\| Microbial Interactions with tlrc Host in perioclontal Diseases . cHAprER 13 tti":,;.;$ tt\r_ :1 . *r,,lrtaPlal ,:<:.'s ,.

g* Gomplement ft-*f: {r ,tt Antibody Phagocytosis o MMP.8 --:)b: Antigen ! r4\- \ \ Antigen \ \\ \ ltal LPS,1 \ -^\ \ MMP-1 1laseh/ MMP.B 1 ,1;i1i.1;i'..r{ r lf il ta .\',::..:;ai1 ,-t-.i-,,.: q1':.. \,.ii,'.'lt Osteoclast activation Serum ( Regional ..

antibody lymph nodes a .PMN Figure 13-6 Schematic illustration .of .key processes of the host bacterial interaction in periodontal diseases-lnteractions of the bacteria or bacteriar antig;n with host tissues leadsto neutrophil recruitment (white orrows), antibody p-Jr.ii""'ig ra y orro*s1, and boneres,orption (light'groy orrows with bloci outtine)-'tnterteu[ in-s''iL-q and interceltularadhesion molecule-l (lcAM-l) production in the epith elial ceils in iurponr" to periodontalbacteria provides a chemotactic signal for neutrophils (pMN). Neutrophils function tocontrol the bacterial assa.u],t by ph igocytosis but also secrete'matiix metalloproteinases(MMP-8), which may contribu ti to tiisu6 destruction. The interaction of bacterial antigenswith peripheral d endritic cells leads to the generation of systemic antibody, whereas interaction with local B.cells leads to production of local antibody. Antibody s pecific tomany of the periodontal .microorganisms is . essential rot prrug6.ytosis. complementcomponents also mav contribute to efficie nt bacterial prtugS.ytiiir. rne prooutti."-"iinterleukin-l.s ft'rp),'tumor necro sis factor arpha (TNF-;), u-no'prortugrandin E2 ecE,) in response to bacterial lioopolysaccharides (LPS) leadi to uon" t"tJrption"through ort".[i"riactivation, proliferation, and differentiation. lvlast cells constitutively transcribe tumor necrosis factor in transendothelial migration of leukocytes (see Figure alpha (TNF-a), transforming growth factor beta (TGF_p), interleukin-4 (IL-4), and "iiterleukin-6 12-4), which results in the movement of leukocytes into (tL_6); when the local tissues.stimulated, they induce transcription of proinflammatory In he althy individuals, complement Ievels in gingivalcytokines such as IL-1, IL-6, in terferon-y (lFN-1), and crevicular fluid (GCF) are about 3o/o of that in seium.o _thers. r2r The stimulation of endothelial cells by C5a, As periodontal inflammation increases, a concomitant IL-iB, TNF-c, and bacterial lipopolysaccharide (LpS) increase in the levels of complement components occurs. results in the expression of seiectlni on the luminal The levels of C3 and C4, for example, can inc.euse to ZSo/o surtace of the endothelial cells and release of chemokines and 859/o of that in serum.rss The levels of complement from the endothelial cells. These processes are central

components in GCF are more than adequate to support