pack 1999 endo perio.pdf

8/13/2019 Pack 1999 endo perio.pdf

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Perio Endo SymposiumBy Dr Angela R.C. Pack BDS Lond , PhD Lond, FDS RCS Eng, Discip lineof Periodonto logy, Schoolof Dentistry, University of Otago, PO Box 647 Dunedin, New Zealand.

PeriodontalEndoperio

Considerations InLesionsEditor s Note:

The following paper was presented to the Perio/Endosymposium of the AN2 Division of the IADR,Dunedin, August I997 and subsequently published. Itis reprinted here from the ournal o f t he NZ Society ofPeriodontology 1999;84: 9- I3 by kind permission ofthe Editor, Dr Angela Pack.

Although the periodontium s constantly subjected to mechanicaland bacterial stress, it efficiently maintains structural and functionalintegnty because of the fast turnover and remodelling ability of itscomponent structures. It functions as one unit anchoring the teethin the jaws, yet the cellular activities and matrices of Its fourdistinctive tissues are interdependent hrough a variety of complexprocesses which coordinate the synthesis of hard and soft tissues.

The mechanisms involved in the initiation nd progression ofperiodontal disease are similar to those influencing the pathogenesisof periapical lesions. The nature and extent of the pathologicalchange is dependant upon factors such as the virulence of theirritant, the host defence mechanisms, and the duration of thedisease process. In both periodontal and endodontic inflammation.the extent nd seventy ofthe respective condition will influence theextent to which the other tissues may be affected. For example,pulpitis will rarely affect the periodontium. and similarly, marginalgingivitis will not evoke any obvious pulpal response. However.untreated endodontic infection is likely to influence periodontalhealing adversely. resulting in a greater risk of attachment lossLikewise, deteriorating periodontal destruction will threaten thein te gr i of the pulp.

The fundamental difference between endodontic and perio-dontal lesions, is their respective origin and the subsequentdirection of their progression. Whereas periodontal destructionmoves apically from an initiating marginal gingivitis. periapical diseasefrom pulpal necrosis can extend apically or coronally. Thus aperiapical lesion which communicates with the oral cavity througha sinus tract along the root surface, may mimic a deep isolatedperiodontal pocket.

It is therefore critically important to determine whether thelesion is primarily periodontal or primarily endodontic in origin,because the accuracy of diagnosis will determine whether or notthe appropriate treatment plan is instigated. Incomplete investi-gation and an error of judgement at this stage could result in anendodontic sinus tract being treated as a deep periodontal pocketby root planing or even surgery. This inappropriate treatmentwould result in failure of the pocket to resolve. and failure of thedisrupted periodontal tissues to heal and repair when eventuallythe endodontic origin is discovered and treated. The diagnosisof a lesion can be further complicated because occasionally bothperiodontal and endodontic lesions may simultaneously andcoincidentally affect the same tooth.

In the embryological development of the tooth. the dentalfollicle, which is the precursor of the perin tiurn . is in closerelationship with the dental papilla from whence comes the pulp.Asthe roots are mapped out by Hertwig's root sheath, and dentinend cementum are deposited. direct anatomical communication

between the pulp nd the periodontium becomes limited to theapical foramina and lateral accessory canals. Once the tooth haserupted however, removal of cementum by root planing and scalingintroduces a further perio/pulpal pathway of communicationthrough exposed dentinal tubules.

The most probable pathway of communication between pulpaland periodontal tissues is by means ofthe common vascular supplyto both regions. and anastomoses through accessory canals formedduringtheearly stagesof tooth development.Bloodsupply reachesthe periodontal ligament from apical vessels, blood vessels from thealveolar bone, and from anastomosis with gingial blood vessels(Cohen 1960). The prevalenceof lateral nd accessory canals wasreported by De Deus (I 975) as being: 17 in the apical third,8.8 in the middle third and I 6 in the gingival third of the root.Subsequently, other studies have reported a higher prevalence oflateral and accessory canals in the coronal and middle thirds of theroots of molar teeth; this being 59 (Lowman et ol 1973).Furthermore, Gutmann in I978 reported that 28.4 of furcationregions had accessory canals.

The significance of the association between pulpal andperiodontal tissues, and the extent to which pathological changesmay be transmitted between the two. are important issues whenconsidenng the common aspects of aetiology and the outcomes ofappropriate treatment and healing.

Sharp ( 1977) and Benenati et 01 ( I98 I) have reviewed therelationship between the periodontium nd the pulp. Controversyexists as to whether or not the presence of periodontalinflammation affects the integnty of the endodontic tissues. Earlyworkers (Fish& Maclean 1936, Sauewein 1956, Mazur & Massler1964) could find no definite relationship between pulpal status andperiodontal disease. Bender & Seltzer (1972) showed that 79 ofteeth with periodontal disease, but without cariesor restorations,exhibited histological evidence of pathological changes in the pulp.Localised necrosis of pulp tissue has been reported adjacent toaccessory canals which have been exposed by periodontal disease(Seltzer et ol 1973. Rubach& Mitchell 1965).Although it seems thatchanges do occur in the pulp as a result of periodontal disease,degeneration of the pulp does not usually occur unless the mainpulp canal, or one of the main pulp canals in the case of multi-rooted teeth, is involved (Langeland et ol 1974).

The response of the pulpal tissues to long standing periodontaldisease appears to result in the deposition of large quantities ofreparative secondary dentine along the pulpal walls, and theinduction of pulpal fibrosis. dystrophic calcifications. reducedvascularity and fewer nerve fibres, rather than an inflammatoryresponse resulting n degeneration and necrosis (Seltzer et ol 1963,

AUSTRALIAN ENDODONTIC JOURNALVOLUME 27 No. I APRIL 2 1 9


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Bender & Seltzer 1972. Lantelme et a1 1976, Sinai & SoltanoffConversely, there is general agreement that pulpal infection c n

both initiate and maintain perdontal disease (Czarnecke &Schilder 1979) hrough the escape of noxious products draining intothe periodontal tissues through apical and accessory root canals.The manifestation of the acute abscess of endodontic origin may beat either a periapical, lateral or furcal location, depending on themajor pathway of drainage.

Many studies have documented the microbiological similaritiesbetween established periodontitis and endodontic infection (Tanneret a1 1982. Kipioti et a/ 1984, Trope et 01 1988. Kerekes& Olsen I990). Recently, Streptococcus, Peptostreptococcus,Eubacterium. Bacteroides and Fusobacterium have been identifiedas the predominant anaerobic species commonly isolated fromboth endodontic and periodontal lesions (Kobayashi et ol 1990).Similar cellular infiltrates in inflamed pulpal and periodontal tissuesprovide further evidence of communication between the two(Bergenholtz et ol 1983).

A study of the effects of various pulpal conditions and endodontictreatment measures on periodontal response by Blomlof et a/I988) suggested that not only the presence of untreated pulpal

disease, but also endodontic dressing materials, could inhibitperiodontal healing and reattachment if patent dentinal tubuleswere present. As a result, Harrington I 79) suggested that toavoid contamination of the periodontium permanent endodontictreatment should be completed before root planing and removal ofthe protective cementum layer during periodontal therapy.

Cementum is a most important component of the perio-dontium. It contributes signifcantly to periodontal function, healing,regeneration nd repair, and itappears to have an important role inmodulating pulpal/periodontal influences. Wasserman et 01 ( 94 Iclaimed that cementum is permeable to diffusion of dyes placedboth pulpally and externally to the root. However, Stallar I968)reported that intact cementum provided a barrier to inwardpenetration of dye. This may be attributable to the highly calcifiedamorphous zone adjacent to the cemento-dentinal unction whichhas been described as intermediate cementum .

lmmunohistochemical studies of intermediate cementum byLindskog (1982) and Lindskog & Hammarstrom I982) havesuggested that this layer is an enameloid layer produced by theepithelial root sheath of Hertwig. More recent studies by AJatili(1996) and Bosshardt & Selvig (1997) further support thishypothesis, fulfilment of which, would require an epithelial-mesenchymal transformation.

Consequently. Harrison & Roda (1995) postulated that thefunction of the intermediate cementum layer may be:

to providea barrier to permeabillty of noxious substancesas a precursor for cementogenesis in root development, ndas a precursor for cementogenesis in wound healing andregenerative procedures.Indeed, it is the latter embryological concept which has resulted

in the development of an enamel matrix protein extract as anadjunct to trigger cementogenesis and periodontal regenerationin periodontal flap surgery. Recent studies also report on thecomplexlty of the connective tissue matrix of cementum withpolypeptide growth factors appearing to mediate cellular attach-ment, proliferation and differentiation in guided tissue regenerationprocedures (MacNeil & Somerman 1993, Narayananet a/ 1995).

Acellular cementum covers the apical two-thirds of the root intowhich Sharpey's fibres are inserted. It has been suggested thatbacteria and toxic substances could enter exposed cementumthrough discrepancies left by the decomposition of these fibres

1973). when periodontal disease has destroyed them. Further enhance-ment of root permeability may be due to root resorption whichcommences in the cementum. Henry & Weinmann ( I95 Ireported cementum resorption in over 90 of teeth of which76.8 occurred apically, 19.2 occurred in the middle third ofthe root, and 4.0 in the coronal third.

The susceptibility of a root to undergo idiopathic resorption hasbeen attributed to the absence of either the uncalcified pre-cementum surface layer or the reduced enamel epithelium withinthe tooth germ. Exposure of dentinal tubules also occurs in 5 10%of people in whom there is a congenital absence of cementumat the cemento-enamel junction. However, inflammation in aperiodontal pocket is also thought to be the stimulus for rootresorption (Lindskoget a/ 1988).

Dentinal sensitivity is frequently a symptom resulting fromexposure of dentinal tubules on the root surface. Patientswho haveundergone periodontal reatment including scaling and root planingfrequent?. complain of increased sensitivlty to thermal, osmotic andmechanical stimuli. The symptoms gradually subside with improvedplaque control, but occasionally the sensiti i persists evoking apulpitis-type oothache with intense pain from the smallest stimulus.Controversy exists as to the aetiology of the dentinal hyper-sensitivity readon. The hydro-dynamic theory of fluid movementwithin the dentinal tubules is generally accepted as being themechanism which stimulates the sensory nerves in the pulp(Br3nnstrom 1966).However, it is probable that the exaggeratedhypersensitivlty may also be related to inflammatory changes in thepulp caused by bacterial products from plaque, which penetratethe exposed and patent dentinal tubules. In this manner, the painthreshold of the sensory nerves in the inflamed pulp would belowered causing a faster and more intense response than thatsolicited from normal teeth, when subjected to the same externalstimuli. This hypothesis is further strengthened by the fact thatscrupulous plaque control at hypersensitive root surfaces usuallyresults in a subsidence of the symptoms. The various treatmentstrategies for root surface hypersensitivity all strive to encourageprecipitation so as to seal the patent dentinal tubws, thus Mockingthe stimuli from reaching the pulp and permitting inflammatorychanges in the pulp to be reversed.

Periodontal treatment measures of the root surface are notmerely mechanical. In the past I 5 years, many periodontal surgicalprocedures have incorporated the chemical conditioning of rootsurfaces by etching agents such as citric acid. tetracyclinehydrochloride. orthophosphoric acid or EDTA. These agentsdemineralise the surface of the root, thereby removing the surfacelayer contaminated by plaque bacteria and endotoxins anddeliberately exposing the collagen fibrils in the dentine. These f ibnlsare thought to be chemotactic to the fibroblasts in the healingwound (Femyhough & Page 1983, Lopez 1984). Hence rootconditioning agents are used to encourage the developmet of newconnective tissue attachment. When tetracycline hydrochloride isused, not only does it etch the surface, but it is also slowly releasedover 48 hours providing substantivty to the antimicrobial actmyin the wound. In addition, tetracycline enhances the binding offibronectin. which further encourages fibroblast attachment andgrowth in guided tissue regeneration GTR) (Baker et 01 1983,Wkesjo et a/ 1986).

In the past I 5 years guided tissue regeneration procedures haveevolved using, first. non-resorbable membranes, and more recentlyresorbable membranes, or various naturally derived or syntheticfillers, with or without incorporated experimental biologicalmediators such as growth factors. The success rates of theseprocedures are encouraging, although still not yet entirely

40 AUSTRALIANENDODONTICJOURNALVOLUME 27 No. APRlL 2001


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predictable. In consideration of the pathways of perio/endocommunication, it is important to realise that root surfacessubjected to conditioning agents during periodontal surgery, maysubsequently become exposed by gingival recession followinghealing. These root surfaces may contribute to symptoms ofhypersensitivity, which could jeopardise the integrity of the pulp, bycontamination.

Notwithstanding these cautionary comments, the use of GTRtherapy, particularly in the treatment of isolated deep periodontaldestruction and frequently involving teeth with combinedperio/endo involvement, has brought astounding benefns topatients who otherwise probably would have lost teeth.

Before embarking upon GTR therapy it is of critical importanceto ascertain the state of vitality of the pulp. Studies have shownthat periodontal healing responses following scaling nd rootplaning are impaired when periapical pathology exists (Ehnevidet olI993a& b).

With respect to GTR procedures. the amount of regeneratedtissue is dependant upon the depth of the intrabony component ofthe original defect. Within a deeper defect, more patent dentinaltubules and lateral canal ramifications are exposed. This providesgreater opportunty for leakage of toxic substances into the healingsurgical wound if periapical pathosis exists. Consequently, it ishypothesised that endodontic infection may play a key role in theoutcome of GTR procedures. However, clearly there is the needfor further research in this field (Chenet ol 1997).

In a long-term retrospective evaluation of I95 teeth which hadreceived both endodontic and periodontal treatment more than8 years previously, Jaouiet ol (1995) showed that 9 I% of caseswere well maintained and only 8.6 had shown deterioration inperiodontal status. Only I 2 teeth had been lost, eight because ofperiodontal diseases, three because of fracture and one becauseof caries. A periapical lesion had formed on one tooth.

Periodontal/endodontic relationships are forged not onlybecause of various anatomical communication pathways, but alsobecause of common microbiological aetiology of pulpal andperiodontal disease. Superimposed on this is the overlying hostimmune response, impairment of which may affect the extent ndseventy of both periodontal and pulpal disease. Consequently, inthe control and treatment of both periodontal nd endodonticdisease it is crucial to observe the fine balance of these inter-relationships if the most successful outcomes are to be achieved.ReferencesAlotli 1 Lundmork, C., Hommontrom, L. The localisation ofepithelial root sheath cells during cementum formation in ratmolars. Journalof Periodontal Research 1996; 3 I 433-40.Armitage, G .C. . Christie. TM. Structural changes in exposed humancementum (i) light microscopic observations. Journalof PeriodontalResearch 1973; 8: 342-55.Baker, 4 Evons, R.T. Cobum, R.A.. Genco, R.j. Tetracycline nd tsderivatives strongly bind to and are released from the tooth surfacein active form.Journalof Periodontology 1983; 54: 58&85.8ender.1.8.. Seltzer, S The effect of periodontal diseaseonthepulp.Oral Surgery, Oral Medicine, Oral Pathology 1972; 33: 458-74.Benenoti. EW. Roone. I .&, Woldrop, TC. The perio-pulpalconnection: an analysis of the periodontic-endodontic lesion. GenDent I98 ; 29: 5 I5-20.Bergenhdtz, G.. Lekholm. U., LIljenberg B., Lindhe j. Morphometricanalysis of chronic inflammatory periapical lesions in root-filledteeth. Oral Surgery, Oral Medicine, Oral Pathology 1983; 55:295-30 I.

Blmlof L.. Lindskog. 5 Hommontrom. L. Influence of pulpaltreatments on cell and tissue reactions in the marginal perio-dontium. Journalof Periontology 1988; 59: 577-83.Bosshordt. D., Selvig K. Dental Cementum: the dynamic tissuecovering of the root. Periodontology 1988; 13: 4 1-75,8ronnstrom. M. Sensitivity of Dentine. ral Surgery 1966; 2 IChen. S Y Wong, H-L ., Glickmon, G.N . The influenceof endodontictreatment upon periodontal wound healing. journal of Clinicolfkriodontology 1997; 24: 449-56.Cohen, L. Further studies into the vascular architecture of themandible. Joumal of Dental Research 1960; 39: 936-46.Gomecki R T Schilder. H. A histolqcal evaluation of the humanpulp in teeth with varying degrees of periodontal disease. JournalofEndodontics 1979; 5: 242-53.De Deus. Q.D. Frequency, location. and direction of the lateral,secondary, and accessory canals. Journal of Endodontics 1975; IEhnevid, H., onsson L.. Linds&og,5 6lmlof L. Periodontal healingin relation to radiographic attachment and endodontic infection.Joumalof Perinto logy 1993; 64: I 199- 1204.Femyhough. W Page, R. Attachment, growth and synthesis byhuman gingival fibroblasts on demineralised or fibronectin treatednormal and diseased tooth roots. Journalof Periodontology 1983;fish E W MocLeon. 1 The distribution of oral streptococci in thetissues. British Dental Journal 1936; 6 I 336-62.Horrington, G.W The perio-endo question: differential diagnosis.Dental Clinics of North America 1979; 23: 673-90.Harrison. j .W W o S Intermediate cementum: Development,structure, composition, and potential functions. Oral Surgery, OralMedicine. Oral Pathology 1995; 79: 624-33.j oour . L.. Mochtou. I? Ouhoyoun. j . P Long-term evaluation ofendodontic and periodontal treatment. International EndodonticKerekes, K.. Olsen. 1 Similarities in the microfloras of root canals anddeep periodontal pockets. Endodontics and Dental TraumatolKpot i . A.. Nokou. M., Legokrs. N.,Mitus I? Microbiological indingof infected root canals and adjacent periodontal pockets in teethwith advanced periodontitis. Oral Surgery, Oral Medicine, OralKobqoshi. T . Hoyoshr, A., Yosh~kawo,R. Ohdo. K.. Horo. K.The microbial flora from root canals and periodontal pockets ofnon-vital teeth associated with advanced periodontitis. InternationalEndodontic Journal 1990; 23: 100-106.Lontelrne. R.L.. Handelmon, S.T. H e h m . R.j. Dentin formation inperiodontally diseased teeth. Joumal of Dental Research 1976; 55:48-5 I.Lindskog, S. Hommontrom. L. Formation of intermediatecementum 111). 3H-tryptophan and 3H-proline uptake into theepithelial root sheath of Herhrvig in vitro. Journal of CraniofacialGenetics and DevelopmentalBiology 1982; 2: I 71-77,Lindskog. S Formation of intermediate cementum (i). Earlymineralisation of aprismatic enamel nd intermediate cementum inmonkeys. Journal of Craniofacial Genetics and DevelopmentalBiology 1982; 2: 147-60.LIndskog 5 Blomlof L.. Hommorstr&n, L. Dentin resorption inreplanted monkey incisors. Morphology of dentinoclast spreading invivo. JournalofClinical Periodontology 1988; 15: 365-70.Lopez. N.j. Connective tissue regeneration to periodontallydiseased roots, planed and conditioned with citric acid andimplanted into the oral mucosa. Journalof Periodontology 1984;

5 17-26.

36 1-66.

54: 133-40.

Journal1995: 28: 249-54.

1990; 6: 1-5.

Pathology 1984; 48: 2 13-20.

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MocNerl. R. Somerman M Molecular factors regulatingdevelopment and regeneration of cementum. Journal ofPeriodontal Research 1993; 28: 550.Mazur 6.. Massler M . The influence of the periodontal disease onthe dental pulp. OralSurgery,Oral Medicine, Oral Pathology 1964;17: 598-603.Narqamn. A. Ikemwa K . MI, D., Pitaru S Cementum specificcomponents which influence periodontal connective tissue cells.Connective Tissue Research 1995; 33: 19-2 I.Seltzer S Bender. 1.8..Zimtz. M . The interrelationship of pulp andperiodontal disease. Oral Surgery. Oral Medicine, Oral Pathology1963; 16: 1474-90.Sharp. R.E. The relationship of the pulp and periodontiurn. J WestSoc Periodontal Periodont Abstr 1977; 25: 13042.Simi. I.H.. Soltonoff; W The transmission of pathologic changesbetween the pulp and the periodontal structures. Oral Surgery,Oral Medicine, Oral Pathology 1973; 36: 558-68.

Preliminary Announcement

Stallard. R.E. Periodontal disease and its relationship to pulpalpathology. Parodontology and Academy Review 1968; 2: 80-6.Tanner A.C.R. Visconti. R.A.. Holdeman. L.V Sundqvist G.Souansky S S Similanty of Wolinella recta strains isdated fromperiodontal pockets and root canals. Journalof Endodontics 1982;Trope M. Tionstad L. Rosenbery 5 stgurten. M. Darkfieldmicroscopy as a diagnostic aid in differentiating exudates fromendodontic and periodontal abscesses. Journal of Endodontics1988; 14: 35-8.Wkesjo. U.M.E.. k k e r fl chnstersson L.A. et a/.A biochemicalapproach to periodontal regeneration: tetracycline treatmentconditions dentin surfaces. Journalof Periodontal Research 1986;

8: 294-300.

2 I 322-29.

Dr Cliff Ruddle To Lecture In May 2002Reward yourself and your staf f in Paradise at the Sheraton Mirage- Gold CoastThe Australian Society of Endodontology Inc in association with Dentsply Australia is pleased to announce thatDr Cliff Ruddle will provide a hands-on programme entitled: Creating Endo do nt ic Excel lenceEndodontic concepts, technology, and techniques have changed dramatically n recent years. This has left manyclinicians uncertainas to what is now possible in endodontics.An all-day presentationwill address essential elements of success including diagnosis, root canal system anatomy,access, irrigants. working lengths, new instrument designs, cleaning and shaping strategies, and verticalcompaction of warm gutta-percha. This will be followed by a half-day hands-on presentation. Or Cliff Ruddle isacclaimed for his contributionsas a clinician, lecturer and writer.

A concurrent programme wil l also run for dental assistants.The dental assistants programme s to reward the dentalassistant with motivation, skills and education in thefield of endodonticsand endodontically related topics. The programme s aimed to funher enhance theintegration of the dentalassistant into the practice. The practiceof endodontics relies on well-trained, highlyskilled, educated and motivated dentalassistants, who c n patticipate more thoroughly in the various dentalprocedures.Use this opportunity to reward yoursetfond your assistants with a few days in Paradise. The result wi//be to producesuperior endodontic results.Further details to be advised when available.42 AUSTPJUIAN ENDODONTIC JOURNALVOLUME 27 No. APfUL 2001

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