2025
,1- In Vthe Vcontext Vof Vjoint Varthroplasty, Vthe Valpha-defensin Vimmunoassay Vtest Vis Vuseful Vfor Vthe
V detection Vof?
1*aseptic Vloosening.
V 2*metal Vcorrosion.
V 3*periprosthetic
V infection. V4*bone
V ingrowth.
Correct Vanswer V3
Alpha-defensin Vis Va Vprotein Vreleased Vby Vactivated Vneutrophils Vin Vresponse Vto Vinfection. VThe
Vdetection Vof Valpha-defensin Vin Vsynovial Vfluid Vis Vhighly Vsensitive Vand Vspecific Vas Va Vmarker Vof
Vperiprosthetic Vinfection. VAseptic Vloosening Vand Vthe Vbone Vingrowth Vof Vprostheses Vgenerally Vare
Vdetected Vradiographically. VMetal Vcorrosion Vissues—in Vmetal-on-metal Vprostheses, Vfor Vexample—
generally Vare Vfollowed Vusing Vblood Vmetal Vion Vlevels.
2- In Vposttraumatic Varthritis, Vthe Vinitial Vinjury Vstimulates Vthe Vproduction Vof Vinflammatory Vcytokines.
V Which V Vcytokine Vis Vproduced Vat Vthe Vhighest Vlevel Von Vthe Vfirst Vday Vafter Vinjury? V
1*Interleukin-6 V(IL-6)
V 2*Interleukin-1 Vbeta V(IL-1β) IL -1B
TNF-a
V 3*Chemokine Vligand V22 V(CCL-
22)
4*Damage-associated Vmolecular Vpatterns V(DAMPs)
Correct Vanswer V2
The Vdevelopment Vof Varthritis Vafter Vjoint Vinjury Vis Vcommon Vand Vcan Vresult Vfrom Vmultiple
V causes, Vincluding Vcartilage Vcontusion, Vmeniscal Vinjury, Vligament Vtear, Vor Vintra-articular Vfracture.
V The Vaccuracy Vof Vreduction Vdoes Vnot Vnecessarily Vprevent Vthe Vdevelopment Vof Vposttraumatic
V arthritis. VData Vfrom Vanimal Vstudies Vof Vposttraumatic Varthritis Vdemonstrate Vthe Vproduction Vof
V inflammatory Vcytokines Vthat Vlead Vto Vchondrocyte Vdeath Vand Vmatrix Vdestruction. VIn Vthe Vfirst
V few Vdays Vafter VinjuryVVIL- V
V1β V(predominantly) Vand Vtumor Vnecrosis Vfactor Valpha Vare Vthe Vprimary Vcytokines Vproduced, Vfollowed
Vby V
nitric Voxide, Vmatrix Vmetalloproteinases, Vand Vaggrecanases, Vwhich Vdegrade Vthe Vchondral Vmatrix
V
V CCL-22 V Vincreases Vat Varound V5 Vdays Vafter Vinjury, Vhowever. VOther Vfactors Vcalled VDAMPs, Vwhich
V are Vgenerated Vthrough Vthe Vmechanical Vor Venzymatic Vdegradation Vof Vjoint Vtissues, Valso
,stimulate Van Vinnate Vinflammatory Vresponse.
V
, 3- What Vis Vthe Vmain Vfunction Vof Vlubricin Vin Vsynovial Vjoints?
1*Serves Vas Va Vcomponent Vof Vthe Vextracellular
matrix V2*Inhibits Vmatrix Vmetalloproteinase
V
3*Increases Vcross-linking Vbetween Vcollagen Vfibers
4*Reduces Vthe Vcoefficient Vof Vfriction Vin Vthe Vjoint
V
Correct Vanswer V4
Lubricin Vreduces Vthe Vfriction Vbetween Vthe Vsurfaces Vin Vthe Vjoint, Vleading Vto Vdecreased Vshear Vforces
Vgoing Vthrough Vthe Vhyaline Vcartilage. VIt Vis Va Vglycoprotein Vthat Vis Vproduced Vby Vthe Vchondrocytes Vin
Vthe Vsuperficial Vzone Vand Vis Vnot Va Vprimary Vcomponent Vof Vthe Vextracellular Vmatrix. VA Vlack Vof
Vlubricin Vhas Vbeen Vassociated V Vwith Vsyndromes Vcausing Varthritic Vchanges Vat Van Vearly Vage V
4- Anti-sclerostin Vantibody Vincreases Vbone Vformation Vby Vtargeting Vwhat Vmolecular
pathway? V V1*Wnt
V
2*Bone Vmorphogenetic Vprotein V(BMP)
3*Notch
V
4*Indian Vhedgehog
Correct Vanswer V1
All Vof Vthe Vlisted Vfactors Vserve Vcritical Vfunctions Vin Vbone Vformation. VOnly VBMP-based Vtherapies
Vcurrently Vare VFDA Vapproved, Vhowever. VSclerostin Vis Van Vextracellular Vantagonist Vof VWnt Vsignaling
Vand, Vto Va Vlesser V Vextent, VBMP Vsignaling. VBlosozumab Vcurrently Vis Van Vinvestigational Vantibody
Vtherapy Vdesigned Vto Vblock Vsclerostin’s Vability Vto Vinhibit VWnt Vsignaling, Vnetting Va Vpositive Veffect Von
Vbone Vformation. VIn Va Vphase V2 Vtrial Vinvolving V120 Vpostmenopausal Vwomen, V1 Vyear Vof Vblosozumab
Vtreatment Vresulted Vin Va V17% Vincrease Vin Vbone Vmineral Vdensity Vin Vthe Vlumbar Vspine.
,1- In Vthe Vcontext Vof Vjoint Varthroplasty, Vthe Valpha-defensin Vimmunoassay Vtest Vis Vuseful Vfor Vthe
V detection Vof?
1*aseptic Vloosening.
V 2*metal Vcorrosion.
V 3*periprosthetic
V infection. V4*bone
V ingrowth.
Correct Vanswer V3
Alpha-defensin Vis Va Vprotein Vreleased Vby Vactivated Vneutrophils Vin Vresponse Vto Vinfection. VThe
Vdetection Vof Valpha-defensin Vin Vsynovial Vfluid Vis Vhighly Vsensitive Vand Vspecific Vas Va Vmarker Vof
Vperiprosthetic Vinfection. VAseptic Vloosening Vand Vthe Vbone Vingrowth Vof Vprostheses Vgenerally Vare
Vdetected Vradiographically. VMetal Vcorrosion Vissues—in Vmetal-on-metal Vprostheses, Vfor Vexample—
generally Vare Vfollowed Vusing Vblood Vmetal Vion Vlevels.
2- In Vposttraumatic Varthritis, Vthe Vinitial Vinjury Vstimulates Vthe Vproduction Vof Vinflammatory Vcytokines.
V Which V Vcytokine Vis Vproduced Vat Vthe Vhighest Vlevel Von Vthe Vfirst Vday Vafter Vinjury? V
1*Interleukin-6 V(IL-6)
V 2*Interleukin-1 Vbeta V(IL-1β) IL -1B
TNF-a
V 3*Chemokine Vligand V22 V(CCL-
22)
4*Damage-associated Vmolecular Vpatterns V(DAMPs)
Correct Vanswer V2
The Vdevelopment Vof Varthritis Vafter Vjoint Vinjury Vis Vcommon Vand Vcan Vresult Vfrom Vmultiple
V causes, Vincluding Vcartilage Vcontusion, Vmeniscal Vinjury, Vligament Vtear, Vor Vintra-articular Vfracture.
V The Vaccuracy Vof Vreduction Vdoes Vnot Vnecessarily Vprevent Vthe Vdevelopment Vof Vposttraumatic
V arthritis. VData Vfrom Vanimal Vstudies Vof Vposttraumatic Varthritis Vdemonstrate Vthe Vproduction Vof
V inflammatory Vcytokines Vthat Vlead Vto Vchondrocyte Vdeath Vand Vmatrix Vdestruction. VIn Vthe Vfirst
V few Vdays Vafter VinjuryVVIL- V
V1β V(predominantly) Vand Vtumor Vnecrosis Vfactor Valpha Vare Vthe Vprimary Vcytokines Vproduced, Vfollowed
Vby V
nitric Voxide, Vmatrix Vmetalloproteinases, Vand Vaggrecanases, Vwhich Vdegrade Vthe Vchondral Vmatrix
V
V CCL-22 V Vincreases Vat Varound V5 Vdays Vafter Vinjury, Vhowever. VOther Vfactors Vcalled VDAMPs, Vwhich
V are Vgenerated Vthrough Vthe Vmechanical Vor Venzymatic Vdegradation Vof Vjoint Vtissues, Valso
,stimulate Van Vinnate Vinflammatory Vresponse.
V
, 3- What Vis Vthe Vmain Vfunction Vof Vlubricin Vin Vsynovial Vjoints?
1*Serves Vas Va Vcomponent Vof Vthe Vextracellular
matrix V2*Inhibits Vmatrix Vmetalloproteinase
V
3*Increases Vcross-linking Vbetween Vcollagen Vfibers
4*Reduces Vthe Vcoefficient Vof Vfriction Vin Vthe Vjoint
V
Correct Vanswer V4
Lubricin Vreduces Vthe Vfriction Vbetween Vthe Vsurfaces Vin Vthe Vjoint, Vleading Vto Vdecreased Vshear Vforces
Vgoing Vthrough Vthe Vhyaline Vcartilage. VIt Vis Va Vglycoprotein Vthat Vis Vproduced Vby Vthe Vchondrocytes Vin
Vthe Vsuperficial Vzone Vand Vis Vnot Va Vprimary Vcomponent Vof Vthe Vextracellular Vmatrix. VA Vlack Vof
Vlubricin Vhas Vbeen Vassociated V Vwith Vsyndromes Vcausing Varthritic Vchanges Vat Van Vearly Vage V
4- Anti-sclerostin Vantibody Vincreases Vbone Vformation Vby Vtargeting Vwhat Vmolecular
pathway? V V1*Wnt
V
2*Bone Vmorphogenetic Vprotein V(BMP)
3*Notch
V
4*Indian Vhedgehog
Correct Vanswer V1
All Vof Vthe Vlisted Vfactors Vserve Vcritical Vfunctions Vin Vbone Vformation. VOnly VBMP-based Vtherapies
Vcurrently Vare VFDA Vapproved, Vhowever. VSclerostin Vis Van Vextracellular Vantagonist Vof VWnt Vsignaling
Vand, Vto Va Vlesser V Vextent, VBMP Vsignaling. VBlosozumab Vcurrently Vis Van Vinvestigational Vantibody
Vtherapy Vdesigned Vto Vblock Vsclerostin’s Vability Vto Vinhibit VWnt Vsignaling, Vnetting Va Vpositive Veffect Von
Vbone Vformation. VIn Va Vphase V2 Vtrial Vinvolving V120 Vpostmenopausal Vwomen, V1 Vyear Vof Vblosozumab
Vtreatment Vresulted Vin Va V17% Vincrease Vin Vbone Vmineral Vdensity Vin Vthe Vlumbar Vspine.
