Putative Periodontopathic Bacteria Far almost 100 years, a bacterial etiology forthe existence of periodontitis has been sought. Early on, the non-specific plaque hypothesis prevailed. but since the 1970s research has indicated specific bacteria as the etiologic agents in periodontal diseases. Nevertheless, it is certain that not all possible periodontopathic microorganisms have yet been ‘identified. With this in mind, Figure 66 {Socransky & Haffa- Jee 1992, Tonetti 1994) presents the most likely periosionto- pathic microorganisms, but this table makes no claim (0 completeness: it will certainly be modified and enhanced by future research, Periodontopathic Bacteria 33 According to Soeransky’s postulates, the pathogenic poten- tial of a microorganism is determined not only by its associ- ation with the disease, but also the pathogen by therapy « Activation of the host immune response tothe speciti fection « Detection of putative virulence factors (pp, $4~35) ‘The elieitation of similar periodontal disease symptoms in animal experiments, | aT 156 Frequency of Research Studies 3 a) ‘Studies That Have Demonstrat [Association Elimination Host | Virulence | Animal | site estes! Rathageniciy [Response | Factors | Studies | ee eee at tates ‘The number af “pis signs" ‘atestheftequency af positive sults inthe stu. For al the microargaisrs st fd, the deect association with the ++ + ‘Bscase (1) was investigated, and an inmost cases io thecthor sted Fr cen e a + | ssitena 2-5) Taree Thelnlersty ofthe backarourd TE ares: ++ + + | calr(red = gramnognve bow = ‘gare pasiive) depicts the asaci Compact 5 {lon al the bacteria withthe vac Cr ives ibe ‘esertera of paviodantls and thus. ea measure the relative + + ++ | jathagenicty. af + Assocation with Pestaois Sg Seemarones =| BR Heh pathogenic Suet [EB] Wodertey pathogenic Fuboctrumnsp. | ke ++ [CE stony sotmogenic Spochetes 4g | 1 rover stsios SSO (57 Rank Ordering ofthe Patho- Moderately Slightly ++ * ‘enicity of tnvidual Bacteria ee | f° Aa Se A. ectinomycetemenmtent ‘comiant 5 interme P singivals : 2° inermecio Tanneretaforsythensis pg eae airecens (2003; former ores Tonnereta oe hee rt be the svi ln Ses appar ine the stv TE seesytpem Suen muceotun periodontal pathogenic mraor> Treponeme Re Euboctertuon sp. ‘anisms. + Te eee E corodens pastes Nuch34 Microbiology—Virulence Virulence Factors The destructive potential of bacteria is related ta their rela- tive concentration (percentage composition of the total bac terial flora}, but also to their so-called virulence factors. Bac- teria (usually gram-negative) possessing virulence factors are usually found in periodontal pockets when periodontal destruction fs actively progressing. Some of these virulence factors have already been mentioned: endotoxin, exotexin, enzymes, chemotactic substances and antigens. These and other virulence factors that have thus far been demonstra ted are listed below, Virulence Transfer Virnfence factors are transferred to daughter cells following cell division, burt such factors can also be transferred from ane bacterium to another or to other species of bacteria by means of plasmid transfer. Plasmids determine various characteristics of bactetla, &.g. the production of toxins (virulence plasmids) and resistance factors (resistance plasmids) against antibiotics. Bacteriophages are viruses that proliferate within bacterial cells and have the ability to transfer DNA Fragments or plas- mids between bacteria (Fig, 70; Preus et al, 1987, Haubek et al, 1997, Will & Meyer 1998). 8 Number {inpercent of A ae aa croorganisms ia Active and inae- tive Pockete(Oaineetal sas) FS Perm Trecoureotpersonttsts gg BOOM tout suface speci ad pi ras ie 1 Peete Theabicutesumberandtheper med centage ampostion cl pion net topategrun-negte bate fosters (iedjaresgicantyerenedin 58 Steportcs ccthepackets hacthelesens, | S27008 Onetinds primacy grapostne ME Atnomee ip Sresdentemsccerpenoms(3se, yp eke sicharelesdarmgingtabost oe tase anc wchto aera de Syeeactualyinbttepathager. ee eee 69 acter Virulence Factor Cans teiooltacies Vnvercanmittanoral tai buaheacactesaaed hemes Fiueaced by theinhecent patho-— ytacestrsaures Teahar adhere ‘penicpotentislof a bacterin ts environment, and is interaction ‘withthe host Virulent bacteria require a gampetited inorder to Colonization, pratiferation = Nutation chain dewcloprnent = foteases fo londstutf metabolism (Host proteins, = Inhibition of inibiors i elicit pertodontitis. micraorga- Host response ~~ Copsaile. mucous: armen TBeciving — —ratiectir tacker «© Establish themselves nearthe —tnhibiting ~ tewhotoains (Aa) é cuemnet Timing imnimogindeainy =| 1 Avoid beng lina by saliva RED cect tees | gence. Penetration into host tissues, — invasins is 1 Fed spose ution ieee 8 hdd thedcenemechlsns | yigdime ark E ‘ofthe host and other microor- Pp ~Gilipenases = ain “fonda. chindotinsatase a Beane tae “Wipes vor ees oversiaptad —_Lrpoye chro kentrouh inet prone so =a et ~~ Capsuile-, membrane substances bees asin the pocket gone asi, boty sel. propionic 36, oles, sponta ‘edrrinptam Sop at tsrpoteti slim compar — Tris tc ese seritathot ofthe hen The olahe ste corpo Eipctectate desta soft and hard tissues iscaused Tiaaise damage indirect _siost inflammatory response bo snainty by the immune defense: ecbidolsaie antes imachntin of tt = Sten euttion 0: iMenmaoymedacrainas | Faceted Tete tesserae |= tis even vent bacterial stains quire partners (comgleves: p37) regulation of the syns af prostaglandin £2 (PCE), matric Ietalloproteinaces (MP) atc,22 Etiology and Pathogenesis—Periodontitis Periodontitis—A Multifactorial Disease In recent years, the conceptual view concerning the etiology ‘of poriadontitis has evolved. Early on, it was the bacteria that were viewed as the determining factor, Certain patho- genic microorganisms were shewn to be associated with ‘various forms of periodontal disease, as well as the speed of progression. However. the existence and distribution of pathogenic hacteria did nat always correlate with the incep- tion and clinical progression of periodontitis. Furthermore, it was demonstrated that the presence of pathogenic bacte- ria in a periodontal pocket is not necessarily the cause of that pocket; rather, it seemed much more important that AY Etiology of Peviodomtitis— Interaction between Dental Plaque and the Host Bacteria 1 The primary etinlogicFacto for the existence of periodontitis pathogenic microorganisms wit inthe subgingival bial, Host 2 The genetical determined nnowspeciic and specific im une responce, 25 wll acs temic syndromes andiseases Influence the exstence andthe linical course of periedoniitis. 33 “Habits” and the patient's oun 2oprmach tngeneralhweatn wil influence plague formatian nd hast immune response, both systemlcally and particularly ‘with regard to oral eal 4 Soxil circumstances influence ‘he systemic anal payee wel being af the patient. Problems fe the sacigeconamic area Feadto negative stress. 55 Pyychic burdens andstress in uence the emma status, In addition to specific microorganisms, diverse host factors: are critical for the development of periodontitis from a pre~ existing gingivitis (cf. Fig. 41, modified from Clarke & Hirsch, 1995), Suc factors include the immune responses triggered by pathogens, and these are well understood today. Such defense reactions may be disproportional to the insult, re sulting in immunopathologic tissue injury. Recently, however, in addition to the genetically determined, immune reactions, a great number of other individual risk factors have been identified, which may be respansible for the initiation and the degree of severity of the clinical course of pesiodtontitis (p.51). the pocket milieu presents a favorable environment for the existence and proliferation of pathogenic organisms. The stage would then be set—Hike a vicinus cycle—far the pro- ‘gression of the disease processes (Mombelli et al, 1991). Nevertheless, the old adage “no bacteria = na periodontitis” still holds true, but on the other hand itis also a fact that bacteria, including pesiodontopathic bacteria, do not with- ‘out exception cause 2 Heredity immune defen Caney Systemic Diseases Viruses Kenmone modulation Negative Stress Psychological Factors. ~tminune modulation 5. Ofthe Fisk factors listed in Figures 41 and 104, only afew are capable of damaging the periodontium directly (e.g, smok- ing); of much greater importance is the influence af such factors on the patient's own immune system. The delicate balance between “attack/destruction™ (bacteria) and de- fense (host response) Is disturbed. It is only logical to sume that the most severe, early-onset and aggressive forms of pesiodantitis will accur when particularly virulent bacteria are present in a weak (immunodeficient) hast.Introduction “Periodontology” is the study of the tooth-supporting tissues, the “periodontium.” The periodon= tium is made up of those tissues that surround each tooth and which anchor each tooth into the alveolar process (Latin: para = adjacent to; Greek: odus = tooth). ‘The following soft and hard tissues constitute the structure of the periodontium: * Periodontal Ligament * Alveolar Bone * Gingiva * Root Cementum, The structure and funetion of these periodontal tissues have been extensively researched (Schroeder 1992). Knowledge of the interplay between and among the cellular and molecular components of the periodontium leads to optimum therapy, and also helps to establish the goals for future intensive research. Periodontal Diseases Gingivitis ~ Periodontitis, ‘There are numerous diseases that affect the periodontium, By far the mast important of these are plaque-associated ‘gingivitis (gingival inflammation without attachment loss} ‘and periodontitis (inflammation-associated loss of peri= ‘odontal supporting tissues). * Gingivitis is limited to the marginal, supracrestal soft tis sues. his manifested clinically by bleedingupon probing of the gingival sulcus, and in more severe cases by erythema and swelling, especially of the interdental papillae (Fig 3}. + Periodantitiscan develop from a pre-existing gingivitis in patients with compromised immune status, the presence ofrisk factors and pro-inflammatory mediators, as well as the presence of a predominately periodontopathic micro- bial flora, The inflammation of the gingiva may then ex- tend! into the deeper structures of the tooth-supporting apparatus. The consequences include destruction of colla- gen and loss of alveolar bone (attachment loss}, The june- tional epithelium degenerates into a “pocket” epithelium, which proliferates apically and laterally. true periadon- tal pocket forms, Such a pocket isa predilection site and a reservoir for opportunistic. pathogenic bacteria: these bacteria sustain periodontitis and enhance the progres- sion ofthe disease processes (Fig.4). Gingival Recession Gingival recession is not actually a “disease,” but rather an anatomic alteration that is elicited by morphology, improp. er oral hygiene (aggressive scrubbing). and possibly func tional overloading. © Teeth are not lost due to classical gingival recession, but patients may experience cervical hypersensitivity and esthetic complications. I gingival recession extends to the mobile oral mucosa, adequate oral hygiene is often no longer possible, Secondary inflammation is the conse- quence. Inaddition to classical gingival recession, apical migration of the gingiva is often observed in patients with long- standing, untreated periodontitis, and it may be a conse quence of periodontitis erapy in elderly patients (“invo- lution”; Fig.2) “These three periodontal disorders ~ gingivitis. periodontitis. gingival recession ~ are observed world-wide; they affect almost the entire population of the earth te greater or lesser degree. In addition ta these common forms of oral patholo~ 2. there are many less frequently encountered diseases and defects of the periodontal tissues, All of these diseases were compretensively classified at an international World Work shop in 1999 (see Appendix, p. 519}.Periodontology Herbert FE. Wolf Edith M. & Klaus H. Rateitschak Thomas M. H Forewords by Samuel B, Low and Maurizio S. Tonetti ard revised and expanded edition | =. spat of wl ae : By asVv Series dors: ous RattschakT Herbert. Walt ‘Authors—Periodontalogy: Herbert. Wot eth Kos Rates Thomas Hassel a ogc» =... paraiprorel Poo Se, Sopareeata area Sete =reein mae sone \Grmancaen 106 guneanen 88 echo Sp ain presen Eien 888 Pisansnedbon 190 Crmony Medimentberscn Rated. Gamnh Pechnnen ssins47som2¢6n9 Dr. Herbert F. Wolf Prat Practienet-Pevodonts SSO/SP Lewenstrese 55/57, 8007 Zurich Sitznand Emaitherertwollabhowineh r. homas M. Hassell Professor DDS. Dr med. dent, Ph. Northern Arona Unversty gst arzona USA Ema thomas hassel @NALEDU Inthe Series “Color Atlas of Dental Medicine” 2 Boor, M.A. Baumann, S. Kim © Endodontology ‘A. Burman, U.Lotemann, }. Mah (© TM Disorders and Orofacial Pain ALH. Geeting,M. Kundert,C.C. Kelsey © Complete Denture and Overdenture Prosthetics G. Graber ‘© Removable Partial Dentures FA.Pasler © Radiology Th. Rakes! I Jonas © Orthodontic Diagnosis LA. Reichart,H.P.Philipsen © Oral Pathology H. Sailer, C.F, Pajarola '© Oral Surgery for the General Dentist |.Schmidseder ‘Aesthetic Dentistry H. Spiekermann,k. Donath T. Hassel 5. Jovanovic, [Richter ‘© Implantology H.E Wolf €.M. 8 K.H, Rateltschak, 7.M. Hassell © Periodontology edition Demers, Sept of Caray and Peiodntoogy Dental nsttute Univestyof ase Clsererstass 19, CH 4056 Basle Fr tenschak blue ch Desks H Ratetschak f Former Profesor nd Chatman Deparumant of arblogy and Dental tute Universtyof ase, itzerand feces ewer eet Ironia, pate ots ‘loro terre toy ore tt ch Teer neta oh erred iepaemoees Seoiicmnarees peony ieciecerens tomer nor ems Sen eee mieten eetecman Ferrer Soeraai Soe Sueaoreine ieneoewonts Eosootroe Setecnerarees Hou spaceingnicensiantae setnroncomntouppctcce ‘tha docu’ poprey ose ‘Dtecomtordn sneer ye paioserturt sine nbieeonah piety aah Sele tino pci I a Sencar sean pod ‘oe Cen memcpy ara {er of met eect de