Domenico Ricucci, MD, DDS, and Jose F.

Siqueira Jr, DDS, MSc, PhDf

Pathways of communication
y The possible pathways for cross-contamination between the pulp and periodontal tissues can be broadly divided into :

y Anatomical y Non-physiological

Ilan Rotstein & James H. S. Simon Periodontology 2000, Vol. 34, 2004, 165203

Anatomical
These are the vascular pathways such as :y Apical foramen Bacterial and inflammatory byproducts may exit readily through the apical foramen to cause periapical pathosis. The apex is also a portal of entry of inflammatory byproducts from deep periodontal pockets to the pulp. y Lateral canals - These accessory canals contain connective tissue and vessels that connect the circulatory system of the pulp with that of the periodontium.
Accessory canals

Apical foramen

Ilan Rotstein & James H. S. Simon Periodontology 2000, Vol. 34, 2004, 165203

Significance y All these aberrations are relatively inaccessible to intracanal instruments. y Not only are all these aberrations largely undebrided, but also bits of tissue and dentin chips may actually be pushed into these areas after being loosened from the main canal

Lateral canals is a canal that is located at approximately right angles to the main root canal.

Root canal morphology and its relationship to endodontic procedures FRANK J. VERTUCCI Endodontic Topics 2005, 10, 3 29

Accessory canals occur in three distinct patterns in mandibular first molars. (A) In 13%, a single furcation canal extends from the pulp chamber to the intraradicular region. (B) In 23%, a lateral canal extends from the coronal third of a major root canal to the furcation region; 80% extend from the distal root canal. (C)10% of the teeth exhibit both lateral and furcation canals.

Accessory canal Is one that branches off from the main root canal

Accessory foramina : Are opening of the accessory and lateral canals in the root surface

y Ramifications can be observed anywhere along the

length of the root, but they occur more commonly in the apical portion and in posterior teeth y In 73.5% in the apical third of the root, 11% middle third 15% coronal third y potential pathways through which bacteria and/or their products y contain connective tissue and blood vessels, is not usually regarded as collateral blood supply --provides little contribution, to pulp function, except --located in the apical 1 2 mm of the canal.

Histologic section of a root showing apical ramifications of the main root canal.

ENDODONTICS ARNALDO CASTELLUCCI MD, DDS

THE FORMATION OF LATERAL CANALS

Lateral canals formed after a localized fragmentation of the epithelial root sheath develops, leaving a small gap, or when blood vessels running from the dental sac through the dental papilla persist. Dentinogenesis does not occur in this specific area, giving rise to a canal containing small blood vessels and sometimes nerves.

Schematic diagram of the formation of lateral canals ENDODONTICS ARNALDO CASTELLUCCI MD, DDS

Schematic diagram of the formation of lateral canals at various root levels ENDODONTICS ARNALDO CASTELLUCCI MD, DDS

y THE FORMATION OF LATERAL CANALS y In some cases, small portions of Hertwig s vertical root sheath

disappear before the odontoblasts have differentiated, and thus before dentin has been formed. A lateral canal will form at just such a point. This small island of lack of cells of Hertwig s root sheath, where odontoblasts do not differentiate and thus dentin does not form, is responsible for the lateral canal s formation y Weinmann states that the development of all the lateral branches of the root canals may be a defect of the epithelial root sheath of Hertwig which occurs during the development of the root because of the presence of a large, supernumerary blood vessel . As a consequence, if the continuity of the root sheath is interrupted before the formation of the dentin, a defect in the dentinal wall will occur. This defect may be also found in the floor of the pulp chamber of a multirooted tooth if the fusion of the tongue-like extensions of the epithelial diaphragm is incomplete due to the presence of a vessel.

y Scott and Symons concur that these aberrant openings are due to defects in the

y y y

formation of Hertwig s root sheath, as a result of which the pulp remains in contact with the dental sac or periodontal tissue. They also believe that these openings in Hertwig s root sheath are probably due to the persistence of anomalous blood vessels reaching the pulp. In studies of the vascularization of the developing tooth of the ape, Cutright and Baskar have observed that a plexus of blood vessels develops in the area of the dental sac. This plexus completely surrounds the enamel organ and the dental papilla. As the tooth develops, this plexus feeds the enamel organ and sends branches into the developing papilla. Once the enamel has been formed, the plexus in the coronal zone degenerates, while the one which surrounds the root forms the periodontal plexus, which gives origin to the vessels that branch around the foramen and enter (or exit) the apical foramen. The formation of the lateral canals has been attributed to the entrapment within Hertwig s membrane of vessels of the periodontal plexus that course around and within the apex of the developing tooth .

y To explain the high incidence of accessory canals near the tip of the root, Cutright and Baskar refer to Kovacs finding that once the tooth enters occlusion the tip of the root grows within the alveolar bone rather than growing outwardly. y According to this theory, each time the vessels of the periodontal plexus are forced to curve apically and then coronally to enter the apex, there is a high pro-bability that they will remain entrapped in Hertwig s root sheath and then be surrounded by dentin. The origin of the accessory canals in the furcation area of multirooted teeth is also attributed to vessels of the periodontal plexus that remain entrapped at points of fusion of the tongue-like extensions of the epithelial diaphragm.

y In confirmation, Grove has noted that no lateral canal

can be found in the apical one third of immature teeth, while they are found in completely developed teeth. Grove hypothesized that if all the vessels reached the pulp from a position directly opposite the foramen, only a single canal would form. If, instead, the vessels entered the pulp from different angles, multiple openings would develop; thus, an apical delta or lateral canals would occur.

To Fill or Not to Fill: Is This the Question?

y Schilder postulated that the main objective of endodontic treatment procedures should be the cleaning and filling of the root canal in its entire extent, also including all lateral canals and apical ramifications. y Buchanan et al those who do 3-D obturation techniques have historically claimed technical and even moral superiority over those who do techniques that only fill primary canals y Rud J, Andreasen Joet al unfilled lateral canals might be associated with post-treatment disease . y Weine FS-- lateral canals harboring inflamed and/or infected material might cause pain during endodontic treatment

y in vitro studies have aimed at evaluating the ability of

different obturation techniques of filling lateral canals-no significant differences y lateral canals are filled less frequently after use of calcium hydroxide medication

Goldberg F, Artaza LP, De S. Influence of calcium hydroxide dressing on the obtu-ration of simulated lateral canals. J Endod 2002;28:99-101.

y Camps and Lambruschini-- filling of lateral canals is

not always necessary for a successful root canal. y endodontic treatment failure --when they are sufficiently large to harbor significant numbers of bacteria and to provide these bacteria with frank access to the periradicular tissues

y Siqueira et al-antibacterial effects of filling materials

are usually weak and only transient, reaching a peak of effectiveness before setting y predictable antibacterial seal provided by the material injected into the small and usually tortuous ramification is highly unlikely

(A)Maxillary lateral incisor with necrotic pulp - a large radiolucency involving the apex and the mesial aspect of the root. Patient presented -spontaneous pain-tender to percussion. (B)After instrumentation and 1-week calcium hydroxide medication, obturated with laterally compacted cold gutta-percha Note that no lateral canal/ramifications were injected with filling material. (C) Three-year follow-up -- completely healed.

(D) maxillary central incisor --necrotic pulp --medicated with an iodoformic paste.--medicament pushed through the sinus tract seen on the buccal mucosa. (E) The material penetrated into a lateral lesion through a large lateral canal and followed the course of the sinus tract. Because of its high radiopacity, it permitted to obtain sort of a fistulography . obturated after 40 days, when the sinus tract appeared clinically healed, with chloroform modified lateral compaction technique and sealer. Postoperative radiograph revealed that the filling material penetrated into the large lateral canal (not shown). (F) Eleven-year follow-up --healed completely, lamina dura following the entire root outline.

Considerations Based on Clinical Observations

y with few exceptions, are not visible in the preoperative

radiographs y suspected only when there is a localized thickening of the periodontal ligament on the lateral surface of the root or when a frank lateral periodontitis lesion is present OR After root canal obturation y more frequently indicated in necrotic cases than in vital pulps; this supposition is based on both clinical impression and the alleged degree of resistance offered by the type of tissue present in the ramification

why lateral periodontitis lesions associated with these ramifications are not so frequent .. y A morphologic study of 100 permanent molars revealed that 79% had lateral/accessory foramina with diameters ranging from 10 200 mm. y The largest diameter was nearly twice to 3 times smaller than the mean diameters of main apical foramen y apical periodontitis is observed far more than lateral periodontitis.
Dammaschke T, Witt M, Ott K, Schafer E. Scanning electron microscopic investiga-tion of incidence, location, and size of accessory foramina in primary and perma-nent molars. Quintessence Int 2004;35:699-705.

Model of Artificial Lateral Canals JOE

Volume 31, Number 12, December 2005

Why a definite lateral lesion often indicates the presence of a significantly large lateral canal with sufficient infected necrotic tissue to give rise to periodontal inflammation . y Large and patent lateral foramina might, however, allow larger numbers of bacteria and bacterial products to reach and contact a larger area of the lateral periodontal ligament to cause disease y The amount of bacterial irritants in small ramifications, with small volume capacity and small exiting foraminal area, might be insufficient to induce significant disease to be discernible radiographically.

why a lateral lesion might heal without squeezing materials into any lateral canal .. y lateral canals is nourished by the rich periodontal blood supply, offering a significant resistance against necrosis and further bacterial invasion. y tissue in lateral canals becomes necrotic and thoroughly colonized by bacteria only in cases with long-standing pulp necrosis

Ricucci D, Siqueira JF Jr. Apical actinomycosis as a continuum of intraradicular and extraradicular infection: case report and critical review on its involvement with treat-ment failure. J Endod 2008;34:1124-9.

Maxillary first molar in a 35-year-old patient--treated endodontically 19 years before -asymptomatic for the whole period until severe symptoms appeared--oblique fracture, and the tooth was extracted. (A)pathologic tissue on the lateral aspect of the palatal root apex. (B) Histologic serial sections revealed a lateral canal connecting the main canal and the lesion. Bacteria are seen at the interface between the root canal wall and the filling material

(C) Section taken approximately 30 sections from that in (B), displaying part of the lateral canal course, and the connection with the main canal (D) Higher magnification of the lateral canal contents. Inflammatory tissue can be visualized, but bacteria are absent

y Bacteria in the main canal elicit inflammation in the

tissue within the lateral canal y Inflammation might extend to the periodontal ligament,being sustained by bacterial products (not necessarily bacterial cells)-- diffuse through the connective tissue and conceivably evoke inflammation at a certain distance from the place where the bacterial cells are located y stimulate the synthesis and release of proinflammatory cytokines, and might act as chemoattractants to polymorphonuclear leukocytes (PMNs) y lesion simply heals because root canal procedures, removing the bacterial content of the main canal
Siqueira JF Jr., Rocas IN. Bacterial pathogenesis and mediators in apical periodon-titis. Braz Dent J 2007;18:267-80.

Weine -3 types of lateral lesions that can be radiographically observed. represent different stages (1) Lateral lesion with no apical lesion: as the infection progresses apically, it might reach a sufficiently large lateral canal to allow a substantial amount of bacteria and bacterial products to reach the lateral periodontium to cause inflammation. In these cases, it is possible that the pulp tissue apical to the ramification is still vital, and the development of an apical lesion is just a matter of time, or it is already established but still cannot be visible on radiographs. (2) Separate lateral and apical lesions: if the pathologic process advances without professional intervention, an apical periodontitis lesion can also be visible radiographically. This means that sufficient numbers of bacteria and their products are concomitantly egressing from the apical and lateral foramina to cause disease (3) Coalescence of lateral and apical lesions: in some cases, the second condition can progress to this third one, also regarded as a wraparound lesion

(A)Maxillary first premolar in 16-year-old girl. treated endodontically and restored with a screw-post and composite. separate radiolucencies, one apical and one lateral, are present--asymptomatic. (B) Nonsurgical retreatment. Canals were obturated after 2 weeks of calcium hydroxide medication. Note that no lateral canals appeared injected with obturation materials. Tooth was restored with a cast post and core and a ceramo-metallic crown.

(C) Eight-month follow-up. Considerable bone formation (D) 2 years and 3 months after treatment with the restoration missing. complete healing of the 2 radiolucencies.

Histopathologic and Histobacteriologic Observations

ACUTE APICAL PERIODONTITIS ( Synonyms: Periapical osteitis, Apical granuloma /cysts, Periapical lesions) Is a painful inflammation of periodontium as a result of trauma, irritation or infection through root canal regardless of pulp is vital or non-vital.
HISTOPATHOLOGIC Classification:

1) Acute apical periodontitis ( PMNL) : Primary & secondary 2) Chronic apical periodontitis ( Lymphocytes, macrophages, plasma cells} 3) Cystic lesions - True cyst, Pocket cyst

FISH s ZONES OF INFECTION

Zone of stimulation Zone of irritation (granulomatous
zone - This zone has histiocytes as the

characterized by fibroblasts and osteoblasts

Zone of contamination Round cell infiltration is observed in this zone Polymorphonuclear zone. leukocytes and macrophages are also seen. Zone of necrosis - The infection is present in the center of inflammation. The dominant cells are poly morphonuclear neutrophils, other cells present in the pus fluid are dead cells and destructive components released from phagocytes.

predominant cell in addition to osteoclasts

Endodontic micro-organisms
Obligate anaerobes Gram- positive cocci Peptostreptococcus Streptococcus Gram- negative cocci Veillonella Facultative anaerobes Gram- positive cocci Streptococcus Enterococcus Gram- negative cocci Neisseria

rods Actinomyces Eubacterium Proprionibacterium Lactobacillus Arachnia

rods Porphyromonas Prevotella Fusobacterium Selenomonas Wolinella

rods Actinomyces

rods Capnocytophaga Eikenella Campylobacter

Sundquist 1994, Le Goff et al. 1997

BACTERIA Fusobacterium nucleatum Streptococcus sp. Bacteroides sp.* Prevotella intermedia Peptostreptococcus micros Eubacterium alactolyticum Peptostreptococcus anaerobius Lactobacillus sp. Eubacterim lentum Fusobacterium sp. Campylobacter sp. Peptostreptococcus sp. Actinomyces sp. Eubacterium timidum Capnocytophaga ochracea Eubacterium brachy Selenomonas sputigena Veillonella parvula Porphyromonas endodontalis Prevotella buccae Prevotella oralis Proprionibacterium propionicum Prevotella denticola Prevotella loescheii Eubacterium nodatum

PERCENTAGE OF INCIDENCE 48 40 35 34 34 34 31 32 31 29 25 15 15 11 11 9 9 9 9 9 8 8 6 6 6

BACTERIA FROM THE ROOT CANALS OF TEETH WITH APICAL RAREFACTION (Adapted form Sundqvist: Taxonomy, ecology and pathogenicity of the root canal, Oral Surg 78:522, 1994)

Bacterial Eclology Of The Infected Root Canals

is governed by the following factors:
1. 2. 3. 4. 5. 6. 7.

Dynamics of the microorganisms Bacteria and the periapical lesion Bacterial interrelationships Coaggregation of bacteria Microbial products & their effects Virulence factors of various oral microbes Enzymes produced by various oral microbes

Nutritional interactions between some common root canal pathogens

Microbial products & their effects

Microbe A.Actinomycetem comitans Gram negative bacteria Product Leukotoxins Effect Inhibition of neutrophils,macrophages & monocytes Activates complement alternate pathway, initiates bone resorption. Activates bone resorption Activates polyclonal Bcells Degradation of collagen & connective tissues Toxic & inhibitory effect on host cells

Endotoxins

Gram positive bacteria Lactobacilli,Neisseria Spirochetes Anaerobic bacteria

Lipoteichoic acid Dexitrans Hydrolytic enzymes Butyric,Propionic acids, Ammonia

STRATEGIES FOR EXTRA CELLULAR SURVIVAL

1. Evading lysis by complement, 2. Evading the professional leukocytes, 3. Evading a specific immune response and 4. Overcoming the nutrient limitations in the tissue. EVADING A PHAGOCYTIC ATTACK can be accomplished by Per-turbing the inflammatory response, 2. Preventing opsonization, 3. Preventing phagocytosis or 4. Killing the phagocyte.
1.

EVADING A PHAGOCYTIC ATTACK can be accomplished by Per-turbing the inflammatory response, 2. Preventing opsonization, 3. Preventing phagocytosis or 4. Killing the phagocyte.
1.

APICAL PERIODONTITIS: ( A DYNAMIC ENCOUNTER b/w Root canal infection & Host response)

Considerations Based on Histopathologic Observations Teeth with Different Preoperative Conditions

(A) Maxillary second premolar with caries penetrating to the pulp. (B) Longitudinal serial sections show a lateral canal at the middle portion of the root (C) Vital uninflamed pulp tissue in the main canal & lateral canal

Generation of host immune responses to microorganisms within the pulp. Silva TA et al. Chemokines in oral inflammatory diseases: apical periodontitis and periodontal disease. Journal of Dental Research (2007); 86: 306 319.

y After pulp exposure to caries, pulp tissue compartments are sequentially subjected to bacterial aggression and become inflamed, necrotic, and eventually infected y compartments are sequentially subjected to bacterial aggression and the time elapsed between pulp exposure and infection of the entire canal is usually a slow process that very often occurs by tissue increments The difference in pressure between inflamed and uninflamed areas can be a result of several edema-preventing mechanisms. y the increase in tissue pressure, in turn, force fluid back into lymphatics and capillaries in the nearby uninflamed tissue, consequently lowering the tissue pressure y Resilience of the ground substance of the pulp tissue might also help prevent spread of the pressure throughout the pulp
Van Hassel HJ. Physiology of the human dental pulp. Oral Surg Oral Med Oral Pathol 1971;32:126-34.

SEQUALAE OF PULPAL INFLAMMATION

Pulpitis Acute chronic Apical perodontitis
acute chronic

Periapical Abscess
acute chronic

Periapical Granuloma Periapical cyst

Osteomyelitis
acute chronic focal diffuse

Periostitis
Cellulitis Abscess

Sixty-year-old woman presenting with an abscess in the mandibular left quadrant. Clinically the mandibular second molar showed a buccal amalgam restoration and a large distal carious lesion. (A)the carious lesion appeared proximal to the pulp chamber, which shows extensive calcification. A small radiolucency is present on the mesial root apex, and bone loss is visible on the mesial aspect of the distal root.

(B) the pulp stone occupying large part of the pulp chamber and a large lateral canal ending on the mesial aspect of the distal root at the transition between the apical and the middle third. (C) Area where the lateral canal joins the main canal. Inflamed connective tissue is present from this point to an apical direction. Note resorptive defects in dentin. Empty spaces in the pulp tissue are shrinkage artifacts

(A, B) Distobuccal root of a maxillary molar extracted with an apical periodontitis lesion attached. Section passing through a lateral canal (arrows) Pulp necrosis reached the level of the entrance of lateral canals and apical ramifications, the tissue therein was partially or completely necrotic

(C) Lateral canal displays necrotic tissue at this level (D) Transition from necrotic to vital tissue (E) Vital tissue free from inflammatory cells

(F, G) Section taken approximately 60 sections distant from that shown in (A, B). Second ramification is present on the opposite root canal wall (arrow), with the lumen completely filled by a bacterial biofilm

clinical implications
In the first condition, y necrotic tissue and bacterial colonization are located only at the entrance of the ramification; irrigating solutions might have a chance to remove the disintegrated tissue. In the second condition, y elimination of the bacterial biofilm in the ramification is virtually impossible with the substances and techniques currently available

(A)Section passing through the main canal of a maxillary incisor with necrotic pulp. Lateral canal is present (B) Detail of the main canal with the lateral canal entrance. The lumen of both is filled with a dense bacterial biofilm Insets show higher power view of the bacterial biofilm adhered to the walls of both main and lateral canals

observations of Langeland
tissue contained in a lateral canal and in apical ramifications reflects the condition of the pulp in the main canal. y healthy pulp tissue healthy tissue is found throughout the lateral canal y adjacent to an area of pulp inflammation also inflamed y necrosis in the main canal necrotic tissue --a transition zone of necrosis/PMNs and then inflamed tissue connected to a lateral inflammatory lesion y necrotic tissue and bacteria occupy all the extent up to the periodontal ligament, which is usually inflamed and associated with bone resorption
Langeland K. Tissue response to dental caries. Endod Dent Traumatol 1987;3: 149-71.

(A)Root apex of a maxillary second premolar extracted with an apical periodontitis lesion. (B)Section passing through the main canal. Note the apical root canal clogged with a bacterial biofilm (C) Section taken approximately 80 sections distant from that shown in (A), displaying a lateral canal that connects the main canal and the lesion

(D) bacterial content of the lateral canal (E) Section taken 30 sections after that shown in (D), passing through the foramen of the lateral canal, also clogged with a dense bacterial biofilm. Empty spaces are shrinkage artifacts

In cases with periodontal disease, when the subgingival biofilm y reached a lateral canal, the corresponding microcirculation was severed, but inflammation of the adjacent pulp tissue was minimal. y reached the main apical foramen, however, the whole pulp became necrotic.

Mandibular second molar with necrotic pulp in a 45-year-old woman. Patient presented complaining of pain at chewing. Tooth did not respond to sensitivity tests and was tender to percussion. Radiograph showed small apical radiolucencies on both roots. (A) lateral canal in the distal root ending in the interradicular area where bone loss is visible

(B) Detail of the interradicular area (C) Magnification from (B). Cavities occupied by necrotic debris in the center. Vital inflamed tissue on the mesial aspect of the distal root Pulp necrosis might simulate a marginal periodontitis lesion or give rise to a typical secondary periodontal involvement

(A)Maxillary second molar in a 38-year-old woman causing a periodontal abscess. (B, C) After extraction, calculus is seen covering the entire distal root up to the apex. (D) Histologic sections showed a wide lateral canal occupied by a biofilm in the mesial root at the furcation area

(E) Detail of lateral canal (F) Higher magnification of exit of lateral canal in the furcation area. Walls of the ramification are covered by a dense bacterial biofilm (G) Section taken at a certain distance from that in (D). Ramifications are present in the distal root

(H) Higher magnification of lateral canal indicated by arrow in (G), with its lumen filled with bacteria (I) Section passing through the mesial root apex. Contrary to what was observed in the distal root where the entire pulp was necrotic, there appears to be some vital pulp in the apical segment of the mesial root (J) Magnification of area indicated by arrow in (I). Transition from necrotic to vital tissue Mesial canal, where the main circulation had not been significantly affected by the periodontal pocket biofilm.

Teeth Subjected to Endodontic Treatment Procedures

y Chemomechanical preparation --partially removed

necrotic tissue from the entrance of ramifications, y In cases with long-standing pulp necrosis and complex internal anatomy--necrotic tissue and bacteria in ramifications remained untouched. y vital cases-- forcing obturation material into this vital tissue might give rise to physical damage and chemical toxicity that result in unnecessary inflammation

KRONFELD'S MOUNTAIN PASS CONCEPT

The aircraft Root apex considered as mountain pass above is the irrigants used in endodontic therapy The root canal infiltrated with microorganisms The periapex infiltrated with defense mechanisms of body

The battle is won with good endodontic therapy, Host defense mechanisms and good biomechanical Preparation. However, the lateral canal i.e. in the mountain pass A microorganism still remains hiding which has to Be destroyed either by host cells or thorough debridement.

Graph showing the mean number of lateral canals successfully penetrated by the irrigant before and after sonic activation. *Traditional needle irrigation alone. Effect of EDTA, Sonic, and Ultrasonic Activation on the Penetration of Sodium Hypochlorite into Simulated Lateral Canals: An In Vitro Study .Cesar de Gregorio, J Endod 2009;35:891 895

Charles H. StuartEnterococcus faecalis: Its Role in Root Canal Treatment Failure and Current Concepts in Retreatment.J Endod 2006;32:93 98

FLOW
AUTHOR Tagger et al (2003) STUDY studied the interaction between sealers (i.e. AH 26, Roth s sealer, Apexit) and gutta-percha cones CONCLUSION AH 26 silver-free had a notable softening effect on most guttapercha resulting in increased flow. Roth s sealer showed least flow. AH Plus had the greatest stability in solution. But, AH Plus also had the greatest film thickness. Flow rates were similar for all sealers.

McMichen et al (2003)

did a comparative study of selected physical properties of four root canal sealers. Roth s 801,Tubliseal EWT,AH Plus, Apexit.

Lacey and coworkers (2005)

Tested the rheologic properties of Tubli-Seal had a thinner film Apexit, Tubli-Seal, Grossman's thickness and lower viscosity and sealer, and Ketac-Endo in a capillary better flow than the other sealers. system

SOLUBILITY
AUTHOR Schafer and Zandbiglari ( 2003) STUDY Studied the solubility of root canal sealers in water. The sealers examined were AH 26, AH Plus, RoekoSeal, Apexit, Sealapex, Ketac-Endo, and Diaket. CONCLUSION Most sealers were of low solubility, although Sealapex and Ketac-Endo showed a marked weight loss. Even after 28 days of storage in water, AH 26, AH Plus, RoekoSeal, and Diaket showed less than 3% weight loss.

Genco et al (2008)

In this study solubility properties of resin based sealers (Epiphany, GuttaFlow, Roekoseal, AH26, AHPlus, Diaket, EndoRez root canal sealers) investigated and compared with Kerr Pulp Canal sealer(ZOE based sealer).

Resin based sealers showed less solubility than ZOE based Kerr Pulp sealer.

LEAKAGE
AUTHOR Pommel et al (2003) STUDY efficacy of four types of sealers in obtaining an impervious apical seal. Pulp Canal Sealer, Sealapex, AH 26 and Ketac endo were the sealers evaluated. Evaluated the bond strength of 3 sealers i.e Roth s sealer,AH26,Sealapex to guttapercha. compared the shear bond strength to dentine with AH Plus, Diaket, and Endo Rez CONCLUSION Sealapex displayed higher apical leakage than the other sealers. No statistically significant difference was found between AH 26, Pulp Canal Sealer, and Ketac Endo. showed AH 26 had a significantly stronger bond to gutta-percha than Sealapex and Roth s sealer AH Plus was superior to both.

Tagger et al (2003)

Eldeniz et al (2005) Hasan et al (2005)

Evaluated the apical leakage of three Diaket showed lower apical root canal sealers AH Plus, Diaket, and leakage than the other two Endo Rez using a computerized fluid sealers. filtration meter.

AUTHOR

STUDY

CONCLUSION

Verdes et al (2006) The sealing ability of sealers - studied It was found that Sealapex in a fluid transport model. Canals were allowed more leakage than laterally compacted with gutta-percha Pulp Canal Sealer. with either Pulp Canal sealer and Sealapex sealer. Cobankara et al (2006) The sealers tested were Rocanal a zinc oxide-eugenol powder-liquid system; AH Plus, an epoxy resin-based sealer, Seala-pex a calcium hydroxide-based sealer; and RC Sealer, an adhesive resin sealer. Apical leakage decreased gradually for all sealers from 7 to 21 days. Sealapex demonstrated poor apical sealing than the other sealers, and AH Plus, RC Sealer and Rocanal all showed similar apical leakage at every time period

AUTHOR Belli et al (2007)

STUDY compared MetaSEAL with Epiphany/Real Seal and AH Plus with gutta-percha

CONCLUSION found less leakage with MetaSEAL after 1 week, but no difference among the sealer groups at 4 and 12 week time periods.

Orstavik et al (2009)

Evaluated the ex vivo coronal bacterial leakage of Epiphany, EndoREZ, Guttaflow and Roekoseal compared with Apexit , AH plus .

Epiphany, Guttaflow and Apexit showed better resistance to bacterial leakage than the other sealers.

ANTIBACTERIAL ACTIVITY
AUTHOR STUDY CONCLUSION found that zinc oxide-eugenol sealers inhibited all the bacteria tested in their study. Sealapex had low antibacterial activity. Overall the sealers containing eugenol and formaldehyde proved to be most effective against the micro- organisms at all the time intervals studied.

Siqueira and Evaluated the antibacterial Gonsalves efficacy of ZnO and Sealapex (1996) using the agar diffusion test. Kaplan et al(1999) Evaluated the antimicrobial activity of different root canal sealers Apexit,AH26,AH plus, Procosol and Ketac Endo.

Leonardo et al (2000)

antimicrobial activity of four All sealers and pastes presented in vitro root canal sealers (AH plus, antimicrobial activity for all bacter-ial strains Sealapex, Ketac-Endo, and Fill after a 24-hour incubation period at 37C. Canal), two calcium hydroxide pastes (Calen and Calasept), and a zinc oxide paste against bacterial strains.

AUTHOR Kayaoglu et al (2005)

STUDY short-term antibacterial activity of root canal sealers toward E. faecalis suspensions exposed to freshly mixed sealers (direct contact test for 30mins) (MCS [Medidenta International, Inc.], AH Plus, Grossman's, Sealapex, Apexit). antibacterial activity of Fill Canal (zinc oxide based sealer), Sealapex, Apexit. (agar diffusion method) antibacterial activity study of four root canal sealers: AH Plus, Endomethasone and Pulp Canal Sealer. The direct contact test was performed.

CONCLUSION MCS, AH Plus, and Grossman s sealer were effective in reducing the number of cultiva-ble cells of E. faecalis. Calcium hydroxide based sealers, Sealapex and Apexit, were less effective in this short- term experiment.

Sipert et al (2005) Pizzo et al (2006)

Fill Canal demonstrated large zones of inhibition against all bacteria tested. All of the freshly mixed sealers showed complete inhibition of bacterial growth. Similar results were obtained after 24 hours.

Root Canal-Treated Teeth

y Ramification contents and adjacent periodontal

tissues after obturation is left relatively undisturbed by chemomechanical procedures. y Therefore, 4 possible situations arise vital or necrotic tissue

into which the filling material was forced or not

Classic spectrum of filling techniques, emphasizing the desirability of minimum sealer volume,from (A) paste only (least desirable), through (B) single cones with paste, and (C) cold lateral condensation, to (D) thermoplastic compaction.

Methods of filling root canals: principles and practices JOHN WHITWORTH Endodontic Topics 2005, 12, 2 24

Mandibular premolar with previously vital pulp. (A)Patient presented after 5 years with loss of coronal restoration and an oblique fracture. Radiograph showed normal periradicular conditions. Note that no lateral canals appear in the postoperative radiograph. (B)Clearing of tooth -- a lateral canal with some obturation material at its entrance. (C) Section passing approximately at center of the canal. A lateral canal is visible

(D) Higher magnification of lateral canal shows loss of tissue for some distance and then a material/ tissue contact area (E) Higher magnification shows vital tissue relatively uninflamed; some hyperemic vessels. Note the limited zone of necrosis at the surface

Part of the tissue proximal to the main canal was damaged by the cumulative effect of the treatment procedures (instrumentation, irrigation,obturation), but the bulk of the tissue in the ramification remainedundisturbed and uninflamed in the absence of bacteria. This is because tissue vitality and relative normality are maintained by the periodontal ligament blood circulation.

(A)Mandibular premolar with necrotic pulp. Postoperative radiograph showed a lateral canal revealed by filling material. (B) After 11 years, the injected lateral canal is no longer visible, and periradicular conditions are normal. After clearing, the injected lateral canal can be seen (inset). (C) the lateral canal is not actually filled. Tissue is present intermixed with the obturation material

(D) upper arrow in (C). Accumulation of inflammatory cells (E)lower arrow in (C). Mononuclear inflammatory cells in a tissue engulfed by obturation material

In some cases of failure after treatment, retreatment, or surgery

y were found to contain bacteria along their entire extent. Failure of the endodontic treatment, y regardless of the presence or not of filling material injected therein. y Located in these areas, bacteria are likely to escape the effects of instruments (because of physical limitations) y Irrigants (because of inactivating chemical reactions and time constraints) y intracanal medication with calcium hydroxide --failure to eliminate bacteria in ramifications--low solubility and inactivation by dentin, tissue fluids, and organic matter, all of which can hamper the pH-dependent antimicrobial effects of calcium hydroxide
Ricucci D, Siqueira JF Jr. Apical actinomycosis as a continuum of intraradicular and extraradicular infection: case report and critical review on its involvement with treat-ment failure. J Endod 2008;34:1124-9.

(A)Maxillary incisor of a 56-year-old man extracted 16 years after endodontic treatment. Root filling had been exposed for long time to the oral environment. A lateral lesion remained attached to the root. (B) After clearing, a lateral canal, apparently empty, can be observed centering the lesion. (C) Section passing through main canal and part of lateral canal

((D) Detail of lateral canal. An amorphous structure is layering the lateral canal walls, faced with an inflammatory reaction (E) At higher magnification, host cells are recognized as PMNs, but no bacterial cells

Concluding Remarks
(1) tissue within ramifications remain relatively unaffected by instruments and irrigants after chemomechanical preparation, regardless of the preoperative pulp conditions; (2) in cases with vital pulp, forcing obturation materials into lateral canals caused unnecessary damage to the tissue, with consequent inflammation; (3) Material that radiographically appears in the lateral canals and apical ramifications was forced into these areas, but this by no means indicates that the ramification is sealed or disinfected; and (4) because bacteria located in large ramifications might reach sufficient numbers to cause or maintain disease, strategies other than finding a technique that better squeezes sealer or guttapercha within ramifications should be pursued to effectively disinfect these regions and optimize the treatment outcome.

References
1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Walton RE, Vertucci FJ. Internal anatomy. In: Torabinejad M, Walton RE, eds. Endodontics: principles and practice. 4th ed. St Louis: Saunders/Elsevier; 2009: 21629. Tronstad L. Clinical endodontics. 3rd ed. Stuttgart: Thieme; 2009. De Deus QD. Frequency, location, and direction of the lateral, secondary, and acces-sory canals. J Endod 1975;1:361-6. Vertucci FJ. Root canal anatomy of the human permanent teeth. Oral Surg Oral Med Oral Pathol 1984;58:589-99. Schilder H. Filling root canals in three dimensions. Dent Clin North Am 1967;11: 72344. Schilder H. Canal debridement and disinfection. In: Cohen S, Burns RC, eds. Path-ways of the pulp. 2nd ed. St Louis: CV Mosby; 1976:111-33. Schilder H. Cleaning and shaping the root canal. Dent Clin North Am 1974;18: 269-96. Buchanan LS. Filling root canal systems with centered condensation: concepts, instruments, and techniques. Dent Today 2004;23. 102, 4, 6 passim. Rud J, Andreasen JO. A study of failures after endodontic surgery by radiographic, histologic and stereomicroscopic methods. Int J Oral Surg 1972;1:311-28. Weine FS. The enigma of the lateral canal. Dent Clin North Am 1984;28:833-52.

11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Reader CM, Himel VT, Germain LP, Hoen MM. Effect of three obturation tech-niques on the filling of lateral canals and the main canal. J Endod 1993;19: 404-8. Wolcott J, Himel VT, Powell W, Penney J. Effect of two obturation techniques on the filling of lateral canals and the main canal. J Endod 1997;23:632-5. DuLac KA, Nielsen CJ, Tomazic TJ, Ferrillo PJ Jr., Hatton JF. Comparison of the obtu-ration of lateral canals by six techniques. J Endod 1999;25:376-80. Venturi M. An ex vivo evaluation of a gutta-percha filling technique when used with two endodontic sealers: analysis of the filling of main and lateral canals. J Endod 2008;34:1105-10. Venturi M, Di Lenarda R, Prati C, Breschi L. An in vitro model to investigate filling of lateral canals. J Endod 2005;31:877-81. Venturi M, Prati C, Capelli G, Falconi M, Breschi L. A preliminary analysis of the morphology of lateral canals after root canal filling using a tooth-clearing technique. Int Endod J 2003;36:54-63. Brothman P. A comparative study of the vertical and the lateral condensation of guttapercha. J Endod 1980;7:27-30. Goldberg F, Artaza LP, De S. Influence of calcium hydroxide dressing on the obtu-ration of simulated lateral canals. J Endod 2002;28:99-101. Camps J, Lambruschini GM. Obturation of lateral canals: necessary therapy or radio-logic satisfaction? RevFr Endod 1991;10:19-26. Barthel CR, Zimmer S, Trope M. Relationship of radiologic and histologic signs of inflammation in human root-filled teeth. J Endod 2004;30:75-9.

21. 22. 23. 24. 25. 26. 27. 28. 29. 30.

Seltzer S, Bender IB, Smith J, Freedman I, Nazimov H. Endodontic failures: an anal-ysis based on clinical, roentgenographs, and histologic findings II. Oral Surg Oral Med Oral Pathol 1967;23:517-30. Seltzer S, Bender IB, Smith J, Freedman I, Nazimov H. Endodontic failures: an anal-ysis based on clinical, roentgenographs, and histologic findings I. Oral Surg Oral Med Oral Pathol 1967;23:500-16. Ricucci D, Siqueira JF Jr., Bate AL, Pitt Ford TR. Histologic investigation of root canaltreated teeth with apical periodontitis: a retrospective study from twenty-four patients. J Endod 2009;35:493-502. Ricucci D, Siqueira JF Jr. Apical actinomycosis as a continuum of intraradicular and extraradicular infection: case report and critical review on its involvement with treat-ment failure. J Endod 2008;34:1124-9. Ricucci D, Siqueira JF Jr., Anatomic and microbiologic challenges to achieving success with endodontic treatment: a case report. J Endod 2008;34:1249-54. Nicholls E. Lateral radicular disease due to lateral branching of the root canal. Oral Surg Oral Med Oral Pathol 1963;16:839-5. Cobankara FK, Altinoz HC, Ergani O, Kav K, Belli S. In vitro antibacterial activities of root-canal sealers by using two different methods. J Endod 2004;30:57-60. Kayaoglu G, Erten H, Alacam T, 0rstavik D. Short-term antibacterial activity of root canal sealers towards Enterococcus faecalis. Int Endod J 2005;38:483-8. Siqueira JF Jr., Goncalves RB. Antibacterial activities of root canal sealers against selected anaerobic bacteria. J Endod 1996;22:89-90. Siqueira JF Jr., Favieri A, Gahyva SM, Moraes SR, Lima KC, Lopes HP. Antimicrobial activity and flow rate of newer and established root canal sealers. J Endod 2000;26: 274-7.

31. 32. 33. 34. 35. 36. 37. 38. 39. 40.

Orstavik D. Antibacterial properties of root canal sealers, cements and pastes. Int Endod J 1981;14:125-33. Shalhav M, Fuss Z, Weiss EI. In vitro antibacterial activity of a glass ionomer endodontic sealer. J Endod 1997;23:616-9. SpangbergLS, Barbosa SV, Lavigne GD. AH 26 releases formaldehyde. J Endod 1993; 19:596-8. Weine FS, Buchanan LS. Controversies in clinical endodontics: part 1 the signifi-cance and filling of lateral canals. Compend Contin Educ Dent 1996;17:1028-32, 1035-6, 1038. Dammaschke T, Witt M, Ott K, Schafer E. Scanning electron microscopic investiga-tion of incidence, location, and size of accessory foramina in primary and perma-nent molars. Quintessence Int 2004;35:699-705. Kuttler Y. Microscopic investigation of root apexes. J Am Dent Assoc 1955;50: 544-52. Ponce EH, Vilar Fernandez JA. The cemento-dentino-canal junction, the apical foramen, and the apical constriction: evaluation by optical microscopy. J Endod 2003;29:214-9. Green D. A stereomicroscopic study of the root apices of 400 maxillary and mandib-ular anterior teeth. Oral Surg Oral Med Oral Pathol 1956;9:1224-32. Siqueira JF Jr., Rocas IN. Bacterial pathogenesis and mediators in apical periodon-titis. Braz Dent J 2007;18:267-80. Weine FS. Endodontic therapy. 4th ed. St Louis: Mosby, 1989.

41. 42. 43. 44. 45. 46. 47. 48. 49. 50.

Ricucci D, Bergenholtz G. Bacterial status in root-filled teeth exposed to the oral environment by loss of restoration and fracture or caries: a histobacteriological study of treated cases. Int Endod J 2003;36:787-802. Ricucci D, Pascon EA, Pitt Ford TR, Langeland K. Epithelium and bacteria in periapical lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101: 239-49. Ricucci D, Martorano M, Bate AL, Pascon EA. Calculus-like deposit on the apical external root surface of teeth with post-treatment apical periodontitis: report of two cases. Int Endod J 2005;38:262-71. Cvek M, Cleaton-Jones PE, Austin JC, Andreasen JO. Pulp reactions to exposure after experimental crown fractures or grinding in adult monkeys. J Endod 1982;8:391-7. Langeland K. Tissue response to dental caries. Endod Dent Traumatol 1987;3: 149-71. Langeland K. Tissue response to dental caries. Endod Dent Traumatol 1987;3: 149-71. Ricucci D. Apical limit of root canal instrumentation and obturation, part 1: litera-ture review. Int Endod J 1998;31:384-93. Kim S. Microcirculation of the dental pulp in health and disease. J Endod 1985;11: 46571. T0nder KJ Kvinnsland I. Micropuncture measurements of interstitial fluid pressure in normal and inflamed dental pulp in cats. J Endod 1983;9:105-9. T0nder KJ Vascular reactions in the dental pulp during inflammation. Acta Odontol Scand 1983;41:247-56. Heyeraas KJ Berggreen E. Interstitial fluid pressure in normal and inflamed pulp. Crit Rev Oral Biol Med 1999;10:328-36.

51. 52. 53. 54. 55. 56. 57.

58. 59. 60.

Van Hassel HJ. Physiology of the human dental pulp. Oral Surg Oral Med Oral Pathol 1971;32:126-34. Yu C, Abbott PV. An overview of the dental pulp: its functions and responses to injury. Aust Dent J 2007;52:S4-16. Langeland K, Rodrigues H, Dowden W. Periodontal disease, bacteria, and pulpal histopathology. Oral Surg Oral Med Oral Pathol 1974;37:257. SiqueiraJF Jr., Araujo MC, GarciaPF, Fraga RC, Dantas CJ. Histological evaluation of the effectiveness of five instrumentation techniques for cleaning the apical third of root canals. J Endod 1997;23:499-502. Langeland K, Liao K, Pascon EA Work-saving devices in endodontics: efficacy of sonic and ultrasonic techniques. J Endod 1985;11:499-510. Walton RE. Histologic evaluation of different methods of enlarging the pulp canal space. J Endod 1976;2:304-11. Nair PN, Henry S, Cano V, Vera J. Microbial status of apical root canal system of human mandibular first molars with primary apical periodontitis after ''one-visit'' endodontic treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005; 99:231-52. SiqueiraJF Jr., Rco^as IN. Clinical implications and microbiology of bacterial persis-tence after treatment procedures. J Endod 2008;34:1291-301. e3. Siqueira JF Jr., Lopes HP. Mechanisms of antimicrobial activity of calcium hydroxide: a critical review. Int Endod J 1999;32:361-9. Haapasalo M, Qian W, Portenier I, Waltimo T. Effects of dentin on the antimicrobial properties of endodontic medicaments. J Endod 2007;33:917-25.

Thank you !!!