Lyme Arthritis: Pathogenesis, Clinical Presentation, and Management

Abstract

l'atl~ogrncsis of :rcn(c and chronic :~rtl~ritis in 1,ymr disrasr Ai'lcr tile initial tielression of scvcral immi~~~o~~tiinul:ilory outst--surl.:icc Iipoj>rotcius that probably play a role ill tiisse:iiiil;~tion to tlic synovial tissue ant1 in tllc patllogencsis of inllammation in the joi~lt itsc11' 101. '1'11~: ;ICLI~C ilrtllritis rcsults from the spirochete-intiuccti i~lliltr:ltion of rnorlonuclc;ir cells into the synovial tissue and tlic :ICCLIIIIU~~I- tion of ncutrophils. i ~ n n ~ u n c complcscs, complcnlcnt, 2und cytokincs in the syi~ovi:~l Ilu~ti. In u~ltl-catcci Ly~nc: :~rtllritis. host i;~etors irivolve(i may incltidc -1'1.,117 alld MyDilH [71. Othcr :utliritogcllic factors may inclucie adhczion molcculcs tI1:~t bi~icl the cstrncclluli~r matrix. sucll :ts P06. riceorin- b1ncii11~ proteins /\ ;~rl(i R. 13gp. and 13BK37 [XI. Matrix n~c.t:illop~~otci~~;~scs [').I(!] may be involvcci tlic p;~thogei~csia oL' erctsivc fe:ituscs in the joint in long-st:~~~di~lg infection (and possibly in arltibiotic-rcl'i-actol-y ;il.th:itis). H /)l~ig(/o~:fi~~.i, I~owevci~, clocs 11ot ~>rotiucc proteases ancl. thel-clhrc, dtxs not caLisc tile r;ipid joint clcstt-uction sect1 it1 cl;~ss!c bac(crinl septic nl.thri[~s. Of the patients who h;ivc illready u~ldcrgons xtantlnrcl antibiotic t1lcr;ipy. a subset mxy h a w pcrsistcrlt 1,ymc al-thritis. .l-hrec major mocicls !'or the inlrn~lnc-)~x~ti~ogcr~csix of antibio~ic-~.cl'r:~etory 1,ymc arthritis h;r\;c Ixcn proposed IOj: pcrsistcnt iilli'ction. -1--cell cpitope mi1nicr-y. :mil hyst:~ndc.r activ;ltion. (A fi)~lrth Iiyl~~tlicsis, that 01' retained sl,iro~licral :intiye~ls, h ; ~ s ~.cccivcc! little stucly ii11tl way 11ot co~lfirnlcd in i ~ ~ ~ m u ~ i l ~ i s t o c l ~ c n ~ i c i ~ l st~~ciies of sy~~o\!ial s;irnplcs fi-o~:~ patients \vho hat1 pcrsistc~lt Lymc arthritis 1.1 I ] . ) The tr~ic etiology ma!; 172 :i combit~ation of thcsc or othcr mcchnnisms, and 11.1~ etiology may vary from