This document provides an overview of joint histopathology. It discusses the articular tissues including cartilage, synovium, and meniscus. It describes the composition and types of cartilage, as well as cartilage healing and lubrication mechanisms. Joint fluid analysis is also covered, distinguishing the characteristics of non-inflammatory versus inflammatory arthritides based on white blood cell count, glucose/protein levels, viscosity, and clot formation.

1. Joint HistopathologyJoint Histopathology
Prepared by:Prepared by:
Dr.Amanj Mohsin MustafaDr.Amanj Mohsin Mustafa
11stst
Year Orthopeadic Trainee At KBMSYear Orthopeadic Trainee At KBMS
SupervisedSupervised
by:by:
Dr.ZainabDr.Zainab
AbdulwahabAbdulwahab

2. ContentsContents
 1.Articular tissues
A.Cartilage
B.Synovium
C.Meniscus
2.Arthroses
 Joint fluid analysis
 Non inflammatory arthritides
 Inflammatory arthritides
 Infectious arthritides
 Hemorrhagic effusions

3. 1.Articular Tissues
A.Cartilage
Function :
-decreases friction and distributes loadsdecreases friction and distributes loads
-avascular, aneural, and alymphaticavascular, aneural, and alymphatic
-Receives nutrients and oxygen from-Receives nutrients and oxygen from
synovial fluid via diffusionsynovial fluid via diffusion
- Ph 7.4- Ph 7.4

4. Types of CartilageTypes of Cartilage
 Growth plate------ (physeal) cartilageGrowth plate------ (physeal) cartilage
 Fibrocartilage ------ tendon & ligamentFibrocartilage ------ tendon & ligament
 Elastic cartilage ---- tracheaElastic cartilage ---- trachea
 Fibroelastic cartilage--- menisciFibroelastic cartilage--- menisci

5. CompositionComposition
1.Water1.Water
(65% to 80% of wet weight)(65% to 80% of wet weight)
Shifts in & out of cartilage to allowShifts in & out of cartilage to allow
deformation of surface in response todeformation of surface in response to
stressstress
-Distribution 80% at surface-Distribution 80% at surface
- responsible for nutrition and- responsible for nutrition and
lubricationlubrication

6. 2.Collagen2.Collagen
 (10% to 20% of wet weight; more than 50% of(10% to 20% of wet weight; more than 50% of
dry weight)dry weight)
 Glycine, proline, hydroxyproline, andGlycine, proline, hydroxyproline, and
hydrogen bonding: responsible for collagen’shydrogen bonding: responsible for collagen’s
unique characteristicsunique characteristics
 Hydroxyproline is unique to collagen,Hydroxyproline is unique to collagen,
measured in urine assess bone turnover.measured in urine assess bone turnover.
 95% of collagen,II in articular cartilage95% of collagen,II in articular cartilage
 Very stable, with a half-life of approximatelyVery stable, with a half-life of approximately
25 years25 years

7. Type Location
I Bone . Tendon . Meniscus, annual vert. disc , skin
II Articular cartilage, nucleus puplosus
III Blood vessels , skin
IV Basement membrane
V Articular cartilage small amount
VI Articular cartilage small amount
VII Basement membrane
VIII Basement membrane
IX Articular cartilage small amount
X Hypertrophic cartilage, callus, G.plate
XI Articular cartilage small amount
XII tendon
XIII Endothelial cell

8. 3.Proteoglycan3.Proteoglycan
 (10% to 15% of wet weight)(10% to 15% of wet weight)
 Have a half-life of 3 monthsHave a half-life of 3 months
 chiefly compressive and elastic strengthchiefly compressive and elastic strength
 Trap and hold waterTrap and hold water
 Composed of subunits glycosaminoglycansComposed of subunits glycosaminoglycans
(disaccharide polymers)(disaccharide polymers)

9. Glycosaminoglycans :Glycosaminoglycans :
 Chondroitin sulfate (most prevalentChondroitin sulfate (most prevalent
glycosaminoglycan in cartilage)glycosaminoglycan in cartilage)
 Chondroitin-4-sulfate concentrationChondroitin-4-sulfate concentration
decreases with age.decreases with age.
 Chondroitin-6-sulfate concentration remainsChondroitin-6-sulfate concentration remains
essentially constant.essentially constant.
 Keratin sulfate concentration increases withKeratin sulfate concentration increases with
age.age.

10. 4.Chondrocytes4.Chondrocytes
 ((5% of wet weight)5% of wet weight)
 mesenchymal precursorsmesenchymal precursors
 active in protein synthesis.active in protein synthesis.
 They produce collagen proteoglycansThey produce collagen proteoglycans
&enzymes.&enzymes.
 least active in the calcified zone.least active in the calcified zone.
 Chondroblasts derived from undifferentiatedChondroblasts derived from undifferentiated
mesenchymal cells (stimulated by motion)mesenchymal cells (stimulated by motion)

11. 5.Other matrix:5.Other matrix:
1.AdhesivesAdhesives
 Noncollagenous proteins, fibronectin,Noncollagenous proteins, fibronectin,
chondronectin & anchorin CIIchondronectin & anchorin CII
 Fibronectin may be associated with osteo­Fibronectin may be associated with osteo­
arthritis.arthritis.
2.Lipid: unknown functionunknown function

13. Articular cartilageArticular cartilage
growth factorsgrowth factors
 Regulate cartilage synthesis; may have a role inRegulate cartilage synthesis; may have a role in
osteoarthritisosteoarthritis
 PDGFPDGF
 TGF-BTGF-B
 Fibroblast growth factor (basic) (b-FGF)Fibroblast growth factor (basic) (b-FGF)
 Insulin-like growth factor-I (IGF-I)Insulin-like growth factor-I (IGF-I)

14. Lubrication & wear mechanisms ofLubrication & wear mechanisms of
articular cartilagearticular cartilage
 The coefficient of friction for human joints variesThe coefficient of friction for human joints varies
from 0.002 to 0.04.from 0.002 to 0.04.
 Factors decreasing articular cartilage coefficient ofFactors decreasing articular cartilage coefficient of
friction:friction:
-Fluid film formation-Fluid film formation
- Elastic deformation of articular cartilage- Elastic deformation of articular cartilage
- Synovial fluid- Synovial fluid
- Efflux of fluid from the cartilage- Efflux of fluid from the cartilage
 Factor increasing the coefficient of friction:Factor increasing the coefficient of friction:
fibrillationfibrillation

15. Specific types ofSpecific types of
lubricationlubrication
1. Elastohydrodynamic lubricationElastohydrodynamic lubrication
 Predominant during dynamic joint functionPredominant during dynamic joint function
 Elastic deformation of articular surfaces & thinElastic deformation of articular surfaces & thin
films of joint lubricants separate the surfaces.films of joint lubricants separate the surfaces.
 Coefficient of friction is generally low.Coefficient of friction is generally low.
2. Boundary lubrication (slippery surfaces)2. Boundary lubrication (slippery surfaces)
 Lubricant only partially separates the surfaces.Lubricant only partially separates the surfaces.
 Superficial zone protein (lubricin) appears to have aSuperficial zone protein (lubricin) appears to have a
role in boundary lubrication.role in boundary lubrication.

16. 3.Boosted lubrication (fluid entrapment)3.Boosted lubrication (fluid entrapment)
 Concentration of lubricating fluid in poolsConcentration of lubricating fluid in pools
trapped by regions of bearing surfaces that aretrapped by regions of bearing surfaces that are
making contactmaking contact
4.Hydrodynamic lubrication4.Hydrodynamic lubrication
 Fluid separates the surfaces when one of theFluid separates the surfaces when one of the
surfaces is sliding on the other.surfaces is sliding on the other.
5.Weeping lubrication5.Weeping lubrication
 Fluid shifts out of articular cartilage in responseFluid shifts out of articular cartilage in response
to load, separating the surfaces by hydrostaticto load, separating the surfaces by hydrostatic
pressure.pressure.

17. Parameter Effect of Aging Effect of
Osteoarthritis
Water content Decrease Increase
Proteoglycan conc. Decrease Decrease
Proteoglycan Syn. Decrease Increase
Proteoglycan Deg. Decrease Increase
Chondroitin 4 sulfate Decrease Increase
Chondrocyte No. Decrease
Collagen Relatively unchaged Decrease in severe OA
Keratin sulfate Increase Decrease
Chondrocyte size Increase
Modulus of elasticity Increase Decrease

18. Articular cartilageArticular cartilage
healinghealing
1.Damage above the tidemark:1.Damage above the tidemark:
 Limited to the chondrocytes (type 1 injury) orLimited to the chondrocytes (type 1 injury) or
articu­lar cartilage surface (type 2 injury)articu­lar cartilage surface (type 2 injury)
2.Lacerations extending below the tidemark:2.Lacerations extending below the tidemark:
 Penetrate underlying subchondral bone (t3Penetrate underlying subchondral bone (t3
injuriesinjuries
 inflammatory response ,heal with fibrocartilageinflammatory response ,heal with fibrocartilage
 Fibrocartilage is not as durable as hyalineFibrocartilage is not as durable as hyaline
cartilage.cartilage.
3.Blunt trauma induce cartilage changes similar to3.Blunt trauma induce cartilage changes similar to
those with osteoarthritisthose with osteoarthritis..

19.  Continuous passive motion is benefit cartilageContinuous passive motion is benefit cartilage
healing.healing.
 immobilization leads atrophy or cartilageimmobilization leads atrophy or cartilage
degeneration.degeneration.
 animal models, 4 weeks of joint immobilizationanimal models, 4 weeks of joint immobilization
decreases proteoglycan/collagen ratio.decreases proteoglycan/collagen ratio.
 This ratio returns to normal after 8 weeks ofThis ratio returns to normal after 8 weeks of
joint mobilization.joint mobilization.
 Joint instability initially decreases theJoint instability initially decreases the
proteoglycan/ collagen ratio (at 4 weeks).proteoglycan/ collagen ratio (at 4 weeks).
 Later (12 weeks), the ratio of proteoglycan toLater (12 weeks), the ratio of proteoglycan to
collagen is elevated, and hydration is increased.collagen is elevated, and hydration is increased.
 Instability markedly decreases hyaluronan,Instability markedly decreases hyaluronan,
disuse does not.disuse does not.

20. B. SynoviumB. Synovium
1.Vascularized connective tissue lacks a1.Vascularized connective tissue lacks a
basement membranebasement membrane
2.2. Mediates nutrient exchange between bloodMediates nutrient exchange between blood
and joint (synovial) fluidand joint (synovial) fluid
Cell typesCell types
 Type A: phagocytosisType A: phagocytosis
 Type B : produce synovial fluidType B : produce synovial fluid
 undifferentiated cells: have a reparative roleundifferentiated cells: have a reparative role

21. Synovial fluidSynovial fluid
 H. acid, lubricin, proteinase, collagenases & PGH. acid, lubricin, proteinase, collagenases & PG
 ultrafiltrate of blood plasma added to fluid producedultrafiltrate of blood plasma added to fluid produced
by synovial membraneby synovial membrane
 Contains no RBCs, clotting factors, or hemoglobinContains no RBCs, clotting factors, or hemoglobin
 Lubricates articular cartilage and provides nourishmentLubricates articular cartilage and provides nourishment
 Exhibits nonnewtonianExhibits nonnewtonian
 Viscosity increases as the shear rate decreases.Viscosity increases as the shear rate decreases.
 Lubricin is key lubricating glycoprotein .Lubricin is key lubricating glycoprotein .
 Hyaluronan molecules knee become entangled &Hyaluronan molecules knee become entangled &
behave like an elastic solid during high-strain activitiesbehave like an elastic solid during high-strain activities
(running, jumping).(running, jumping).

22. C. MeniscusC. Meniscus
1.1. Deepens articular surface synovial jointsDeepens articular surface synovial joints
The meniscus broadens contact area & distributes load.The meniscus broadens contact area & distributes load.
joints include AC, SC, GH, hip & knee .joints include AC, SC, GH, hip & knee .
2.2. More elastic & less permeable than articular cartilageMore elastic & less permeable than articular cartilage
3. 50% force in extension, 90% deep flexion3. 50% force in extension, 90% deep flexion
4.3 years after total meniscectomy , 20% of patients have4.3 years after total meniscectomy , 20% of patients have
significant arthritic lesions and 70% have radiographicsignificant arthritic lesions and 70% have radiographic
changes.changes.
5.All patients experience arthrosis after 20 years.5.All patients experience arthrosis after 20 years.
The severity of degenerative changes is proportional to theThe severity of degenerative changes is proportional to the
amount of meniscus excised.amount of meniscus excised.

23. 5.Anatomy (knee meniscus)5.Anatomy (knee meniscus)
Triangular semilunar structureTriangular semilunar structure
Peripheral border attached to the joint capsulePeripheral border attached to the joint capsule
medial meniscus: semicircular; lateral meniscus: circularmedial meniscus: semicircular; lateral meniscus: circular
6.Histologic findings6.Histologic findings
 Fibroelastic cartilageFibroelastic cartilage
 An interlacing network of collagen fibers (90% type I)An interlacing network of collagen fibers (90% type I)
 Proteoglycans, glycoproteins, and cellular elementsProteoglycans, glycoproteins, and cellular elements
 a The concentration of mechanoreceptors is highest ina The concentration of mechanoreceptors is highest in
the posterior horns.the posterior horns.

24.  Blood supply ----- geniculate arteries.Blood supply ----- geniculate arteries.
 peripheral 25% of meniscus.peripheral 25% of meniscus.
 remaining meniscus receives nutrition throughremaining meniscus receives nutrition through
diffusion.diffusion.
 Tears peripheral, vascularized region (“red zone”)Tears peripheral, vascularized region (“red zone”)
can heal by means of fibrovascular scar formation.can heal by means of fibrovascular scar formation.
 central tears in the avascular region (“white zone”)central tears in the avascular region (“white zone”)
cannot.cannot.
 The fibrochondrocyte is responsible for meniscalThe fibrochondrocyte is responsible for meniscal
healing.healing.

26. II. ARTHROSESII. ARTHROSES
A.Joint fluid analysisA.Joint fluid analysis
1.1. Noninflammatory arthritidesNoninflammatory arthritides
 (WBC) count: 200/mm(WBC) count: 200/mm33
, 25% (PMN), 25% (PMN)
 Equal serum values of glucose and proteinEqual serum values of glucose and protein
 Normal viscosity (high)Normal viscosity (high)
 Straw colorStraw color
 Firm mucin clotFirm mucin clot

27. 2.Inflammatory2.Inflammatory
arthritidesarthritides
 WBC count: 2000/mmWBC count: 2000/mm33
to 75,000/mmto 75,000/mm33
, 50%, 50%
PMNsPMNs
 Moderately decreased glucose level (25Moderately decreased glucose level (25
mg/dL lower than serum glucose level)mg/dL lower than serum glucose level)
 Low viscosityLow viscosity
 Yellow-greenYellow-green
 Friable mucin clotFriable mucin clot
 Synovial fluid complement decreased inSynovial fluid complement decreased in
(RA), normal in ankylosing spondylitis(RA), normal in ankylosing spondylitis

28. 3.Infectious arthritides3.Infectious arthritides
 WBC count: more than 80,000/mmWBC count: more than 80,000/mm33
75%75%
PMNPMN
 Positive Gram stain (positive culturesPositive Gram stain (positive cultures
later)later)
 Low glucose level (25 mg/dL lower thanLow glucose level (25 mg/dL lower than
serum glucose level)serum glucose level)
 Opaque fluidOpaque fluid
 Increased synovial lactateIncreased synovial lactate

29. B.Noninflammatory ArthritidesB.Noninflammatory Arthritides
1. Osteoarthritis1. Osteoarthritis
 (degenerative Joint disease)(degenerative Joint disease)
 Inflammation, overload, or decreased matrixInflammation, overload, or decreased matrix
productionproduction
 Osteoarthritic cartilageOsteoarthritic cartilage
 Collagen abnormalities (disrupted by collagenase)Collagen abnormalities (disrupted by collagenase)
 Binding of proteoglycans to hyaluronic acidBinding of proteoglycans to hyaluronic acid
 Cathepsins B and D levels and metalloproteinasesCathepsins B and D levels and metalloproteinases
(collagenase, gelatinase, stromelysin) increase.(collagenase, gelatinase, stromelysin) increase.
 IL-1 enhances enzyme synthesis and have aIL-1 enhances enzyme synthesis and have a
catabolic effect leading to cartilage degeneration.catabolic effect leading to cartilage degeneration.
 a Genetic predisposition important in osteoarthritisa Genetic predisposition important in osteoarthritis

30. AreasAreas thatthat OsteoarthritisOsteoarthritis
AffectsAffects

31. A Rapidly destructiveA Rapidly destructive
osteoarthritisosteoarthritis
 common in the hip.common in the hip.
 mimic septic arthritis, RA, seronegativemimic septic arthritis, RA, seronegative
arthritis, neuropathic arthritis, orarthritis, neuropathic arthritis, or
osteonecrosis.osteonecrosis.
 The femoral head may be so flat as toThe femoral head may be so flat as to
appear sheared off.appear sheared off.

33. General characteristicsGeneral characteristics
 primary or secondary (trauma, infection,primary or secondary (trauma, infection,
congenital)congenital)
 Begins with deterioration & loss of theBegins with deterioration & loss of the
weight­bearing surfaceweight­bearing surface
 Followed by osteophyte development andFollowed by osteophyte development and
osteochondral junction breakdownosteochondral junction breakdown
 Later, cartilage disintegration andLater, cartilage disintegration and
subchondral microfractures expose the bonysubchondral microfractures expose the bony
surface,surface,

35. Radiographic findings:Radiographic findings:
 Subchondral cysts (secondary toSubchondral cysts (secondary to
microfracture, may contain amorphousmicrofracture, may contain amorphous
gelatinous material)gelatinous material)
 OsteophytesOsteophytes
 Joint space narrowingJoint space narrowing
 Ebumation of boneEbumation of bone
 Best shown on tomograms or CT scansBest shown on tomograms or CT scans

37. Microscopic changesMicroscopic changes
 Loss of superficial chondrocytesLoss of superficial chondrocytes
 Chondrocyte cloning (more than 1Chondrocyte cloning (more than 1
chondrocyte per lacuna)chondrocyte per lacuna)
 Replication and breakdown of the tidemarkReplication and breakdown of the tidemark
 FissuringFissuring
 Cartilage destruction with eburnation ofCartilage destruction with eburnation of
subchondral “pagetoid” bonesubchondral “pagetoid” bone

39. Physical examinationPhysical examination
 Decreased ROMDecreased ROM
 CrepitusCrepitus
 Knee: asymmetric involvementKnee: asymmetric involvement
 Hand: (DIP),(PIP), and CMC jointsHand: (DIP),(PIP), and CMC joints
 Hip: superolateral involvementHip: superolateral involvement

40. TreatmentTreatment
 a Supportive measures ( activitya Supportive measures ( activity
modification, use of a cane), includingmodification, use of a cane), including
NSAIDs ,NSAIDs ,
 Surgical proceduresSurgical procedures
range from arthroscopic debridement torange from arthroscopic debridement to
total joint arthroplastytotal joint arthroplasty

41. 2.Neuropathic Arthropathy2.Neuropathic Arthropathy
(charcot Joint Disease)(charcot Joint Disease)
 extreme form of osteoarthritis caused by disturbed sensoryextreme form of osteoarthritis caused by disturbed sensory
innervationinnervation
CausesCauses
1.Diabetes (Most common)1.Diabetes (Most common)
 Charcot joint disease develops in 1% of patientsCharcot joint disease develops in 1% of patients
with diabetic neuropathywith diabetic neuropathy
 Foot and ankle most commonlyFoot and ankle most commonly
 Other anatomic sites , including knee and hipOther anatomic sites , including knee and hip
2.Tabes dorsalis2.Tabes dorsalis (syphilitic myelopathy; lower(syphilitic myelopathy; lower
extremity)extremity)

42. 3. Syringomyelia3. Syringomyelia
 most common cause of upper-extremitymost common cause of upper-extremity
neuropathic arthropathy (shoulder andneuropathic arthropathy (shoulder and
elbow).elbow).
 Charcot joint disease develops in 25% ofCharcot joint disease develops in 25% of
patients with syringomyelia; 80% of casespatients with syringomyelia; 80% of cases
involve the upper extremity.involve the upper extremity.

43.  4. Hansens disease4. Hansens disease
Second most common cause of upperSecond most common cause of upper
extremity neuropathic arthropathyextremity neuropathic arthropathy
5. Myelomeningocele5. Myelomeningocele : ankle and foot: ankle and foot
6.Congenital insensitivity to pain6.Congenital insensitivity to pain : ankle: ankle
and footand foot
7.Other neurologic problems7.Other neurologic problems (such as(such as
spinal cord injury)spinal cord injury)

44. DiagnosisDiagnosis
 Typically in older patient withTypically in older patient with
unstable, painless, swollen jointunstable, painless, swollen joint
 May manifest with hemarthrosisMay manifest with hemarthrosis

45. a Radiographic findingsa Radiographic findings
 Advanced (severe) destructiveAdvanced (severe) destructive
changes on both sides of the jointchanges on both sides of the joint
 Scattered “chunks” of bone embeddedScattered “chunks” of bone embedded
in fibrous tissuein fibrous tissue
 Joint distension by fluidJoint distension by fluid
 Heterotopic ossificationHeterotopic ossification

47.  Charcot’s arthropathy & osteomyelitis byCharcot’s arthropathy & osteomyelitis by
physical examination & radiographsphysical examination & radiographs
 Symptoms : swelling, warmth, erythema,Symptoms : swelling, warmth, erythema,
minimal pain, a variable WBC count &minimal pain, a variable WBC count &
(ESR)(ESR)
 Both common in diabeticBoth common in diabetic
 Technetium bone scan: may look “hot”Technetium bone scan: may look “hot”
(positive)(positive)
 Indium leukocyte scan: “hot” (positive)Indium leukocyte scan: “hot” (positive)

48. TreatmentTreatment
 Limitation activity, bracing or castingLimitation activity, bracing or casting
 Skin temperature involved side that isSkin temperature involved side that is
similar to uninvolved side is best indicatorsimilar to uninvolved side is best indicator
for discontinuing a total contact cast.for discontinuing a total contact cast.
 Charcot joint disease: usually aCharcot joint disease: usually a
contraindication for TJA andcontraindication for TJA and
use orthopaedic hardwareuse orthopaedic hardware

49. 3.Acute rheumatic fever3.Acute rheumatic fever
 most common cause of childhood arthritis.most common cause of childhood arthritis.
 Rare since the advent of antibioticsRare since the advent of antibiotics
 Arthritis and arthralgias can followArthritis and arthralgias can follow
untreated group A hemolytic streptococcaluntreated group A hemolytic streptococcal
infections.infections.
 The onset of red, tender, extremely painfulThe onset of red, tender, extremely painful
joint effusions is acute.joint effusions is acute.

50.  Systemic manifestations include :Systemic manifestations include :
 CarditisCarditis
 Erythema marginatum (painless macules with red margins, usuallyErythema marginatum (painless macules with red margins, usually
on the abdomen but never on the face)on the abdomen but never on the face)
 Subcutaneous nodules (extensor surfaces of the upperSubcutaneous nodules (extensor surfaces of the upper
extremities)extremities)
 ChoreaChorea
 Arthritis is migratory and typically involves multiple large joints.Arthritis is migratory and typically involves multiple large joints.

51. Jones criteriaJones criteria
Preceding streptococcal infection with two of the followingPreceding streptococcal infection with two of the following
major criteria:major criteria:
 Carditis, polyarthritis, chorea, erythema marginatum,Carditis, polyarthritis, chorea, erythema marginatum,
subcutaneous nodulessubcutaneous nodules
 Or with one major criterion and two of the following minorOr with one major criterion and two of the following minor
criteria:criteria:
 Fever, arthralgia, prior rheumatic fever, elevated ESR,Fever, arthralgia, prior rheumatic fever, elevated ESR,
prolonged PR interval on ECG studyprolonged PR interval on ECG study
 Antistreptolysin O titers are elevated in 80% of affectedAntistreptolysin O titers are elevated in 80% of affected
patients.patients.

52. TreatmentTreatment
penicillin and salicylates.penicillin and salicylates.

53. 4.Ochronosis4.Ochronosis
 Degenerative arthritis resulting from alkaptonuriaDegenerative arthritis resulting from alkaptonuria
 A rare inborn defect of the homogentisic acidA rare inborn defect of the homogentisic acid
oxidase enzyme system (tyrosine andoxidase enzyme system (tyrosine and
phenylalanine catabolism)phenylalanine catabolism)
 Excess homogentisic acid deposited in the jointsExcess homogentisic acid deposited in the joints
 can be deposited in other tissues , heart valves.can be deposited in other tissues , heart valves.
 Affected patients may present with black urineAffected patients may present with black urine
 Ochronotic spondylitisOchronotic spondylitis
 Usually occurs during the 4Usually occurs during the 4thth
decade of life Includesdecade of life Includes
progressive degenerative changes, disc spaceprogressive degenerative changes, disc space
narrowing, and calcificationnarrowing, and calcification

55. 5.5. Secondary pulmonarySecondary pulmonary
hypertrophic osteoarthropathyhypertrophic osteoarthropathy
 A clinical diagnosisA clinical diagnosis
 Involves a lung tumor mass, jointInvolves a lung tumor mass, joint
pain and stiffness, periostitis of thepain and stiffness, periostitis of the
long bones, and clubbing of thelong bones, and clubbing of the
fingersfingers

56. C. Inflammatory arthritidesC. Inflammatory arthritides
 Radiographic findings: generallyRadiographic findings: generally
evidence of destruction on both sidesevidence of destruction on both sides
of a jointof a joint
 Laboratory findings: confusingLaboratory findings: confusing

57. Finding Positive Negative
Rheumatoid Factor R.A
Sjogren Syndrome
Sarcoid
SLE
A.Spondylitis
Gout
Psoriatic Arthritis
Reiter Syndrome
HLA A.Spondylitis
Reiter Syndrome
Psoriatic Arthritis
Enteropathic aryhritis
ANA SLE
Sjogren Syndrome
Scleroderma

58. 1.1. Rheumatoid arthritisRheumatoid arthritis
 The most common inflammatory arthritisThe most common inflammatory arthritis
 Affects 3% of women and 1% of menAffects 3% of women and 1% of men
 Diagnostic criteria of the AmericanDiagnostic criteria of the American
Rheumatism Association:Rheumatism Association:
 Morning stiffnessMorning stiffness
 Swelling a NodulesSwelling a Nodules
 a Positive laboratory test resultsa Positive laboratory test results
 Radiographic findingsRadiographic findings

59. CausesCauses
 Unclear; a cell-mediated immune response (T cell):Unclear; a cell-mediated immune response (T cell):
Incites an inflammatory responseIncites an inflammatory response
Response is initially against soft tissuesResponse is initially against soft tissues
Response is later against cartilage (chondrolysis) &Response is later against cartilage (chondrolysis) &
bone (periarticular bone resorption)bone (periarticular bone resorption)
 Mononuclear cells: primary cellular mediators of tissueMononuclear cells: primary cellular mediators of tissue
destruction in RAdestruction in RA
 associated with infectious cause or human leukocyteassociated with infectious cause or human leukocyte
antigen (HLA) locus (HLA-DR4 and HLA-DW4)antigen (HLA) locus (HLA-DR4 and HLA-DW4)
 Lymphokines, cytokines and other inflammatoryLymphokines, cytokines and other inflammatory
mediators: initiate a destructive cascade that leads tomediators: initiate a destructive cascade that leads to
joint destructionjoint destruction

60. General characteristicsGeneral characteristics
1.Insidious onset, morning stiffness, and1.Insidious onset, morning stiffness, and
polyarthritispolyarthritis
2.Hands (ulnar deviation and subluxation of2.Hands (ulnar deviation and subluxation of
the meta­carpophalangeal [MCP] joints) andthe meta­carpophalangeal [MCP] joints) and
feet (metatarso­phalangeal joints, claw toes,feet (metatarso­phalangeal joints, claw toes,
and hallux valgus) affected earlyand hallux valgus) affected early
3.Also common in the knees, elbows,3.Also common in the knees, elbows,
shoulders, ankles, and cervical spineshoulders, ankles, and cervical spine

61. 4.Subcutaneous nodules Observed in 20% of RA4.Subcutaneous nodules Observed in 20% of RA
patients during their lifetimepatients during their lifetime
5. Synovium and soft tissues affected first5. Synovium and soft tissues affected first
 Joints significantly involved only laterJoints significantly involved only later
A. Early disease processA. Early disease process, the RA-inflamed, the RA-inflamed
synovium shows a proliferation of blood vesselssynovium shows a proliferation of blood vessels
B. Late synovial changesB. Late synovial changes
 Hyperplastic cellsHyperplastic cells
 Intimal hyperplasiaIntimal hyperplasia
 Increased blood vesselsIncreased blood vessels
 Abundant lymphocytes and rare neutrophilsAbundant lymphocytes and rare neutrophils

62. Laboratory findingsLaboratory findings
 ESR and CRP are elevated.ESR and CRP are elevated.
 (RF) positive in 80% affected patients.(RF) positive in 80% affected patients.
 RF autoantibodies are directed againstRF autoantibodies are directed against
crystallizable fragment (Fc) portion ofcrystallizable fragment (Fc) portion of
immunoglobulin G (IgG).immunoglobulin G (IgG).
 RF is most commonly (IgM) but any can beRF is most commonly (IgM) but any can be
immunoglobulin type.immunoglobulin type.
 Joint fluid assays also demonstrate RF,Joint fluid assays also demonstrate RF,
decreased complement levelsdecreased complement levels

63. SystemicSystemic
manifestationsmanifestations
 Rheumatoid vasculitisRheumatoid vasculitis
 PericarditisPericarditis
 Pulmonary disease (pleurisy, nodules,Pulmonary disease (pleurisy, nodules,
fibrosis)fibrosis)
 Popliteal cysts in rheumatoid patientsPopliteal cysts in rheumatoid patients
(U/S), which can mimic thrombophlebitis(U/S), which can mimic thrombophlebitis

64. Felty’s syndromeFelty’s syndrome
 RA with splenomegaly and leukopeniaRA with splenomegaly and leukopenia
Still’s diseaseStill’s disease
 (JRA) with fever, rash, and splenomegaly(JRA) with fever, rash, and splenomegaly
Sjogren’s syndromeSjogren’s syndrome
 autoimmune exocrinopathy associated with RA.autoimmune exocrinopathy associated with RA.
 Decreased salivary and lacrimal gland secretionDecreased salivary and lacrimal gland secretion
and lymphoid proliferationand lymphoid proliferation

65.
RadiographicRadiographic
characteristicscharacteristics
 Periarticular erosions and osteopeniaPeriarticular erosions and osteopenia
 All three knee compartments may showAll three knee compartments may show
osteoporosis and erosions.osteoporosis and erosions.
 Protrusio acetabuliProtrusio acetabuli
Medial displacement of the acetabulum beyond theMedial displacement of the acetabulum beyond the
radiographic teardrop with medial migration of theradiographic teardrop with medial migration of the
femoral head into the pelvisfemoral head into the pelvis
Common in RA, ankylosing spondylitis, Paget’sCommon in RA, ankylosing spondylitis, Paget’s
disease, metabolic bone diseases, Marfan’sdisease, metabolic bone diseases, Marfan’s
syndrome, Otto’s pelvissyndrome, Otto’s pelvis

67. TreatmentTreatment
 Goals:Goals:
Control synovitis and painControl synovitis and pain
Maintain joint functionMaintain joint function
Prevent deformitiesPrevent deformities

68. ““pyramid” approachpyramid” approach
to RA drug therapyto RA drug therapy
 Begins with NSAIDsBegins with NSAIDs
 antimalarials, remittent agents (methotrexate,antimalarials, remittent agents (methotrexate,
sulfasalazine, gold &penicillamine), steroid & cytotoxicsulfasalazine, gold &penicillamine), steroid & cytotoxic
drugsdrugs
 Doxycycline has shown early promise in reducingDoxycycline has shown early promise in reducing
inflammation in RA.inflammation in RA.
 DMARDs address underlying causes for diseaseDMARDs address underlying causes for disease
( autoimmune ) rather than only effects ( inflammation).( autoimmune ) rather than only effects ( inflammation).
 methotrexate, azathioprine & anakinra (IL-1 inhibitor).methotrexate, azathioprine & anakinra (IL-1 inhibitor).
 Most new DMARDs, infliximab & etanercept target TNF-Most new DMARDs, infliximab & etanercept target TNF-
a.a.
 a These drugs should be discontinued before elec­tivea These drugs should be discontinued before elec­tive
surgery, to decrease risk of infection.surgery, to decrease risk of infection.

69. SurgerySurgery
 Synovectomy, only if aggressive drug therapy failsSynovectomy, only if aggressive drug therapy fails
 Soft tissue realignments Usually not favored becauseSoft tissue realignments Usually not favored because
deformity progressesdeformity progresses
 Various reconstructive proceduresVarious reconstructive procedures
Risk of infection after TJA is increasedRisk of infection after TJA is increased
 Operative synovectomy in the kneeOperative synovectomy in the knee
1.Decreases pain and swelling1.Decreases pain and swelling
2. Does not prevent radiographic progression or the need2. Does not prevent radiographic progression or the need
for future y (TKA)for future y (TKA)
3.Does not improve joint ROM3.Does not improve joint ROM
 a Preoperative evaluation of the cervical spine witha Preoperative evaluation of the cervical spine with
radiographs is important.radiographs is important.

70. 2.Systemic lupus2.Systemic lupus
erythematosuserythematosus
 SLE is a chronic inflammatory disease ofSLE is a chronic inflammatory disease of
unknown origin.unknown origin.
 Usually affects women (especially AfricanUsually affects women (especially African
Americans)Americans)
 related to the immune complexrelated to the immune complex
 Patients with SLE typically have positivePatients with SLE typically have positive
(ANA) & HLA-DR3 titers and may have(ANA) & HLA-DR3 titers and may have
positive RF titers.positive RF titers.

71. ManifestationsManifestations
 FeverFever
 Butterfly malar rashButterfly malar rash
 PancytopeniaPancytopenia
 PericarditisPericarditis
 NephritisNephritis
 PolyarthritisPolyarthritis
 Joint is most common feature, more than 75% ofJoint is most common feature, more than 75% of
patients with SLEpatients with SLE
 arthritis in SLE typically manifests as acute, red, tenderarthritis in SLE typically manifests as acute, red, tender
swelling of the PIP joints, MCP joints, carpus, kneesswelling of the PIP joints, MCP joints, carpus, knees
 SLE is typically not as destructive as RASLE is typically not as destructive as RA

72. TreatmentTreatment
 same medications as for RA.same medications as for RA.
 Mortality in SLE is usuallyMortality in SLE is usually
related to renal disease.related to renal disease.
 DDX:DDX:
polymyositispolymyositis
dermatomyositisdermatomyositis..

73.
3.Polymyalgia3.Polymyalgia
rheumaticarheumatica
 elderly personselderly persons
 Aching and stiffness of the shoulder and pelvic girdle,Aching and stiffness of the shoulder and pelvic girdle,
associated with malaise, headaches, and anorexiaassociated with malaise, headaches, and anorexia
 Physical examination :unremarkablePhysical examination :unremarkable
 laboratory, Markedly elevated ESR ,ALP,Immunelaboratory, Markedly elevated ESR ,ALP,Immune
comlpex, Anemiacomlpex, Anemia
 Usually treated symptomaticallyUsually treated symptomatically
 Steroids for refractory casesSteroids for refractory cases
 May be associated with temporal arteritisMay be associated with temporal arteritis
Biopsy for definitive diagnosisBiopsy for definitive diagnosis
requires treatment high-dose steroids;requires treatment high-dose steroids;
if untreated, may rapidly result in total blindnessif untreated, may rapidly result in total blindness

74. 4.Juvenile rheumatoid4.Juvenile rheumatoid
arthritisarthritis
 Seronegativity negative RF titers.Seronegativity negative RF titers.
 Seropositivity positive RF titers.Seropositivity positive RF titers.
-incidence of seropositivity is estimated less than 15% of JRA-incidence of seropositivity is estimated less than 15% of JRA
- incidence of chronic, active, and progressive dis. is higher.incidence of chronic, active, and progressive dis. is higher.
- In early-onset JRA, onset of disease occurs before the teens;In early-onset JRA, onset of disease occurs before the teens;
in late-onset JRA, onset of disease occurs during the teens orin late-onset JRA, onset of disease occurs during the teens or
later.later.

75. Types :Types :
1.Systemic (20%)1.Systemic (20%)
2.Polyarticular (50%)2.Polyarticular (50%)
Five or more joints are involved.Five or more joints are involved.
Seronegative polyarticular JRA is moreSeronegative polyarticular JRA is more
frequent in girls.frequent in girls.
Seropositive polyarticular JRA is also moreSeropositive polyarticular JRA is also more
frequent in girls.frequent in girls.
Exhibits destructive degenerative jointExhibits destructive degenerative joint
disease Frequently develops into adult RAdisease Frequently develops into adult RA
aa

76. 3. Pauciarticular (30%)3. Pauciarticular (30%)
Four or fewer joints are involved.Four or fewer joints are involved.
Onset peaks at ages 2 to 4 years.Onset peaks at ages 2 to 4 years.
Average duration of disease is 2 years, 9 months.Average duration of disease is 2 years, 9 months.
Early-onset pauciarticular JRA has two distinctiveEarly-onset pauciarticular JRA has two distinctive
characteristics:characteristics:
 More frequent in girlsMore frequent in girls
 Associated with iridocyclitis in 50%Associated with iridocyclitis in 50%
Late-onset pauciarticular JRA has one distinctiveLate-onset pauciarticular JRA has one distinctive
characteristic:characteristic:
 Observed in boys more commonly than in girlsObserved in boys more commonly than in girls

77. Treatment:Treatment:
 High-dose aspirinHigh-dose aspirin
 Occasionally gold or remittent agentsOccasionally gold or remittent agents
(refractory polyarticular)(refractory polyarticular)
 Frequent ophthalmologic examinations (withFrequent ophthalmologic examinations (with
a slit lamp) for asymptomatic oculara slit lamp) for asymptomatic ocular
involvementinvolvement
 Most common joint affected: the knee,Most common joint affected: the knee,
followed by the finger/wrist, ankle, hip, andfollowed by the finger/wrist, ankle, hip, and
cervical spinecervical spine
 C-spine fusion or instability can occurC-spine fusion or instability can occur

78. 5.Relapsing5.Relapsing
polychondritispolychondritis

79. 6.Spondyloarthropathies/enthesopathies6.Spondyloarthropathies/enthesopathies
A.Ankylosing Spondylitis
 Diagnostic criteriaDiagnostic criteria::
1.Bilateral sacroiliitis1.Bilateral sacroiliitis
2.With or without acute anterior uveitis2.With or without acute anterior uveitis
3.HLA-B27-positive male patient3.HLA-B27-positive male patient
Insidious onset of back painInsidious onset of back pain
 Associated morning stiffnessAssociated morning stiffness
 Hip painHip pain
 Third to fourth decades of life)Third to fourth decades of life)
 Squaring of the vertebraeSquaring of the vertebrae
 Obliteration of sacroiliac jointsObliteration of sacroiliac joints
 ° Spinal manifestation “Chin on chest” deformity° Spinal manifestation “Chin on chest” deformity

80. B.Reiters SyndromeB.Reiters Syndrome
 Classical presentation is of a young man with theClassical presentation is of a young man with the
triad of conjunctivitis, urethritis, and oligoarticulartriad of conjunctivitis, urethritis, and oligoarticular
arthritis.arthritis.
 Mnemonic: “Mnemonic: “Can’t see, pee, or bend theCan’t see, pee, or bend the
kneeknee””
 Other common findings include :Other common findings include :
 Painless oral ulcersPainless oral ulcers
 Penile lesionsPenile lesions
 Pustular lesions on the extremities, palms, andPustular lesions on the extremities, palms, and
soles (keratoderma blennorrhagicum)soles (keratoderma blennorrhagicum)
 Plantar heel painPlantar heel pain

81. c.Psoriatic arthropathyc.Psoriatic arthropathy
 Affects approximately 5% to 10% of patients withAffects approximately 5% to 10% of patients with
psoriasispsoriasis
 HLA-B27 is found in 50% of patients.HLA-B27 is found in 50% of patients.
 Many forms exist; most patients have theMany forms exist; most patients have the
oligoarticular form.oligoarticular form.
 Asymmetrically affects small joints of the hands andAsymmetrically affects small joints of the hands and
feetfeet
 Nail pitting (also fragmentation and discoloration)Nail pitting (also fragmentation and discoloration)
 ““Sausage” digitsSausage” digits
 ““Pencil-in-cup” deformityPencil-in-cup” deformity
 Treatment is similar to that for RA.Treatment is similar to that for RA.

83. D.D. Enteropathic arthritisEnteropathic arthritis
 of patients with Crohn’s disease and ulcerativeof patients with Crohn’s disease and ulcerative
colitis,colitis,
 10% to 20% experience peripheral joint arthritis.10% to 20% experience peripheral joint arthritis.
 Five percent or more experience axial disease, aFive percent or more experience axial disease, a
Non deforming arthritisNon deforming arthritis
 Occurs more commonly in large, weight-bearingOccurs more commonly in large, weight-bearing
jointsjoints
 Usually manifests as an acute monarticularUsually manifests as an acute monarticular
synovitis that may precede any bowel symptomssynovitis that may precede any bowel symptoms
 50% HLA-B27 positive.50% HLA-B27 positive.
 10-15% of cases are associated with anky­losing10-15% of cases are associated with anky­losing
spondylitisspondylitis..

85. 7.7. Crystal depositionCrystal deposition
diseasedisease
A. GoutA. Gout
 Disorder of nucleic acid metabolism causingDisorder of nucleic acid metabolism causing
hyperuricemiahyperuricemia
 Deposition of monosodium urate crystals inDeposition of monosodium urate crystals in
jointsjoints

86. CauseCause
 The crystals activate inflammatory mediators.The crystals activate inflammatory mediators.
 mediators include proteases, chemotactic factors, PG,mediators include proteases, chemotactic factors, PG,
leukotriene Bleukotriene B44, and free oxygen radicals., and free oxygen radicals.
 inflammatory mediators are inhibited by colchicine.inflammatory mediators are inhibited by colchicine.
 crystals also activate platelets, IL-1 production, andcrystals also activate platelets, IL-1 production, and
complement system.complement system.
 Local polypeptides may inhibit the crystal inflammatoryLocal polypeptides may inhibit the crystal inflammatory
response by means of a glycoprotein “coating.”response by means of a glycoprotein “coating.”
 Gout may be precipitated by chemotherapy forGout may be precipitated by chemotherapy for
myeloproliferative disorders.myeloproliferative disorders.

87. □□ DiagnosisDiagnosis
 Recurrent arthritis attacks, in men 40 to 60Recurrent arthritis attacks, in men 40 to 60
 Usually in the lower extremity, great toeUsually in the lower extremity, great toe
 Crystal deposition as tophiCrystal deposition as tophi
- Ear helix, eyelid, olecranon, Achilles tendonEar helix, eyelid, olecranon, Achilles tendon
- Usually observed in the chronic formUsually observed in the chronic form
 Renal disease or stonesRenal disease or stones
 Kidneys are second most commonly affected.Kidneys are second most commonly affected.
 not diagnostic.not diagnostic.

88. Radiographic findings:Radiographic findings:
 Soft tissue changesSoft tissue changes
 ““Punched-out” periarticular erosions withPunched-out” periarticular erosions with
sclerotic overhanging borderssclerotic overhanging borders
 Monosodium urate crystals—thin, taperedMonosodium urate crystals—thin, tapered
intra­cellular crystals that are stronglyintra­cellular crystals that are strongly
negatively birefringent in joint aspiratenegatively birefringent in joint aspirate
must be present for the diagnosis.must be present for the diagnosis.
 Elevated serum uric acid level is notElevated serum uric acid level is not
diagnosticdiagnostic

90. Treatment:Treatment:
 acute attacks with indomethacin (50 mg three timesacute attacks with indomethacin (50 mg three times
daily)daily)
 A rheumatology consultation is necessary afterwards.A rheumatology consultation is necessary afterwards.
 intravenous colchicine for pt. with GIT diseaseintravenous colchicine for pt. with GIT disease
 Allopurinol for chronic gout.Allopurinol for chronic gout.
-xanthine oxidase inhibitor; xanthine oxidase is needed-xanthine oxidase inhibitor; xanthine oxidase is needed
for the conversion of hypoxanthine to xanthine andfor the conversion of hypoxanthine to xanthine and
xanthine to uric acid.xanthine to uric acid.
 Colchicine is used for prophylaxis after recurrentColchicine is used for prophylaxis after recurrent
attacks.attacks.

91. B.ChondrocalcinosisB.Chondrocalcinosis
C.Calcium hydroxyapatiteC.Calcium hydroxyapatite
crystal deposition diseasecrystal deposition disease

92. E. Infectious arthritidesE. Infectious arthritides
1. Pyogenic arthritis1. Pyogenic arthritis
 CauseCause
Hematogenous spreadHematogenous spread
Extension of osteomyelitisExtension of osteomyelitis
Posttraumatic (fight bites, open injuries)Posttraumatic (fight bites, open injuries)
Postoperative (iatrogenic)Postoperative (iatrogenic)
 Commonly occurs in childrenCommonly occurs in children
 Adults at high risk include the following:Adults at high risk include the following:
Intravenous drug abusersIntravenous drug abusers
Sexually active young adults (Neisseria gonorrhoeae)Sexually active young adults (Neisseria gonorrhoeae)
Patients with DMPatients with DM
Patients with RA

93. Histologic findings:Histologic findings:
 Synovial hyperplasia may be demonstrated.Synovial hyperplasia may be demonstrated.
 Numerous PMNs are present.Numerous PMNs are present.
 Cartilage destruction is evident.Cartilage destruction is evident.
direct (from proteolytic enzymes)direct (from proteolytic enzymes)
indirect (from pressure and lack of nutrition)indirect (from pressure and lack of nutrition)
 Treatment:Treatment:
 ° Incision and drainage ° Antibiotics for up to° Incision and drainage ° Antibiotics for up to
several weeksseveral weeks

94. B.Tuberculous arthritisB.Tuberculous arthritis
 Chronic granulomatous infection nChronic granulomatous infection n
Mycobacterium tuberculosisMycobacterium tuberculosis
 Usually invades joints by hematogenousUsually invades joints by hematogenous
spreadspread
 Spine and lower extremities most oftenSpine and lower extremities most often
involvedinvolved
 Common in Mexico and AsiaCommon in Mexico and Asia
 85% are monarticular85% are monarticular

95. CharacteristicCharacteristic
radiographic findings:radiographic findings:
 Osteolytic changes on both sides of the jointOsteolytic changes on both sides of the joint
° Subchondral osteoporosis° Subchondral osteoporosis
 Cystic changesCystic changes
 Notchlike, bony destruction at the joint edgeNotchlike, bony destruction at the joint edge
n Joint space narrowingn Joint space narrowing

96. DiagnosisDiagnosis
 Positive results of purified protein derivative testPositive results of purified protein derivative test
 Acid-fast bacilli and “rice bodies” (fibrin) in synovial fluidAcid-fast bacilli and “rice bodies” (fibrin) in synovial fluid
 Cultures may take several weeks to yield positiveCultures may take several weeks to yield positive
resultsresults
 Histologic study: may demonstrate characteristicHistologic study: may demonstrate characteristic
granulomas with Langerhans giant cellsgranulomas with Langerhans giant cells
Treatment:Treatment:
 Incision and drainageIncision and drainage
 Long-term (6 months) antibiotics (isoniazid, rifampin orLong-term (6 months) antibiotics (isoniazid, rifampin or
rifabutin, pyrazinamide, and pyridoxine)rifabutin, pyrazinamide, and pyridoxine)

97. 3.Fungal arthritis3.Fungal arthritis
AIDSAIDS
CandidiaCandidia
AntifungalAntifungal
4.Lyme Disease
USAUSA
Self limitingSelf limiting
Tick biteTick bite

98. E Hemorrhagic effusionsE Hemorrhagic effusions
 1. Hemophilic arthropathy1. Hemophilic arthropathy
 X-linked recessive disorderX-linked recessive disorder
 Factor VIII deficiency: hemophilia A (classic)Factor VIII deficiency: hemophilia A (classic)
 Factor IX deficiency: hemophilia B (Christmas disease)Factor IX deficiency: hemophilia B (Christmas disease)
 repeated hemarthrosis by minor traumarepeated hemarthrosis by minor trauma
 leads to synovitis, cartilage destruction & jointleads to synovitis, cartilage destruction & joint
deformity,Repeated episodes lead to replacement ofdeformity,Repeated episodes lead to replacement of
the normal joint capsule with dense scar tissue.the normal joint capsule with dense scar tissue.

99. severity related to degree of factor VIIIseverity related to degree of factor VIII
deficiency:deficiency:
 Mild disease: levels of factor VIII are 5% toMild disease: levels of factor VIII are 5% to
25%25%
 Moderate disease: 1% to 5%Moderate disease: 1% to 5%
 Severe disease: 0% to 1%Severe disease: 0% to 1%
Home factor treatment has reduced incidenceHome factor treatment has reduced incidence
substantiallysubstantially..

100. Diagnosis:Diagnosis:
 Most commonly: kneeMost commonly: knee
 Followed by elbow, ankle, shoulder, and spine n JointFollowed by elbow, ankle, shoulder, and spine n Joint
swelling, decreased ROM, and painswelling, decreased ROM, and pain
 a Concomitant infection: ruled out by examination of jointa Concomitant infection: ruled out by examination of joint
aspirateaspirate
 Radiographic :Radiographic :
 ““Squared off’ patella (Jordan’s sign)Squared off’ patella (Jordan’s sign)
 Widening of the intercondylar notchWidening of the intercondylar notch
 Enlarged femoral condyles,Enlarged femoral condyles,
 appearing to “fall off’ the tibiaappearing to “fall off’ the tibia
 U/S: diagnose & monitor IM bleedingU/S: diagnose & monitor IM bleeding
 Iliacus hematomas can cause femoral nerve palsies.Iliacus hematomas can cause femoral nerve palsies.

101. Treatment:Treatment:
 Correction of factor levelsCorrection of factor levels
 Factor VIII: to 40% to 50% of normal levelsFactor VIII: to 40% to 50% of normal levels
 Splints and bracingSplints and bracing
 Compressive dressings a AnalgesicsCompressive dressings a Analgesics
 Steroids (occasionally helpful)Steroids (occasionally helpful)

102. Surgical managementSurgical management
Synovectomy for recurrent hemarthrosesSynovectomy for recurrent hemarthroses
refractory to medical treatmentrefractory to medical treatment
Reduces incidence of recurrentReduces incidence of recurrent
hemarthroses; causes less pain andhemarthroses; causes less pain and
swellingswelling
 TJA for end-stage arthropathyTJA for end-stage arthropathy
 Arthrodesis, especially for the ankleArthrodesis, especially for the ankle

103. 2. Sickle cell disease2. Sickle cell disease
 Hemoglobin SS is found in 1% of black North Americans.Hemoglobin SS is found in 1% of black North Americans.
 This hemoglobin type leads to local infarction as a resultThis hemoglobin type leads to local infarction as a result
of capillary stasis.of capillary stasis.
 Bony infarcts and ischemic necrosis may occur inBony infarcts and ischemic necrosis may occur in
multiple bones.multiple bones.
 a Osteonecrosis, femoral head, is common among SCAa Osteonecrosis, femoral head, is common among SCA
 Dactylitis with metacarpal/metatarsal periosteal new boneDactylitis with metacarpal/metatarsal periosteal new bone
formation may also be observed.formation may also be observed.
 Osteomyelitis is not uncommon (Salmonella)Osteomyelitis is not uncommon (Salmonella)
 Staphylococcus species are the most common infectingStaphylococcus species are the most common infecting
organismsorganisms

104. Pigmented villonodularPigmented villonodular
synovitissynovitis
 Synovial disease often affects young adultsSynovial disease often affects young adults
with PVNS.with PVNS.
 Synovium is frequently rust colored orSynovium is frequently rust colored or
brown, a Extensive hemosiderin depositsbrown, a Extensive hemosiderin deposits
are present.are present.
 Pain, swelling, synovitis, and a rust coloredPain, swelling, synovitis, and a rust colored
or bloody effusionor bloody effusion
 The knee is the most frequent site.The knee is the most frequent site.

105. Radiographic findings:Radiographic findings:
 Well-defined juxtacortical erosions with scleroticWell-defined juxtacortical erosions with sclerotic
marginsmargins
 Histologic findings:Histologic findings:
 Pigmented synovial histiocytes n Foam cellsPigmented synovial histiocytes n Foam cells
(lipid-laden histiocytes)(lipid-laden histiocytes)
 Multinucleated giant cellsMultinucleated giant cells
Treatment:Treatment:
Surgical Excision (total Synovectomy)Surgical Excision (total Synovectomy)
Local PVNS only nodule resectionLocal PVNS only nodule resection

106. RefferenceRefference
 Review of Orthopeadic
Six Edition
Mark D. Miller
 Apleys
System of orthopedic and Fracture
 Internet for pictures