J Clin Periodontol 2002: 29: 663–671 Copyright C Blackwell Munksgaard 2002
Printed in Denmark . All rights reserved
664 Zehnder et al.
vested along with the strains at the
front of the lesion. In patients with lo-
calized aggressive perio...
Pulpal and periodontal tissue pathways 665
1976). The number of dentinal tubules
per mm2
decreases from the pulp to the
666 Zehnder et al.
pathology, and have been termed ‘retro-
grade periodontitis’ (Simring & Gold-
berg 1964).
Similarly, te...
Pulpal and periodontal tissue pathways 667
vital functions of the pulp unless the
disease process has reached a terminal
668 Zehnder et al.
of tissue reactions, regardless of
whether a root canal infection is present
or not (Ehnevid et al. 199...
Pulpal and periodontal tissue pathways 669
Cameron, C. E. (1964) Cracked-tooth syn-
drome. Journal of the American Dental ...
670 Zehnder et al.
Oral Radiology and Endodontics 90, 224–
Madison, S. & Wilcox, L. R. (1988) An
evaluation of corona...
Pulpal and periodontal tissue pathways 671
Vertucci, F. J. & Williams, R. G. (1974) Fur-
cation canals in the human mandib...
Pulpa y perio
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Pulpa y perio

  1. 1. J Clin Periodontol 2002: 29: 663–671 Copyright C Blackwell Munksgaard 2002 Printed in Denmark . All rights reserved 0303-6979 M. Zehnder1 , S. I. Gold2 and Pathologic interactions in pulpal G. Hasselgren1 1 Columbia University, School of Dental and Oral Surgery, Division of Endodontics, New York, NY, 2 Columbia University, School ofand periodontal tissues Dental and Oral Surgery, Division of Periodontics, New York, NY, USA Zehnder M, Gold SI, Hasselgren G. Pathologic interactions in pulpal and periodontal tissues. J Clin Periodontol 2002; 29: 663–671. C Blackwell Munksgaard, 2002. Abstract Both endodontic and periodontal disease are caused by a mixed anaerobic infec- tion. The pathways for the spread of bacteria between pulpal and periodontal tissues have been discussed with controversy. This article is an attempt to provide a rational approach to the perio-endo/endo-perio question based on a review of Key words: combined lesion; endo-perio, infection; pathways; PDL; perio-endo; pulp;the relevant literature. In the light of evidence, clinical concepts for the diagnosis reviewand treatment of lesions involving both periodontal and pulpal tissues are dis- cussed. Accepted for publication 31 July 2001 A lesion involving both periodontal and pulpal tissues can be of primary endo- dontic, primary periodontal or stem from separate origins (meaning that both the endodontic lesion and the marginal periodontal lesion have de- veloped independently). Different authors have created varying nomencla- tures for these pathologies, based on either aetiological or clinical criteria, or a combination of these (Oliet & Pollock 1968, Simon et al. 1972, Guldener 1985). The clinical aspects of perio- endo lesions have been discussed in depth (Hiatt 1977, Harrington 1979, Gargiulo 1984, Meng 1999). However, scientific support for the current under- standing of the matter is sparse. Much of what is in the literature consists of anecdotal reports. There is general agreement today that the vast majority of pulpal and periodontal lesions are a result of bacterial infection. Under which conditions and especially in which direction spread of the disease occurs in the pulpo-periodontal con- tinuum remains a matter of controversy. This article attempts to provide a ra- tional approach to the perio-endo ques- tion based on a review of the relevant literature. Special attention is given to the natural and man-made gates con- necting the involved tissues and the communication of microorganisms and their products within these pathways. Clinical considerations are discussed for each type of lesion, using the classi- fication of Simon et al. (1972), separat- ing lesions involving both periodontal and pulpal tissues into the following groups: O primary endodontic lesions with sec- ondary periodontal involvement, O primary periodontal lesions with sec- ondary endodontic involvement, and O true combined lesions. Microbiology of endodontic and periodontal lesions In a letter to the Royal Society of Lon- don in 1683, Antoni van Leeuvenhoek, the father of microbiology, described the ‘animalcules’ contained in dental plaque and tartar and produced the first drawing of bacteria (Dobell 1958). The presence of bacteria in necrotic hu- man pulp tissue was first described by Miller (1894). It was not until the groundbreaking experiments in animal models by Gupta et al. (1957) and Kakehashi et al. (1965) that micro- organisms were established as the main cause of periodontal and pulpal disease. The concepts obtained from the pre- viously cited animal studies were later confirmed in man (Löe et al. 1965, Sundqvist 1976). Periodontal disease is now thought by most researchers to be caused by a mixed anaerobic infection, modulated by a complex interplay with local and host factors (for review, see Loesche 1999, Page 1999). Similarly, en- dodontic infection of necrotic pulp tissue is of an anerobic nature (Sundqv- ist 1976). An exception to this rule seems to be the microaerophilic A. acti- nomycetemcomitans, which has been as- sociated with aggressive periodontitis (Newman & Socransky 1977). Most of the species that have been found in in- fected root canals can also be present in the periodontal pocket (Moore 1987, Sundqvist 1994). However, Porphyro- monas endodontalis seems to be very rare in oral infections other than those of endodontic origin (VanWinkelhoff et al. 1988). Overall, the root canal flora does not appear to be as complex as the periodontal flora of adjacent pockets (Kurihara et al. 1995). However, it is an inherent problem in bacterial sampling of periodontal pockets that strains from more shallow levels of the site are har-
  2. 2. 664 Zehnder et al. vested along with the strains at the front of the lesion. In patients with lo- calized aggressive periodontitis, more than 50% of the flora from the deepest portion of the pocket consists of Gram- negative rods (Newman & Socransky 1977). When classifying microbiota by morphological criteria with interference microscopy, no significant difference was found between infected root canals and adjacent periodontal pockets (Ko- bayashi et al. 1990). Using anaerobic culturing techniques, the overall flora also appears similar in deepened pockets and adjacent necrotic pulps (Kipioti et al. 1984). Similar conditions favoring anaerobic growth appear to be present in both deepened periodontal pockets and infected pulpal tissues. In addition, it should not be forgotten that the source of both infections is the same, namely, the more than 400 bac- terial species that are present in the flora of the oral cavity. As in any opportunistic infection, in both pulpal and periodontal disease it is quite difficult to evaluate which microbiota actually cause the problem and which bacteria are found simply because the environment favors their selection. Exacerbations of periapical lesions appear to be linked to the pres- ence of black-pigmented, Gram-nega- tive anaerobic rods in the root canal system (Sundqvist 1976, Yoshida et al. 1987, Haapasalo 1989, Sundqvist et al. 1989, Gomes et al. 1994). At least in the case of Prevotella oralis, these bacteria appear to depend on other strains to develop their full pathogenic potential in the root canal system, and were found to be unable to survive if mono- inoculated in root canals of monkeys (Fabricius et al. 1982). The idea of posi- tive microbial interaction in endodontic infections was underlined further by Sundqvist (1992), who demonstrated that certain bacteria are more likely to be found together in the root canal flora. In a study on 13261 plaque samples, Bacteroides forsythus, Porphy- romonas gingivalis and Treponema denticola, if found together, were highly correlated with pocket depth and bleeding on probing (Socransky et al. 1998). This complex was also found in two of 28 infected root canals (Siqueira et al. 2000). However, the sample size in the latter study was much too small for any definite conclusions. It has been noted that the endodontic flora can ap- pear in clusters of mixed bacterial con- tent similar to the arrangement seen in subgingival plaque (Nair 1987). Such matrix-enclosed communities of bac- teria evolved to permit survival of the whole community, and are called bi- ofilms (Costerton et al. 1994). In conclusion, the similarities be- tween the endodontic and periodontal microflora suggest that cross-infection between the root canal and the peri- odontal pocket can occur. This idea is supported by the presence of anatomi- cal pathways between the pulp and the periodontal ligament (Kerekes & Olsen 1990). Pathways connecting endodontic and periodontal tissues There are two forms of possible path- ways for bacteria and their products connecting the two tissues: anatomical and non-physiological. Anatomical pathways The major connections between peri- odontal and pulpal tissues are the api- cal foramina. In addition to these main avenues of communication, there are a multitude of branches connecting the main root canal system with the peri- odontal ligament. These root canal ramifications were first described some 100years ago (Preiswerk 1901, Fischer 1907), and have since been subdivided into furcated, collateral, lateral, second- ary, accessory, intercanal and reticular canals (DeDeus 1975), as well as fur- cation canals (Vertucci & Williams 1974). For simplicity’s sake, this paper will use the term ‘accessory canal’ for any ramification that connects the root canal system to the periodontal liga- ment. It has been speculated that these channels are created by the interference of persistent blood vessels during the downward growth of the sheath of Hertwig (Barrett 1925). This hypothesis is underlined by the finding that acces- sory canals usually contain blood ves- sels (Russell & Kramer 1956). Acces- sory canals are most frequent in the apical third of the root (DeDeus 1975), with ramifications at the very tip of the root having the highest incidence (Hess 1917). In the latter study, maxillary third molars had the highest incidence of accessory canals, followed by maxil- lary lateral and central incisors (Hess 1917). Several authors have described the existence of accessory canals lead- ing from the pulp chamber and/or the main canals into the furcation area of multirooted teeth (Barrett 1925, Seltzer et al. 1963b, Lowman et al. 1973, Ko- enigs et al. 1974, Burch & Hulen 1974, Vertucci & Williams 1974, Gutmann 1978, Perlich et al. 1981, Vertucci & An- thony 1986). A variety of techniques have been employed for these studies, which may explain the divergent results. While scanning electron microscopy studies reveal a high incidence of open- ings on the periodontal surface of mo- lar furcations (Vertucci & Anthony 1986), fewer such openings can be found on the floor of the pulp chamber (Perlich et al. 1981). This phenomenon is explained by the finding that the ma- jority of these ‘canals’ are present only in the cementum layer that covers the furcation; they do not reach the dentin and contain connective tissue rather than blood vessels (Schroeder & Scherle 1987). Patent canals leading from the pulp chamber into the furcation only occur in about 10% of all molars (Vert- ucci & Williams 1974). However, patent canals connecting the main root canal system to the periodontal ligament in the whole furcation area of molars are found in 30–60% of investigated molars (Lowman et al. 1973, Gutmann 1978), predisposing this area to be a zone of intense communication between pulpal and periodontal tissues. In addition to the apical foramina and accessory canals, there is a third possible route for bacteria and their products, the dentinal tubules. Dentinal tubules are formed or, better, left out during tooth development by odonto- blasts, which trail their processes as they grow centripetally while secreting the dentin matrix. The extent of these processes in the dentinal tubules of fully formed dentin is a matter of dispute; however, it is most likely that the odontoblastic process does not reach further than 0.5mm into the dentin (Garberoglio & Brännström 1976). Dentinal tubules are filled with a fluid (Spreter von Kreudenstein & Stüben 1955) similar in composition to extra- cellular fluid (Coffey et al. 1970). In a mature tooth, each individual dentinal tubule can be regarded as an inverted cone with the smallest dimension at the periphery and the largest dimension at the pulp. The opening of each of these small tunnels facing the periodontal ligament is sealed with cementum. At 3.5mm distance from the pulp, the mean tubule diameter was found to be 0.8mm, compared to 2.5mm at the pul- pal wall (Garberoglio & Brännström
  3. 3. Pulpal and periodontal tissue pathways 665 1976). The number of dentinal tubules per mm2 decreases from the pulp to the periphery (Garberoglio & Brännström 1976). Furthermore, the total density of tubules is significantly lower in the api- cal root region than in the midroot and cervical areas (Carrigan et al. 1984). The odontoblastic process, collagenous fibers and the sheet-like lamina limitans in the tubule are tissue structures that further diminish the functional tubule radius to 5–40% of the anatomical ra- dius (Michelich et al. 1978). Non-physiological pathways Iatrogenic root canal perforations are serious complications during dental treatment and have a rather poor prog- nosis (Petersson et al. 1985). Perfor- ations may be produced by powered ro- tary instruments during the attempt to gain access to the pulp, or during prep- aration for a post. Improper manipula- tion of endodontic instruments can also lead to a perforation of the root. The second group of artificial path- ways between periodontal and pulpal tissues are vertical root fractures. Verti- cal root fractures are caused by trauma and have been reported to occur in both vital and non-vital teeth (Chan et al. 1999). In vital teeth, vertical fractures can be continuations of coronal frac- tures in the ‘cracked tooth syndrome’ (Cameron 1964) or can occur solely on root surfaces (Chan et al. 1999). In en- dodontically treated teeth, the incidence of vertical root fractures is higher in teeth that were filled with lateral con- densation technique as compared to teeth filled with single cone technique (Morfis 1990). Teeth restored with in- tracanal posts are more susceptible to fracture than root-filled teeth without posts, and the extension of posts be- yond the coronal half of root canals has a significant negative effect on the inci- dence of root fractures as compared to shorter posts (Morfis 1990). Spread of the disease and clinical considerations The transfer of bacterial flora between periodontal and pulpal tissues is sum- marized in a schematic diagram in Fig. 1. In the following, a more detailed dis- cussion will be given, according to the classification of lesions involving both periodontal and pulpal tissues by Si- mon et al. (1972). Some clinical con- siderations are discussed for each type of lesion, based on the evidence of its bacterial aetiology. Primary endodontic lesions with secondary periodontal involvement The root canal system primarily be- comes infected as a result of dental caries (Reeves & Stanley 1966), trau- matic injuries (Sundqvist 1976) and co- ronal microleakage (Madison & Wilcox 1988). The influence of infected pulp tissue on a healthy periodontium has been directly correlated with the total microbial content in the root canal sys- tem (Byström et al. 1987), and with the length and time the periapical tissues are exposed to the infecting micro- organisms (Korzen et al. 1974). As in periodontal disease, certain host factors or a lack thereof may also play a roˆle in the development of periapical pathosis. For instance, when exposed to the same endodontic pathogens, rats with strep- tozotocin-induced diabetes develop sig- nificantly larger periapical lesions than healthy control animals (Kohsaka et al. 1996). In general, individuals with de- fects in the non-specific immune system have increased susceptibility to bac- terial infections, including periodontitis (Van Dyke & Hoop 1990). Although not yet investigated, it might be antici- pated that patients suffering from dis- eases affecting the non-specific immune response are also more susceptible to the progression of pulpal infection and to increased periapical destruction (Sta- shenko et al. 1998). Fig.1. Schematic diagram illustrating possible pathways as well as the direction within these pathways (small arrowheads) for spread of infection between pulpal and periodontal tissues. If a pulp is only inflamed, but not yet necrotic, it should essentially be re- garded as non-infected and no major breakdown of the periapical tissues should be expected. It has been estab- lished histologically that bacteria do not invade vital pulp tissue (Langeland 1987). However, minor periapical radio- lucencies can occur in spite of the fact that vital pulp functions prevail (Lange- land 1987). Moreover, it is a common clinical observation that in multirooted teeth, vital tissue can be found in canals adjacent to ones containing completely necrotic pulp tissue. Breakdown prod- ucts from necrotic uninfected pulps do not seem to be sufficient to cause peri- apical pathosis (Bergenholtz 1974, Sundqvist 1976, Möller et al. 1981). In addition, there does not seem to be much breakdown from dead, uninfected tissue. In contrast, breakdown products from the cell walls of Gram-negative bacteria found in infected root canals (Dahle´n & Bergenholtz 1980) can cause inflammatory alterations in the peri- apical area (Dwyer & Torabinejad 1981). Hence, infected necrotic pulps will always lead to periapical tissue re- actions if not treated (Sundqvist 1976, Möller et al. 1981). The location of this inflammation is most often at the apex of the tooth. However, periodontal tissue breakdown due to endodontic in- fection not infrequently occurs around the opening of an accessory canal on lateral root surfaces or in the furcation region of multirooted teeth. Such lesions can mimic marginal periodontal
  4. 4. 666 Zehnder et al. pathology, and have been termed ‘retro- grade periodontitis’ (Simring & Gold- berg 1964). Similarly, teeth with iatrogenic root perforations cause inflammatory reac- tions in the periodontal ligament. After an observation period of 1year, a severe inflammation was noted in the peri- odontal ligament surrounding the site of experimental root perforation in 37 of 51 dog teeth (Petersson et al. 1985). In the same study, epithelial down- growth towards the perforation was noted, creating a marginal periodontal defect. This phenomenon seems to be more likely with the perforation site close to the epithelial attachment, and may explain the poorer prognosis of perforations in the furcation area of molars (Strömberg et al. 1972a). A substantial effect of infected pulp tissue on the healthy periodontium via dentinal tubules is very unlikely. Due to its physiological features, discussed above, dentin and the overlying ce- mentum form a natural barrier against bacterial penetration. In fact, it was found that healthy dentin alone signifi- cantly restricts the diffusion of Porphyr- omonas gingivalis proteins in vitro (Pis- siotis & Spångberg 1992). However, in heavily infected root canals, bacteria are found from a few micrometers into the dentin to approximately halfway to the cementodentinal junction, and de- generative alterations can be observed in the cementum (Armitage et al. 1983). The host tissue response to bacterial spread from an infected root canal can initially take two forms: an acute abscess or a chronic inflammatory reaction. Which direction the infectious process takes is in large measure dependent on the virulence and the amount of bacteria present in the root canal. In acute forms of periapical lesions, bacteria can be found in periapical tissues (Nair 1987). Acute periapical lesions or exacer- bations of chronic lesions may drain through sinus tracts, sometimes reaching the gingival sulcus. Following the initial expansion, which involves destruction of the periodontal ligament and the ad- jacent alveolar bone, a balanced host– parasite relationship is usually estab- lished (Yu & Stashenko 1987). The in- flammatory process may then remain unchanged for years. Periapical lesions unaffected by marginal periodontal dis- ease are periapical cysts in 15%, granu- lomas in 50% and periapical abscesses in 35% of the cases (Nair et al. 1996). Chronic, non-symptomatic periapical lesions are usually free of bacteria, but are maintained by endodontic infection (Nair 1987). Clinical considerations If a tooth with an unusual periodontal breakdown does not have a root filling, the first step for proper perio-endo di- agnosis will be a vitality test. It is well- known that pulp tests cannot provide an accurate assessment of the histologi- cal status of the pulp (Greth 1933, Selt- zer et al. 1963a). However, it has been shown that the probability of a non- sensitive reaction representing a ne- crotic pulp is 89% with the cold test and 88% with the electric pulp test (Petersson et al. 1999). As mentioned above, a necrotic pulp in association with a deep periodontal defect should always be suspected to harbor bacteria and should therefore be treated endo- dontically. If the rest of the dentition is periodontally healthy and a vertical root fracture has been ruled out, heal- ing of the attachment apparatus can be expected after endodontic treatment without any periodontal treatment (Fig.2). Some clinical folklore still exists as to the belief that fistulas of en- dodontic origin can cause a periodontal problem. However, it has been demon- strated that, after proper root canal treatment, fistulas originating from an endodontic lesion heal even if they have been present for a long time (Strömberg et al. 1972b). In this context, it should be noted that cleaning and shaping of the root canal in combination with irrigation Fig.2. Male, age 45, presenting with severe bone loss around the distal root and in the furcation area of the mandibular left second molar. Pus was draining through the sulcus. The rest of the dentition was in fair to good periodontal condition. The tooth was non- responsive to cold test (Endo IceA , Hygenic, Akron, OH, USA). Endodontic treatment was administered in two visits, with an in- tervisit calcium hydroxide medication. No periodontal treatment was rendered. At the 6-month recall visit, repair of the bony lesion could be observed (Courtesy of Dr Joshua Most, New York, NY, USA). with sodium hypochlorite alone can not render the root canal system free of cul- tivable bacteria, but an additional in- terappointment medication with a cal- cium hydroxide dressing can (Byström & Sundqvist 1983, Byström et al. 1985). In root-filled, non-vital teeth with periapical lesions, it should be kept in mind that the periapical radiolucency does not necessarily indicate an infec- tion of the root canal system. It has been shown that periapical lesions in endodontically treated teeth take up to 4years to heal (Strindberg 1956). The importance of following up each lesion can therefore not be overemphasized. The prognosis of root canal perfor- ations can be augmented by a stringent aseptic technique and immediate clo- sure of the via falsa with a material that provides maximal bacterial sealing abil- ity and minimal tissue irritation (Seltzer et al. 1970). Primary periodontal lesions with secondary endodontic involvement The formation of bacterial plaque on exposed root surfaces following peri- odontal disease theoretically has the chance to induce pathological changes in the healthy pulp tissue along the very same pathways, as an endodontic infec- tion can affect the periodontium in the opposite direction. Only a few studies have dealt with the matter of bacterial transfer from the infected periodontium towards the uninfected pulp and pulpal reactions to periodontal disease. Find- ings have been very contradictory. Some researchers have reported sub- stantial pathological change and fre- quent necrosis in the pulp tissue due to periodontal disease, especially when ac- cessory canals are present (Bauchwitz 1932, Seltzer et al. 1963b, Rubach & Mitchell 1965). Other investigators have stated that pulps in periodontally affected teeth remain within normal limits regardless of the severity of the periodontal pathosis (Mazur & Massler 1964, Czarnecki & Schilder 1979). In a well-designed histological study on 60 caries-free teeth with various degrees of periodontitis, Langeland et al. (1974) convincingly demonstrated that patho- logic changes do occur in the pulp when periodontal disease is present; however, the pulp does not succumb as long as the apical foramen is not involved. It therefore seems evident that peri- odontal disease rarely jeopardizes the
  5. 5. Pulpal and periodontal tissue pathways 667 vital functions of the pulp unless the disease process has reached a terminal stage and involves the main pulpal blood supply. Some controversy remains as to whether the removal of cementum dur- ing scaling and root planing has an untoward effect on the pulp by opening the dentinal tubules to bacterial pene- tration. In 21 human teeth affected by terminal periodontal attachment loss, invading bacteria were found in the outer third of the dentinal tubules in eight of 15 teeth that had received root planing and in three of six untreated teeth (Adriaens et al. 1987). Unfortu- nately, no attention was given to the state of the pulp in that study. In mon- keys, teeth subjected to scaling and sub- sequent plaque accumulation in com- parison with teeth with periodontitis alone exhibit no obvious aggravation or increased incidence of pathologic pulp reactions (Bergenholtz & Lindhe 1978). As long as the pulp maintains its vital functions, an outward flow of dentinal fluid may be expected upon removal of the cementum barrier (Vongsavan & Matthews 1991). This fluid flow may have a protective, flushing action, which may reduce the inward diffusion of nox- ious bacterial products in exposed den- tin (Pashley & Matthews 1993). Indeed, in a well-controlled in vivo study using human third molars bound for extrac- tion, it was found that bacteria invade dentinal tubules of devitalized teeth much more readily than the tubules of vital control teeth (Nagaoka et al. 1996). On a more long-term basis, the pulp tissue will protect itself against noxious agents by formation of repara- tive dentin (Seltzer & Bender 1959). It therefore seems unlikely that, in vital teeth, careful scaling has a negative ef- fect on the pulp tissue. It furthermore does not seem very plausible that peri- odontal disease can be maintained by a bacterial ‘depot’ contained in infected dentinal tubules after scaling and root planing, as has been suggested (Adria- ens et al. 1987). Clinical considerations If a tooth presenting with a breakdown of the attachment apparatus all the way to the apex reacts positively to cold or electric pulp test, endodontic treatment is not necessary and should be avoided. The probability of a sensitive reaction representing a vital pulp is 90% with the cold test and 84% with the electric pulp test (Petersson et al. 1999). Vital teeth with apparent periapical lesions that stem from primary periodontal break- down are not uncommon (Figs3 and 4). In these cases, periodontal treatment alone should be administered (Gold & Moskow 1987), but complete healing of the attachment apparatus is unlikely. Teeth that did become necrotic as a se- quela of periodontal disease are very rare, and are usually bound for extrac- tion (Zehnder 2001). Fig.3. Male, age 57, long-standing peri- odontal disease in multiple sites. Advised root resection and endodontic treatment on maxillary right first molar. Patient declined recommended treatment but agreed to surgi- cal debridement. The patient was on periodic periodontal (non-surgical) maintenance treatment throughout the observation period. At the 18-year recall visit, the tooth was still in place and the gain of clinical attachment was 6mm in the furcation area. The tooth is vital (positive response to cold test). Fig.4. Female, age 50, long-standing recur- rent periodontal infection. The periodontal disease on the mandibular left central incisor was treated surgically. Routine periodontal maintenance was carried out in 3–4-month intervals. Three years postoperatively, the gain of clinical attachment was 5mm on the distal aspect of this tooth. The tooth has re- mained vital throughout the observation period. True combined lesions These lesions occur when an endodont- ically induced periapical lesion exists at a tooth that is also affected by marginal periodontitis. The two lesions can either merge or exist separately. Merged lesions form by ongoing marginal attachment loss or by exacerbations of apical periodontitis. Teeth with vertical root fractures also belong in this cat- egory, and have been found to have ra- diolucencies involving the periodontal ligament in 75% of the cases (Meister et al. 1980). If apical foramina and acces- sory canals are referred to as avenues of communication for bacteria between pulpal and periodontal tissues, vertical root fractures should be called bacterial highways. As a result of bacterial growth in a fracture space, the adjacent periodontal ligament and (in vital cases) pulp tissue will become the seat of an inflammatory lesion, causing breakdown of connective tissue fibers and alveolar bone. Combined endo-perio lesions that exist separately on the same tooth (meaning that they are not physically merged) have recently gained a lot of attention. The roˆle of an endodontic in- fection as a local modifying risk factor of periodontal disease has been studied in retrospective clinical studies on peri- odontitis-prone patients. Single-rooted teeth with an endodontic infection evident as a periapical radiolucency are significantly correlated to deeper peri- odontal pockets (Jansson et al. 1993a), more radiographic attachment loss (Jansson et al. 1993b, Jansson et al. 1995) and less probing depth reduction over time (Ehnevid et al. 1993a, Ehnev- id et al. 1993b) compared to teeth with- out endodontic infection. Furthermore, endodontic infection is associated with additional attachment loss in the fur- cation area of molars (Jansson & Ehne- vid 1998). Dentinal tubules devoid of the covering cementum layer have been suggested as possible pathways for bac- teria in endodontically infected teeth, leading to further periodontal break- down (Ehnevid et al. 1995). Indeed, in intentionally replanted, infected mon- key teeth, denuded dentin surfaces are associated with epithelial downgrowth (Hammarström et al. 1986), and ex- posed dentin surfaces show significantly larger areas of resorption in infected roots compared to non-infected roots. On the other hand, cementum surfaces exhibit an almost identical distribution
  6. 6. 668 Zehnder et al. of tissue reactions, regardless of whether a root canal infection is present or not (Ehnevid et al. 1995). However, the latter study employed a model that involved trauma to the periodontal liga- ment, and the results obtained can therefore not be directly transferred to the situation of a combined peri- odontal-endodontic lesion. Interest- ingly, in a well-controlled study on ex- perimentally induced periapical in- flammation in monkey teeth, colonies of bacteria could be observed along the entire length of the dentinal tubules ad- jacent to inflamed periodontal tissue, whereas bacteria penetrated to no more than about one third of the tubular length towards the cemento-dentinal junction adjacent to a healthy peri- odontal ligament (Valderhaug 1974). Hence, healthy periodontal tissue, simi- lar to healthy pulp tissue, appears to have more defense mechanisms to resist bacterial penetration than a diseased tissue. Whether an intact cementum layer is an important part of this de- fense system remains elusive. Clinical considerations Root-filled teeth with unusual marginal bone loss should be carefully inspected for vertical root fractures and root per- forations. Here, the comparison of ac- tual radiographs with previous pictures of the same area are very helpful. A sudden and severe breakdown of bony attachment is indicative of a vertical root fracture. It has also been found that vertically fractured, endodontically treated teeth are associated with a typi- cal, V-shaped osseous defect on the buc- cal plate (Lustig et al. 2000). An ex- ploratory surgical procedure is often necessary to obtain the correct diag- nosis. If a vertical root fracture is diag- nosed, extraction or amputation of the affected root remains the only good treatment option. Even if a fracture has been ruled out, the treatment of teeth with combined lesions remains challenging. It is often hard or impossible to assess where the defect caused by the marginal peri- odontal disease starts and the endodon- tic lesion ends. Yet the root canal sys- tem, unlike the periodontal tissues, can be freed from bacteria and then sealed. In addition, overzealous deep scaling and root planing may create the risk of interfering with reattachment. Hence, the treatment should always start with the root canal treatment, followed by an observation period of at least 3months. Concluding remarks In conclusion, it can be stated that in the vast majority of the lesions involv- ing the pulpo-periodontal complex, the bacterial aetiology dictates the clinical course of the disease and therefore the treatment plan. Therefore, the classifi- cation by Simon et al. (1972) has stood the test of time and is very useful in reaching sound clinical decisions. The guidelines for treatment planning given in this text are general. Other factors, such as patient cooperation, restor- ability and economics will influence treatment decisions. However, the pri- mary goal of all treatment efforts must be to rid the patient of the infection. In this article, cystic and neoplastic processes, which are not related to bac- terial invasion of either periodontal or endodontic tissues, yet appear in these tissues, have not been discussed, be- cause the authors feel that they are rare and not perio-endo lesions in the true sense of the expression. Furthermore, lesions that are in part caused by exter- nal traumatic injuries to the dentition, such as external inflammatory resorp- tion, have also not been included. Many of the articles cited here are quite old; the majority of the references were published before 1990. There are two reasons for this: 1) some outstand- ing studies, especially anatomical obser- vations, are as valid today as when they were first published; and 2) there is a clear lack of recent documentation re- lated to the present topic. The need for new data can not be overemphasized. Hopefully, some of the unanswered questions raised in this article will pro- vide ideas for new research projects. Zusammenfassung Pathologische Interaktionen bei pulpalen und parodontalen Geweben Sowohl die endodontalen als auch parodon- talen Erkrankungen sind durch eine gemisch- te anaerobe Infektion verursacht. Die patho- genetischen Muster für die Ausbreitung der Bakterien zwischen pulpalen und parodonta- len Geweben sind kontrovers diskutiert wor- den. Dieser Artikel ist ein Versuch für einen rationalen Ansatz zu den paro-endo bzw. endo-paro Fragen, basierend auf einer Über- sicht der relevanten Literatur. Im Blick der Evidence werden die klinischen Konzepte für die Diagnose und Therapie der Läsionen, die sowohl parodontale als auch pulpale Gewebe einbeziehen, diskutiert. Re´sume´ Interactions pathologiques entre les tissus pul- paires et parodontaux. Les maladies endodontiques et parodontales sont toutes deux causes par une infection mixte anae´robique. Les voies de disse´mina- tion des bacte´ries entre les tissus pulpaires et parodontaux ont e´te´ discute´e avec controver- se. Cet article est une tentative d’apporter une approche rationnelle a` la question paro- endo/endo-paro a` partir d’une revue critique de la litte´rature approprie´e. A la lumie`re des preuves, des concepts cliniques pour le dia- gnostic et le traitement des le´sions impli- quant a` la fois les tissus parodontaux et pul- paires sont discute´s. References Adriaens, P. A., Edwards, C. A., De Boever, J. A. & Loesche, W. J. 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