Perio/Endo Symposium

By Dr Angela R.C. Pack, BDS Lond, PhD Lond, FDS RCS Eng, Discipline of Periodontology,School of Dentistry, University of Otago, PO Box 647, Dunedin, New Zealand.

Periodontal Considerations In Endoperio Lesions

Editor's Note: The following paper was presented to the Perio/Endo symposium of the AN2 Division of the IADR, Dunedin, August I997 and subsequently published. It is reprinted here from the journal ofthe NZ Society of Periodontology 1999; 84: 9- I 3 by kind permission of the Editor, Dr Angela Pack.
Although the periodontiumis constantly subjected to mechanical and bacterial stress, it efficiently maintains structural and functional integnty because of the fast turnover and remodelling ability of its component structures. It functions as one unit anchoring the teeth in the jaws, yet the cellular activities and matrices of Its four distinctive tissues are interdependentthrough a variety of complex processes which coordinate the synthesis of hard and soft tissues. The mechanisms involved in the initiation and progression of periodontal disease are similar to those influencing the pathogenesis of periapical lesions. The nature and extent of the pathological change is dependant upon factors such as the virulence of the irritant, the host defence mechanisms, and the duration of the disease process. In both periodontal and endodontic inflammation. the extent and seventy of the respective condition will influence the extent to which the other tissues may be affected. For example, pulpitis will rarely affect the periodontium. and similarly, marginal gingivitis will not evoke any obvious pulpal response. However. untreated endodontic infection is likely to influence periodontal healing adversely. resulting in a greater risk of attachment loss. Likewise, deteriorating periodontal destruction will threaten the integri of the pulp. The fundamental difference between endodontic and periodontal lesions, is their respective origin and the subsequent direction of their progression. Whereas periodontal destruction moves apically from an initiatingmarginal gingivitis. periapical disease from pulpal necrosis can extend apically or coronally. Thus a periapical lesion which communicates with the oral cavity through a sinus tract along the root surface, may mimic a deep isolated periodontal pocket. It is therefore critically important to determine whether the lesion is primarily periodontal or primarily endodontic in origin, because the accuracy of diagnosis will determine whether or not the appropriate treatment plan is instigated. Incomplete investigation and an error of judgement at this stage could result in an endodontic sinus tract being treated as a deep periodontal pocket by root planing or even surgery. This inappropriate treatment would result in failure of the "pocket" to resolve. and failure of the disrupted periodontal tissues to heal and repair when eventually the endodontic origin is discovered and treated. The diagnosis of a lesion can be further complicated because occasionally both periodontal and endodontic lesions may simultaneously and coincidentally affect the same tooth.
AUSTRALIAN ENDODONTIC JOURNALVOLUME 27 No. I APRIL 2001

In the embryological development of the tooth. the dental follicle, which is the precursor of the perintiurn. is in close relationship with the dental papilla from whence comes the pulp. As the roots are mapped out by Hertwig's root sheath, and dentine and cementum are deposited. direct anatomical communication between the pulp and the periodontium becomes limited to the apical foramina and lateral accessory canals. Once the tooth has erupted however, removalof cementum by root planing and scaling introduces a further perio/pulpal pathway of communication through exposed dentinal tubules. The most probable pathway of communication between pulpal and periodontal tissues is by means of the common vascular supply to both regions. and anastomoses through accessory canals formed during the early stages of tooth development. Blood supply reaches the periodontal ligament from apical vessels, blood vessels from the alveolar bone, and from anastomosis with gingial blood vessels (Cohen 1960). The prevalence of lateral and accessory canals was reported 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 of lateral and accessory canals in the coronal and middle thirds of the roots of molar teeth; this being 59% (Lowman et ol 1973). Furthermore, Gutmann in I978 reported that 28.4% of furcation regions had accessory canals. The significance of the association between pulpal and periodontal tissues, and the extent to which pathological changes may be transmitted between the two. are important issues when considenng the common aspects of aetiology and the outcomes of appropriate treatment and healing. Sharp ( 1977) and Benenati et 01 ( I98 I) have reviewed the relationship between the periodontium and the pulp. Controversy exists as to whether or not the presence of periodontal inflammation affects the integnty of the endodontic tissues. Early workers (Fish & Maclean 1936, Sauewein 1956, Mazur & Massler 1964) could find no definite relationship between pulpal status and periodontal disease. Bender & Seltzer ( 1972) showed that 79% of teeth with periodontal disease, but without caries or restorations, exhibited histological evidence of pathological changes in the pulp. Localised necrosis of pulp tissue has been reported adjacent to accessory canals which have been exposed by periodontal disease (Seltzer et ol 1973. Rubach & Mitchell 1965). Although it seems that changes do occur in the pulp as a result of periodontal disease, degeneration of the pulp does not usually occur unless the main pulp canal, or one of the main pulp canals in the case of multirooted teeth, is involved (Langeland et ol 1974). The response of the pulpal tissues to long standing periodontal disease appears to result in the deposition of large quantities of reparative secondary dentine along the pulpal walls, and the induction of pulpal fibrosis. dystrophic calcifications. reduced vascularity and fewer nerve fibres, rather than an inflammatory response resultingin degeneration and necrosis (Seltzer et ol 1963,
39

Bender & Seltzer 1972. Lantelme et a 1 1976, Sinai & Soltanoff 1973). Conversely, there is general agreement that pulpal infection can both initiate and maintain perdontal disease (Czarnecke & Schilder 1979)through the escape of noxious productsdraining into the periodontal tissues through apical and accessory root canals. The manifestation of the acute abscess of endodontic origin may be at either a periapical, lateral or furcal location, depending on the major pathway of drainage. Many studies have documented the microbiological similarities between established periodontitisand endodontic infection (Tanner et a 1 1982. Kipioti et a/ 1984, Trope et 01 1988. Kerekes & Olsen I 990). Recently, Streptococcus, Peptostreptococcus, Eubacterium. Bacteroides and Fusobacterium have been identified as the predominant anaerobic species commonly isolated from both endodontic and periodontal lesions (Kobayashi et ol 1990). Similar cellular infiltrates in inflamed pulpal and periodontal tissues provide further evidence of communication between the two (Bergenholtz et ol 1983). A study of the effects of various pulpal conditions and endodontic treatment 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 inhibit periodontal healing and reattachment if patent dentinal tubules were present. As a result, Harrington (I979) suggested that to avoid contamination of the periodontium permanent endodontic treatment should be completed before root planing and removal of the protective cementum layer during periodontal therapy. Cementum is a most important component of the periodontium. It contributes signifcantly to periodontal function, healing, regenerationand repair, and it appears to have an important role in modulating pulpal/periodontal influences. Wasserman et 01 ( I 94 I) claimed that cementum is permeable to diffusion of dyes placed both pulpally and externally to the root. However, Stallar (I968) reported that intact cementum provided a barrier to inward penetration of dye. This may be attributable to the highly calcified amorphous zone adjacent to the cemento-dentinaljunction which has been described as "intermediate cementum". lmmunohistochemical studies of intermediate cementum by Lindskog (1982) and Lindskog & Hammarstrom (I982) have suggested that this layer is an enameloid layer produced by the epithelial root sheath of Hertwig. More recent studies by AJatili (1996) and Bosshardt & Selvig (1997) further support this hypothesis, fulfilment of which, would require an epithelialmesenchymal transformation. Consequently. Harrison & Roda (1995) postulated that the function of the intermediate cementum layer may be: to provide a barrier to permeabillty of noxious substances as a precursor for cementogenesis in root development, and as a precursor for cementogenesis in wound healing and regenerative procedures. t is the latter embryological concept which has resulted Indeed, i in the development of an enamel matrix protein extract as an adjunct to trigger cementogenesis and periodontal regeneration in periodontal flap surgery. Recent studies also report on the complexlty of the connective tissue matrix of cementum with polypeptide growth factors appearing to mediate cellular attachment, proliferation and differentiation in guided tissue regeneration procedures (MacNeil & Somerman 1993, Narayanan et a/ 1995). Acellular cementum covers the apical two-thirds of the root into which Sharpey's fibres are inserted. It has been suggested that bacteria and toxic substances could enter exposed cementum through discrepancies left by the decomposition of these fibres
40

when periodontal disease has destroyed them. Further enhancement of root permeability may be due to root resorption which commences in the cementum. Henry & Weinmann ( I95 I) reported cementum resorption in over 90% of teeth of which 76.8% occurred apically, 19.2% occurred in the middle third of the root, and 4.0% in the coronal third. The susceptibility of a root to undergo idiopathic resorption has been attributed to the absence of either the uncalcified precementum surface layer or the reduced enamel epithelium within the tooth germ. Exposure of dentinal tubules also occurs in 5- 10% of people in whom there is a congenital absence of cementum at the cemento-enamel junction. However, inflammation in a periodontal pocket is also thought to be the stimulus for root resorption (Lindskog et a/ 1988). Dentinal sensitivity is frequently a symptom resulting from exposure of dentinal tubules on the root surface. Patientswho have undergone periodontaltreatment including scaling and root planing frequent?. complain of increased sensitivlty to thermal, osmotic and mechanical stimuli. The symptoms gradually subside with improved plaque control, but occasionally the sensitii persists evoking a pulpitis-typetoothache with intense pain from the smallest stimulus. Controversy exists as to the aetiology of the dentinal hypersensitivity readon. The hydro-dynamic theory of fluid movement within the dentinal tubules is generally accepted as being the mechanism which stimulates the sensory nerves in the pulp (Br3nnstrom 1966). However, it is probable that the exaggerated hypersensitivlty may also be related to inflammatory changes in the pulp caused by bacterial products from plaque, which penetrate the exposed and patent dentinal tubules. In this manner, the pain threshold of the sensory nerves in the inflamed pulp would be lowered causing a faster and more intense response than that solicited from normal teeth, when subjected to the same external stimuli. This hypothesis is further strengthened by the fact that scrupulous plaque control at hypersensitive root surfaces usually results in a subsidence of the symptoms. The various treatment strategies for root surface hypersensitivity all strive to encourage precipitation so as to seal the patent dentinal tubws, thus Mocking the stimuli from reaching the pulp and permitting inflammatory changes in the pulp to be reversed. Periodontal treatment measures of the root surface are not merely mechanical. In the past I 5 years, many periodontal surgical procedures have incorporated the chemical conditioning of root surfaces by etching agents such as citric acid. tetracycline hydrochloride. orthophosphoric acid or EDTA. These agents demineralise the surface of the root, thereby removing the surface layer contaminated by plaque bacteria and endotoxins and deliberately exposing the collagen fibrils in the dentine. These fibnls are thought to be chemotactic to the fibroblasts in the healing wound (Femyhough & Page 1983, Lopez 1984). Hence root conditioning agents are used to encourage the developmet of new connective tissue attachment. When tetracycline hydrochloride is used, not only does it etch the surface, but it is also slowly released over 48 hours providing substantivty to the antimicrobial actmy in the wound. In addition, tetracycline enhances the binding of fibronectin. which further encourages fibroblast attachment and growth in guided tissue regeneration (GTR) (Baker et 01 1983, Wkesjo et a/ 1986). In the past I 5 years guided tissue regenerationprocedures have evolved using, first. non-resorbablemembranes, and more recently resorbable membranes, or various naturally derived or synthetic fillers, with or without incorporated experimental biological mediators such as growth factors. The success rates of these procedures are encouraging, although still not yet entirely
AUSTRALIAN ENDODONTICJOURNALVOLUME 27 No. I APRlL 2001

predictable. In consideration of the pathways of perio/endo communication, it is important to realise that root surfaces subjected to conditioning agents during periodontal surgery, may subsequently become exposed by gingival recession following healing. These root surfaces may contribute to symptoms of hypersensitivity, which could jeopardise the integrity of the pulp, by contamination. Notwithstanding these cautionary comments, the use of GTR therapy, particularly in the treatment of isolated deep periodontal destruction and frequently involving teeth with combined perio/endo involvement, has brought astounding benefns to patients who otherwise probably would have lost teeth. Before embarking upon GTR therapy it is of critical importance to ascertain the state of vitality of the pulp. Studies have shown that periodontal healing responses following scaling and root planing are impaired when periapical pathology exists (Ehnevid et ol I993a & b). With respect to GTR procedures. the amount of regenerated tissue is dependant upon the depth of the intrabony component of the original defect. Within a deeper defect, more patent dentinal tubules and lateral canal ramifications are exposed. This provides greater opportunty for leakage of toxic substances into the healing surgical wound if periapical pathosis exists. Consequently, it is hypothesised that endodontic infection may play a key role in the outcome of GTR procedures. However, clearly there is the need for further research in this field (Chen et ol 1997). In a long-term retrospective evaluation of I95 teeth which had received both endodontic and periodontal treatment more than 8 years previously, Jaoui et ol ( 1995) showed that 9 I% of cases were well maintained and only 8.6% had shown deterioration in periodontal status. Only I 2 teeth had been lost, eight because of periodontal diseases, three because of fracture and one because of caries. A periapical lesion had formed on one tooth. Periodontal/endodontic relationships are forged not only because of various anatomical communication pathways, but also because of common microbiological aetiology of pulpal and periodontal disease. Superimposed on this is the overlying host immune response, impairment of which may affect the extent and seventy of both periodontal and pulpal disease. Consequently, in the control and treatment of both periodontal and endodontic disease it is crucial to observe the fine balance of these interrelationships if the most successful outcomes are to be achieved.

Blmlof L.. Lindskog. 5. Hommontrom. L. Influence of pulpal treatments on cell and tissue reactions in the marginal periodontium. Journalof Periontology 1988; 59: 577-83. Bosshordt. D., Selvig, K. Dental Cementum: the dynamic tissue coveringof the root. Periodontology 1988; 13: 4 1-75, 8ronnstrom. M. Sensitivity of Dentine. Oral Surgery 1966; 2 I :

5 17-26.
Chen. SY. Wong, H-L., Glickmon, G.N. The influence o f endodontic treatment upon periodontal wound healing. journal of Clinicol fkriodontology 1997; 24: 449-56. Cohen, L. Further studies into the vascular architecture of the mandible. Joumalof Dental Research 1960; 39: 936-46. Gomecki. R.T. Schilder. H. A histolqcal evaluation of the human pulp in teeth with varying degrees of periodontal disease. Journalof Endodontics 1979; 5: 242-53. De Deus. Q.D. Frequency, location. and direction of the lateral, secondary, and accessory canals. Journalof Endodontics 1975; I:

36 1-66.
Ehnevid, H., jonsson, L.. Linds&og,5.. 6lmlof L. Periodontal healing in relation to radiographic attachment and endodontic infection. Joumalof Perintology 1993; 64: I 199- 1204. Femyhough. W , Page, R. Attachment, growth and synthesis by human gingival fibroblasts on demineralised or fibronectin treated normal and diseased tooth roots. Journalof Periodontology 1983;

54: 133-40.
fish. E.W. MocLeon. 1. The distribution of oral streptococci in the tissues. 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 . R.S. Intermediate cementum: Development, structure, composition, and potential functions. Oral Surgery, Oral Medicine. Oral Pathology 1995; 79: 624-33. joour. L.. Mochtou. I?, Ouhoyoun. j.P Long-term evaluation of endodontic and periodontal treatment. International Endodontic Journal 1995: 28: 249-54. Kerekes, K.. Olsen. 1. Similarities in the microflorasof root canals and deep periodontal pockets. Endodontics and Dental Traumatol

1990; 6: 1-5.
Kpoti. A.. Nokou. M., Legokrs. N., Mitus, ? I Microbiologicalfinding of infected root canals and adjacent periodontal pockets in teeth with advanced periodontitis. Oral Surgery, Oral Medicine, Oral Pathology 1984; 48: 2 13-20. Kobqoshi. T . Hoyoshr, A., Yosh~kawo,R., Ohdo. K.. Horo. K. The microbial flora from root canals and periodontal pockets of non-vital teeth associated with advanced periodontitis. International Endodontic Journal 1990; 23: 100-106. Lontelrne. R.L.. Handelmon, S.T. H e h m . R.j. Dentin formation in periodontally diseased teeth. Joumalof Dental Research 1976; 55: 48-5 I. Lindskog, S., Hommontrom. L. Formation of intermediate cementum (111). 3H-tryptophan and 3H-proline uptake into the epithelial root sheath of Herhrvig in vitro. Journal of Craniofacial Genetics and Developmental Biology 1982; 2: I 7 1-77, Lindskog. S. Formation of intermediate cementum (i). Early mineralisation of aprismatic enamel and intermediate cementum in monkeys. Journal of Craniofacial Genetics and Developmental Biology 1982; 2: 147-60. LIndskog, 5.. Blomlof L.. Hommorstr&n, L. Dentin resorption in replantedmonkey incisors. Morphology of dentinoclast spreading in vivo. Journalof Clinical Periodontology 1988; 15: 365-70. Lopez. N.j. Connective tissue regeneration to periodontally diseased roots, planed and conditioned with citric acid and implanted into the oral mucosa. Journal of Periodontology 1984;

References
Alotli, 1.. Lundmork, C., Hommontrom, L. The localisation of epithelial root sheath cells during cementum formation in rat molars. Journalof Periodontal Research 1996; 3 I: 433-40. Armitage, G.C.. Christie. TM. Structural changes in exposed human cementum (i) light microscopic observations. Journalof Periodontal Research 1973; 8: 342-55. Baker, 4..Evons, R.T., Cobum, R.A.. Genco, R.j. Tetracycline and its derivatives strongly bind to and are released from the tooth surface in active form. Journalof Periodontology 1983; 54: 58&85. 8ender. 1.8.. Seltzer, S. The effect of periodontaldisease on the pulp. Oral Surgery, Oral Medicine, Oral Pathology 1972; 33: 458-74. Benenoti. EW. Roone. I.&, Woldrop, TC. The perio-pulpal connection: an analysis of the periodontic-endodontic lesion. Gen Dent I98 I ; 29: 5 I 5-20. Bergenhdtz, G.. Lekholm. U., LIljenberg, B., Lindhe,j. Morphometric analysis of chronic inflammatory periapical lesions in root-filled teeth. Oral Surgery, Oral Medicine, Oral Pathology 1983; 55: 295-30 I.
AUSTRALIAN ENDODONTICJOURNALVOLUME 27 No. I APRIL 200 I

55: 38 1-90.
41

MocNerl. R., Somerman, M . Molecular factors regulating development and regeneration of cementum. Journal of Periodontal Research 1993; 28: 550. Mazur, 6.. Massler, M. The influence of the periodontal disease on the dental pulp. Oral Surgery, Oral Medicine, Oral Pathology 1964;

Stallard. R.E. Periodontal disease and its relationship to pulpal pathology. 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 from periodontal pockets and root canals. Journalof Endodontics 1982;

17: 598-603.
Narqamn. A., Ikemwa. K., M I , D., Pitaru, S. Cementum specific components which influence periodontal connective tissue cells. Connective Tissue Research 1995; 33: 19-2 I. Seltzer, S.. Bender. 1.8.. Zimtz. M. The interrelationshipof pulp and periodontal disease. Oral Surgery. Oral Medicine, Oral Pathology

8: 294-300. Trope, M., Tionstad, L., Rosenbery 5. Lstgurten. M. Darkfield

microscopy as a diagnostic aid in differentiating exudates from endodontic and periodontal abscesses. Journal of Endodontics

1988; 14: 35-8.

Wkesjo. U.M.E.. kker, fl.. chnstersson, L.A. et a/. A biochemical approach to periodontal regeneration: tetracycline treatment conditions dentin surfaces. Journalof Periodontal Research 1986; 2 I: 322-29.

1963; 16: 1474-90. Sharp. R.E. The relationship of the pulp and periodontiurn. J West Soc Periodontal Periodont Abstr 1977; 25: 13042.
Simi. I.H.. Soltonoff; W The transmission of pathologic changes between the pulp and the periodontal structures. Oral Surgery, Oral Medicine, Oral Pathology 1973; 36: 558-68.

Preliminary Announcement

Dr Cliff Ruddle T o Lecture In May 2002

Reward yourself and your staff in Paradise at the Sheraton Mirage Gold Coast
The Australian Society of Endodontology Inc in association with Dentsply Australia is pleased to announce that Dr Cliff Ruddle will provide a hands-on programmeentitled:

Creating Endodontic Excellence

Endodontic concepts, technology, and techniques have changed dramatically in recent years. This has left many clinicians uncertain as to what is now possible in endodontics.

An all-day presentation will address essential elements of success includingdiagnosis, root canal system anatomy, access, irrigants. working lengths, new instrument designs, cleaning and shaping strategies, and vertical compaction of warm gutta-percha. This will be followed by a half-day hands-on presentation. Or Cliff Ruddle is acclaimed for his contributionsas a clinician, lecturer and writer. A concurrent programme will also run for dental assistants.
The dental assistants programme is to reward the dental assistant with motivation, skills and education in the field of endodontics and endodontically related topics. The programme is aimed to funher enhance the integration of the dental assistant into the practice. The practice of endodontics relies on well-trained, highly skilled, educated and motivated dental assistants, who can patticipate more thoroughly in the various dental procedures. Use this opportunity to reward yoursetfond your assistants with a few days in Paradise. The result wi// be to produce superior endodontic results.

Further details to be advised when available.

42

AUSTPJUIAN ENDODONTIC JOURNALVOLUME 27 No. I APfUL 2001