditions

InfectionSuppurative arthritisTuberculosis

Tumors around knee jointTumors of boneTumors of soft tissue

Metabolic conditionsRicketsScurvyGoutOchronotic ArthritisOsteoporosis

Congenital and Developmental conditionsGenu valgumGenu varumGenu recurvatumCongenital dislocation of patellaCongenital discoid meniscus

Fractures around kneeSupra condyler femur fractureFractures of the isolated condyleTibial condyle and plateau fractureFracture patellaTibial tuberosity avulsion

Fractures of the femoral condyle at metaphysis level extending in to knee joint

Fractures of the isolated condyleHoffa’s FractureEpicondyler avulsions

Both condyle fractures Isolated condyle fractures Tibial spine fracture

>200,000 injuries/year>100,000 reconstructions/yearHigher incidence in femalesMales = contact

Females = noncontact

1. MOI: twisting of knee forced hyperextension lateral blow to knee

*foot must be firmly anchored to playing surface

2. 50% of people describe a “pop” in knee 3. Knee fills with blood quickly

Hemarthrosis4. Usually immediate loss of motion5. Knee feels unstable

Anterior Drawer Test:

examiner attempts to slide the tibia forward which may indicate a torn ACL ligament

Who needs surgery? - Activity level? - Level of Competition - Age?

ArthroscopicGraft options

Patellar TendonSemitendinosusGracilisCadaverSynthetic

1. MOI: excessive hyperextension hyperflexion

tibia forced posteriorly (blow to front of knee)“dashboard knee”

Possibly 90% of all PCL injuries due to motor vehicle accidents?

2. Mild hemarthrosis3. Posterior knee pain4. Walk with knee

slightly flexed, avoid full extension

5. Posterior sag of tibia6. Surgery?

MOI: Blow to the outside of the knee = Valgus Force Possible overuse – breaststroke in swimmers

Commonly associated with meniscal injuries – attached to medial meniscus

No surgery

Valgus Stress Test:tests for injury to the MCL ligament

MOI: Blow to inside of the knee – Varus force

Grade III tear may require surgery

Varus Stress Test:tests for injury to the LCL ligament

1. MOI: Rotation of the knee as the knee extends during rapid cutting or pivoting

2. Signs and Symptoms:- pain- joint line tenderness- catching or locking- knee buckling or giving way- swelling- incomplete flexion- clicking on stair climbing

3. Surgery?Meniscectomy: removal of the

meniscus- Total meniscectomy = osteoarthritis

Depends on location of tear, type of tear, and blood supply

- bucket handle- Flap tear- Transverse tear- Horn tear

Apley’s Compression

Tear of the medial meniscus, anterior cruciate ligament (ACL), and medial collateral ligament (MCL)

Osteoarthritis of knee jointOsteochondritis dessicansTraumatic arthritis

Disease of the joints characterized by:

– Progressive articular cartilage loss

– New subchondral bone formation

– New bone and cartilage formation at joint margins

– Low level synovitis

& PAIN!

– Joint Pain

– Typical Pain Pattern

– Xray FindingsStanding filmsAP with 30 deg

flexion

– No Sign of Zebras

Pathogenesis of Osteoarthritis

An Interplay of Factors

Dieppe, American Academy of Orthopaedic Surgeons, 1995

Age10-fold increase from

3065Genetics (generalized)Gender

Men <50: higher riskWomen >50: higher

riskNutritional

Low vitamin C and D intake

Joint Biomechanical Risk FactorsJoint traumaObesity (knee, hip, hand)OccupationAbnormal joint

biomechanicsDysplasia,

malalignment, instability, abnormal innervation

Knee extensor wknessSports w/ joint risk

50% decrease in OA with with 11#

wt lossLarger effect in

women (Felson et. al.

Ann Int Med 1992, Framingham Heart

Cohort data)

Jobs requiring repetitive knee

bending/moderate activity predict higher rates of osteoarthritis

Felson et alAnnals of Int Med 1992

11 lb / 50% risk reduction rule

Break that vicious cycle:

Team approach is critical

Disuse

Weight Gain

Pain and stiffness

Regular aerobic walking for knee OA LOE 1a for knee OA LOE IV for hip OA

Home-based quad strength exercises LOE 1a for knee OA LOE IV for hip OA

Water-based exercise for hip OA LOE 1b

Medial or lateral unloading

Medial tibio-femoral OA

TENS effective in some with knee or hip OA Short-term, 2-4 weeks

Acupuncture relieves pain (no effect on function)

Pulsed Electromagnetic Field Therapy Meta-analysis 2009

Thermotherapies

Tylenol, max 4 gm/day analgesic of choiceLOE 1a, but modest pain relief if OA

mild/modNSAIDs—LOE 1aTramadol: LOE 1a in short-term trials

No long-term trialsMore side-effects than Tylenol

Glucosamine

No disease modifying drug for OA (yet)

Considerations before treatment:Surgical candidate?

Don’t waste the timePrevious injections?

Beneficial in KNEEBeneficial in HIPShort-duration benefits: 2-4 weeks

Effective in knee and hip (LOE 1a)Delayed effect (1-3 weeks)Long duration (6 months)Weekly injections, 3-5xMight delay need for joint replacement

X

Arthroscopy Joint replacementCartilage transplantation

Cochrane review 2008: NO BENEFIT for undiscriminated OA (mechanical or inflammatory causes)

LOE IIIUniversally

recommended to improved pain, function, QOLUnicompartmentalTotal joint replacement

                                                            

Osteo-Articular Transplant (OAT) procedures

Autologous Chondrocyte Implantation (ACI)

Cadaver allografts

Due to intraarticular fractures

Malunions lead to joint arthrosis

Primary cartilage insult leading to repair by fibrocartilage and arthrosis

Treatment is TKR if tri compartmental OA

In children and adolescents

Small segments of nactrotic subchondral bone

Pain stiffness and locking

Rest/ debridment of joint/ replacment

Rheumatoid arthritisJuvenile RheumatismNeuropathic jointHemophilic arthritisBursitisOther conditions

Synovitis chronic infl, synovial hypertrophy, effusion Destruction proteolytic enzymes, pannus Deformity articular destruction, capsular stretching,

tendon rupture

nodules tendon sheath vasculitis myopathy and neuropathy reticulo-endothelial system visceral - lungs, heart, kidneys, brain, GI

myopathy, tiredness, weight loss, malaise proximal finger joints wrists, feet, knees, shoulders start up pain tendon crepitus

joint destruction pain deformity instability

joint space narrowing peri-articular osteopenia erosions

stop synovitis prevent deformity reconstruct rehabilitate

10% improve 60% intermittent, slowly worsening 20% severe joint erosion, multiple surgery 10% completely disabled

Diabetes is the leading cause:1/700, 0.16-2.5% of all diabeticsUsually in the 5th or 6th decade of lifeRelated to duration and control of diabetesInvolvement includes:

Tarsometatarsal/metatarsophalangeal joints Ankles Knees Upper limbs (rare)

Giurini. Charcot's disease in diabetic patients. Postgrad Med 1991; Brower. Sinha. Neuro-arthropathy (Charcot joints) in diabetes mellitus (clinical study of 101 cases). Medicine (Baltimore) 1972; 51:191 .

Reported associations: Leprosy Alcoholism Uremia Amyloidosis Pernicious anemia Syphillis (tertiary) Syringomyelia Spina Bifida Myelomeningocele Cord compression Cauda Equina lipoma

MS Poliomyelitis Connective Tissue disorder Charcot-Marie-Tooth disease Congential sensory neuropathies Ehlers-Danlos syndrome Familial dysautonomia Thalidomide embryopathy Intraarticular steroids

Radiographics. 2000;20:S279-S293

Storey GO.Charcot joints. Rheumatol Phys Med. 1970 Aug;10(7):312-20.

Problems with patella – most common cause of knee pain

Anatomy:- Patella is a sesamoid bone formed in Quad tendon- Patellofemoral joint – patella and femur- Compression forces –

<body weight during walking2.5 x body weight during stairs

“Jumper’s Knee”Inflammation and degeneration of the tendon

that connects the kneecap (Patella) to the shin bone (Tibia).

A gradual degenerative change that occurs beneath the patella

Caused by acute trauma, repeated microtrauma, or improper alignment of the patella in the trochlear groove

Weak vastus medialis (VMO) can cause improper alignment

Prevention: strengthen quadsMinimize squats, downhill

running, biking with low seat

1. Painful swelling over tibial tuberosity(patellar tendon insertion)

2. Usually occurs between 9-13 years of age3. Pain increases with activity

Occurs where IT Band rubs over femur at the knee joint

Common in running (esp. downhill) or any activity with repetitive flexion

Hills or stairs increase painLots of IT Band stretching

“Baker’s Cyst”Fluid accumulation in posterior knee

(popliteal space)Patient usually complains of a mass behind

the knee

“Housemaid’s Knee”Tender swelling over

the kneecap (prepatellar bursa)

Pes anserine bursitis is an irritation or inflammation of a bursa in your knee. The pes anserine bursa is located on the inner side of the knee just below the knee joint.

Tendons of three muscles attach to the shin bone (tibia) over this bursa

Suppurative arthritisTuberculosis

Bacterial: staphylococcus

streptococcus

Gonococcus

H. pneumonia

gram negative organisms

Mycobacterium:TB, atypical TB

Fungi: candida

Spirochete: lyme (borrelia burgdorfi)

Viral: HIV, Hepatitis B, C

Tumors of boneTumors of soft tissue

Signs/Symptoms:Pain, characteristically more intense at night,

relieved by NSAIA and eliminated by excisionVertebral lesions may cause scoliosis

Age:10-30 years

Sex:M > F (2:1)

Anatomic Distribution:Nearly every location, most frequent in femur,

tibia, humerus, bones of hands and feet, vertebrae and fibula

Over 50% of cases in femur or tibiaMetaphysis of long bones

Central radiolucent nidus with or without a radiodense center; surrounded by thickened sclerotic bone

Central hemorrhagic nidus surrounded by dense rim of

sclerotic bone

Nidus contains interlacing network of osteoid and bony

trabeculae with variable amount of mineralization, lying in vascular fibrous tissue

Signs/Symptoms:PainGait disturbances

Age:80% of patients < 30 years

Sex:M >> F (3:1)

Anatomic Distribution:Predilection for vertebral columnMetaphysis of long bones

Radiographic Findings:Similar to osteoid osteoma, though much larger (up

to 11.0 cm)

Gross and Microscopic Findings:Similar to osteoid osteoma, though much larger nidus

Ancillary Testing:N/A

Prognosis/Treatment:Curettage followed by bone graftingIf incompletely removed, tumor may recurMalignant change to osteosarcoma has been rarely

reported

Most frequent primary malignant bone tumor

Malignant cells must produce osteoidMost tumors arise de novo, though others

arise in the setting of:Paget’s diseasePrevious RTPrevious chemo (especially alkylating agents)Fibrous dysplasiaOsteochondromatosisChondromatosisChronic osteomyelitis

Signs/Symptoms:Pain and swellingPathologic fracture is uncommon

Age:Peak in 2nd decade with gradual decrease thereafter

Sex:M > F

Anatomic Distribution:50% arise around the kneeMetaphysis of long bones

An 11-year-old male was seen in consultation for an increasingly painful distal femoral lesion associated with a soft tissue mass.

Plain radiograph shows an ill-defined destructive tumor in the distal femur. Fluffy radiodense infiltrates represent malignant tumor osteoid.

Biopsy material shows two major components of this neoplasm: highly pleomorphic cells and haphazard deposits of osteoid. Note that the malignant cells fill the spaces between osteoid deposits. Lace-like osteoid deposition is very characteristic of this neoplasm.

The tan-white tumor fills most of the medullary cavity of the metaphysis and proximal diaphysis. It has infiltrated through the cortex, lifted the periosteum, and formed soft tissue masses on both sides of the bone.

Benign:ChondromaOsteochondromaChondroblastomaChondromyxoid Fibroma

Malignant:Chondrosarcoma

Benign tumor of mature hyaline cartilage

Most within bone (enchondroma)2 syndromes characterized by multiple

chondromas:Ollier’s disease

Multiple enchondromas, usually unilateralMaffucci’s syndrome

Multiple enchondromas associated with soft tissue hemangiomas

Both disorders have 25% risk of malignant transformation to chondrosarcoma

Enchondroma is the most common tumor of the bones of the hand

Signs/Symptoms:Usually asymptomatic lesions; pain with pathologic

fracture

Age:Evenly distributed

Sex:F > M

Anatomic Distribution:50% of lesions within small bones of hands and feet

(mostly the phalanges)

Localized central lytic lesion surrounded by sharp rim of sclerosis; cortex usually not involved, though

may be thin

An incidental finding of a bone lesion in the distal femur of a 38-year old female. The lesion was completely asymptomatic.

Plain radiograph showed an intarmedullary zone of stippled and ring-shaped calcifications in the distal femoral metaphysis. This mineralization pattern with radiodense stipples and rings is characteristic of mature hyaline cartilage.

Low-power microscopic examination of the biopsy specimen shows three characteristic features of this lesion: a) vague lobularity; b) abundant cartilaginous matrix, which can be focally calcified; c) low cellularity.

High-power view shows clustered and scattered chondrocytes with small, uniform, darkly stained nuclei. Occasional bi-nucleated chondrocytes are present. Importantly, there were no mitotic figures.

Ollier’s disease

Composed of mature lobules of hyaline cartilage with foci of

myxoid degeneration, calcification and endochondral

ossification; may be quite cellular

Ancillary Testing:N/A

Prognosis/Treatment:Solitary chondromas of long or flat bones need no

treatmentIf fracture occurs, treat with curettage and bone

graftingRecurrence unusual

Most frequent benign bone tumorProbably not a true neoplasm, but rather a

tumor produced by growth of aberrant foci of cartilage on the surface of bone

Autosomal dominant disorder of osteochrondromatosis with risk of malignant transformation to chondrosarcoma

Signs/Symptoms:Palpable mass of long durationPain from compression of regional structures

Age:60% of patients < 20 yearsAverage age 10 years

Sex:M > F

Anatomic Predilection:May occur in any bone; usually metaphysis of long

bones (lower end of femur, upper end of humerus and upper end of tibia are most frequent)

Projection with cortex continuous with underlying bone; may be pedunculated; cartilaginous cap with frequent calcification

A 20-year-old male presented with a painless, hard subcutaneous mass in the popliteal fossa. He stated that the mass had been present for several years and did not change in size. Two words, "painless" and "non-growing" (or very slow growing), suggest that the lesion described here is probably benign.

Plain radiograph demonstrated a pedunculated bony outgrowth at the proximal tibial metaphysis. The lesion had a uniform, cartilagenous cap with stippled calcifications. The tibial cortex and medulla were continuous with those of the lesion.

The specimen consisted of a pedunculated lesion, 3 x 3 x 2cm, with a lobulated cartilage cap measuring up to 0.9cm in thickness

Osteochondroma, the most common benign bone tumor, is not a neoplasm but a hamartoma. It is thought to arise from a portion of growth plate cartilage entrapped beneath the periosteum during skeletal growth. These entrapped pieces continue to grow and ossify at the same rate as the adjacent bone. When skeletal maturity is reached, osteochondromas usually stop growing.

Rare benign tumorMost common primary epiphyseal

tumor in childrenSigns/Symptoms:

Local pain and swelling; tumors 1.0 to 7.0 cm

Age:2nd decade of life

Sex:M > F

Anatomic Distribution:Epiphysis of long bones40% in distal femur or proximal tibia

Lytic lesion of epiphysis with thin sclerotic rim; thinning

without destruction of cortex

Rare benign tumorSigns/Symptoms:

Pain and swelling

Age:2nd and 3rd decades

Sex:M > F

Anatomic Distribution:Metaphysis of long bones, though may abut the

epiphysis30% of tumors in tibia

Eccentric, sharply defined radiolucency in metaphysis of long

bones; may destroy cortex

Signs/Symptoms:Local swelling and pain

Age:Adulthood (60% between 30-60 years)Rare in childhood

Sex:M > F

Anatomic Distribution:Trunk, shoulder girdle, upper ends of femur and

humerus

Ill-defined margins; fusiform thickening of shaft; perforation of

cortex

Myxoid Chondrosarcoma

Mesenchymal Chondrosarcoma

Ancillary Testing:IHC

S100 – positive

Prognosis/Treatment:Must completely excise; biopsy leads to soft tissue

implantationRADIORESISTANT; surgery is Tx of choiceRecurrence may occur 5-10 years after primary5-year survival 80%Hematogenous metastasis to lung in high grade

lesions

Giant Cell TumorEwing’s Sarcoma / Primitive

Neuroectodermal Tumor (PNET)Chordoma

Signs/Symptoms:Pain, loss of mobility, fracture

Age:80% of patients > 20 years

Sex:F > M

Anatomic Distribution:Epiphysis of long bones50% around knee with most in distal femurMost common primary epiphyseal tumor of adults

A 45-year old female presented with increasing pain and swelling around the knee. She mentioned that the symptoms had progressed over a 4-month period. Age of the patient is an important diagnostic clue. If a pathologic fracture is excluded, pain and swelling imply active growth of the lesion. Plain film demonstrates a

large, lobulated, ill-defined lesion centered in the distal femoral metaphysis. There is endosteal scalloping and periosteal thickening. Central stippled and "ring and arc" calcifications are apparent and are typical of cartilaginous matrix. Small radiolucent areas are seen at the periphery of the lesion.

Low magnification shows a moderately cellular, lobulated cartilaginous tumor.

High-power view shows scattered plump, moderately pleomorphic chondrocytes. Binucleated cells are present. Mitotic rate averaged 1 per 10 hpf.

Tumor

Geographic and Expansile

Sharp Zone of Transition between Tumor and Normal Bone/Fibula

CT scan shows a thin cortical shell around the tumor indicating the periosteum is intact and the tumor is likely benign

There was no ossification or calcification within the tumor indicating that the tumor was probably not a bone or cartilage producing tumor

Peroneal Nerve

Tumor

Peroneal Muscles

Soleus Muscle

Signs/Symptoms:May simulate osteomyelitis as patients often

present with pain, fever and leukocytosis

Age:5-20 years

Sex:M > F

Anatomic Distribution:Long bones of extremities

Gross Findings:Solid masses of degenerating gray-white tumor

Signs/Symptoms:Usually found incidentally; may cause pain

Age:Children and adolescents

Sex:M > F

Anatomic Distribution:Metaphysis of long bones, usually distal femur and

tibia

Genu valgumGenu varumGenu recurvatumCongenital dislocation of patellaCongenital discoid meniscus

Genu Valgum: “knock knees”

Genu Varum: “bowlegs”

Genu Recurvatum:

hyperextension of the knee joint

Dislocation usually occurs as a result of sudden direction changes while running and the knee is under stress or it may occur as a direct result of injury.

Usually lateral

Rehab: strengthen quads, especially VMO to hold patella in place

Each dislocation will damage cartilage which can eventually lead to traumatic arthritis

RicketsScurvyGoutOchronotic ArthritisOsteoporosis

Mineralization defect are classified according to the mineral deficiency.

Calcipenic rickets ( vit D↓, 1-alpha hydroxylase defect, vit D receptor dysfunction, dietary Ca ↓, CRF) .

Phosphopenic ricket: Inadequate intake  (Premature infants (rickets of prematurity) , Aluminum-containing antacids).

Deficient Intake: Ca, Ph, Vit D.

Poor absorption: vit D ↓, pseudo vit D↓, vit D resistance, high phytin content( soy formula), antacids, anticonvulsants, renal insufficiency, Fanconi syndrome, hepatic insufficiency, fat malabsorption (cystic fibrosis).

Increased excretion: furosemide, renal tubular dysfunction( phosphaturia, RTA with hypercalciuria), renal tubular damage e.g. cystinosis, tyrosinosis, galactosemia, fructose intolerance, wilson disease.

Local effect on bone matrix: hypophosphatasia(alp↓)

VITAMIN D DISORDERS Nutritional vitamin D deficiency; Congenital vitamin D deficiency; Secondary vitamin D deficiency;  Malabsorption ; Increased degradation; Decreased liver 25-hydroxylase; Vitamin D-dependent rickets type 1; Vitamin D-dependent rickets type 2 ;Chronic renal failure.

CALCIUM DEFICIENCY Low intake  Diet  Premature infants (rickets of prematurity) Malabsorption  Primary disease  Dietary inhibitors of calcium absorption

PHOSPHORUS DEFICIENCY Inadequate intake  Premature infants (rickets of prematurity)  Aluminum-containing antacids

RENAL LOSSES X-linked hypophosphatemic rickets; Autosomal dominant hypophosphatemic rickets; Hereditary hypophosphatemic rickets with hypercalciuria; Overproduction of phosphatonin ( Tumor-induced rickets,  McCune-Albright syndrome’  Epidermal nevus syndrome,  Neurofibromatosis) ,Fanconi syndrome, Dent disease

DISTAL RENAL TUBULAR ACIDOSIS

Skeletal findings:

1. Delay in closure of the fontanelles.

2. Parietal & frontal bossing.

3. Craniotabes ( soft skull bones).

4. Enlargement of the costochondral junction (rachitic rosary).

5. The development of Harrison sulcus ( caused by pull of the diaphragmatic attachments to the lower ribs).

6. Enlargement of the wrist & bowing of the distal radius & ulna.

7. Progressive lateral bowing of the femur & tibia.

GENERAL Failure to thrive; Listlessness; Protuding abdomen; Muscle weakness (especially proximal); Fractures.

HEAD Craniotabes; Frontal bossing; Delayed fontanelle closure; Delayed dentition; caries; Craniosynostosis

CHEST Rachitic rosary; Harrison groove; Respiratory infections and atelectasis

BACK Scoliosis ,Kyphosis ,Lordosis

EXTREMITIES Enlargement of wrists and ankles; Valgus or varus deformities Windswept deformity (combination of valgus deformity of 1 leg with varus deformity of the other leg); Anterior bowing of the tibia and femur; Coxa vara; Leg pain.

HYPOCALCEMIC SYMPTOMS Tetany ; Seizures; Stridor due to laryngeal spasm

Extraskeletal manifestation of rickets vary depending upon the 1ry mineral deficiency.

Hypoplasia of the dental enamel is typical for hypocalcemic rickets, whereas abscesses of the teeth occur more often in phosphopenic rickets.

Hypocalcemic seizures, decreased muscle tone leading to delayed motor milestones, recurrent infections, increased sweating.

AntioxidantNot produced in the human bodyNecessary for collagen synthesisProlyl and lysyl hydroxylaseProcollagen triple helix4-8 months of deficiency to develop clinical

signs

Figure 2 : Corkscrew hair [3]

Figure3: gingivitis

Male>>>FemaleAssociated conditions

Hyperlipidemia, obesity, HT, CAD, DMPrecipitating Conditions

ETOH, dietary excess, traumaStress: surgery, GI bleed, MIDrugs: low dose ASA, diuretics, allopurinol

Clinical:Monoarticular ->Cluster ->Polyarticular1st MTP > 90%; any jointPeaks in 12 hoursRed, hot, swollenVery painfulDesquamation of skinTophi

Soft tissue swelling; tophi1st MTP -> any jointOverhanging edgeDestructive +++ if not treated

Aspirate the joint and look for MSU crystals under polarized microscopy