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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, 165²203
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.
Ilan Rotstein & James H. S. Simon Periodontology 2000, Vol. 34, 2004, 165²203
y Not only are all these aberrations largely undebrided.Significance y All these aberrations are relatively inaccessible to intracanal instruments. 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.
. (B) In 23%. (A) In 13%. 80% extend from the distal root canal. a lateral canal extends from the coronal third of a major root canal to the furcation region. a single furcation canal extends from the pulp chamber to the intraradicular region.Root canal morphology and its relationship to endodontic procedures FRANK J. VERTUCCI Endodontic Topics 2005. 3 29 Accessory canals occur in three distinct patterns in mandibular first molars. 10. (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 .
except --located in the apical 1 2 mm of the canal. is not usually regarded as collateral blood supply --provides little contribution.y Ramifications can be observed anywhere along the length of the root.5% in the apical third of the root. to pulp function. 11% middle third 15% coronal third y potential pathways through which bacteria and/or their products y contain connective tissue and blood vessels. but they occur more commonly in the apical portion and in posterior teeth y In 73. .
DDS . ENDODONTICS ARNALDO CASTELLUCCI MD.Histologic section of a root showing apical ramifications of the main root canal.
THE FORMATION OF LATERAL CANALS Lateral canals formed after a localized fragmentation of the epithelial root sheath develops. . leaving a small gap. Dentinogenesis does not occur in this specific area. or when blood vessels running from the dental sac through the dental papilla persist. 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 .
DDS .Schematic diagram of the formation of lateral canals at various root levels ENDODONTICS ARNALDO CASTELLUCCI MD.
if the continuity of the root sheath is interrupted before the formation of the dentin. A lateral canal will form at just such a point. supernumerary blood vessel . a defect in the dentinal wall will occur. 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. where odontoblasts do not differentiate and thus dentin does not form. 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. This small island of lack of cells of Hertwig s root sheath. As a consequence.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.
As the tooth develops. as a result of which the pulp remains in contact with the dental sac or periodontal tissue. which gives origin to the vessels that branch around the foramen and enter (or exit) the apical foramen. 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. 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 Scott and Symons concur that these aberrant openings are due to defects in the y y y y formation of Hertwig s root sheath. the plexus in the coronal zone degenerates. while the one which surrounds the root forms the periodontal plexus. this plexus feeds the enamel organ and sends branches into the developing papilla. . This plexus completely surrounds the enamel organ and the dental papilla. Once the enamel has been formed. They also believe that these openings in Hertwig s root sheath are probably due to the persistence of anomalous blood vessels reaching the pulp.
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. there is a high pro-bability that they will remain entrapped in Hertwig s root sheath and then be surrounded by dentin. 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. 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.
If. while they are found in completely developed teeth. thus. an apical delta or lateral canals would occur. instead. .y In confirmation. only a single canal would form. Grove hypothesized that if all the vessels reached the pulp from a position directly opposite the foramen. multiple openings would develop. the vessels entered the pulp from different angles. Grove has noted that no lateral canal can be found in the apical one third of immature teeth.
also including all lateral canals and apical ramifications.lateral canals harboring inflamed and/or infected material might cause pain during endodontic treatment . 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 .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. y Weine FS-.
Artaza LP. Influence of calcium hydroxide dressing on the obtu-ration of simulated lateral canals.filling of lateral canals is not always necessary for a successful root canal.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.28:99-101. De S. y Camps and Lambruschini-. J Endod 2002. 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 .
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 .y Siqueira et al-antibacterial effects of filling materials are usually weak and only transient.
obturated with laterally compacted cold gutta-percha Note that no lateral canal/ramifications were injected with filling material. Patient presented -spontaneous pain-tender to percussion.completely healed.a large radiolucency involving the apex and the mesial aspect of the root.(A)Maxillary lateral incisor with necrotic pulp . (C) Three-year follow-up -. (B)After instrumentation and 1-week calcium hydroxide medication. .
with chloroform modified lateral compaction technique and sealer. Because of its high radiopacity. . obturated after 40 days. (E) The material penetrated into a lateral lesion through a large lateral canal and followed the course of the sinus tract.--medicament pushed through the sinus tract seen on the buccal mucosa.(D) maxillary central incisor --necrotic pulp --medicated with an iodoformic paste. when the sinus tract appeared clinically healed. it permitted to obtain sort of a fistulography . 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.
this supposition is based on both clinical impression and the alleged degree of resistance offered by the type of tissue present in the ramification .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.
Schafer E. location. Dammaschke T. and size of accessory foramina in primary and perma-nent molars.35:699-705. . 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.. Scanning electron microscopic investiga-tion of incidence. Witt M.why lateral periodontitis lesions associated with these ramifications are not so frequent . Ott K. Quintessence Int 2004.
Model of Artificial Lateral Canals JOE Volume 31. December 2005 . Number 12.
however. . might be insufficient to induce significant disease to be discernible radiographically.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 . with small volume capacity and small exiting foraminal area. y Large and patent lateral foramina might. 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.
y lateral canals is nourished by the rich periodontal blood supply. .34:1124-9..why a lateral lesion might heal without squeezing materials into any lateral canal . offering a significant resistance against necrosis and further bacterial invasion. J Endod 2008. Siqueira JF Jr. y tissue in lateral canals becomes necrotic and thoroughly colonized by bacteria only in cases with long-standing pulp necrosis Ricucci D. Apical actinomycosis as a continuum of intraradicular and extraradicular infection: case report and critical review on its involvement with treat-ment failure.
(A)pathologic tissue on the lateral aspect of the palatal root apex. and the tooth was extracted. (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 .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 connection with the main canal (D) Higher magnification of the lateral canal contents. Inflammatory tissue can be visualized.(C) Section taken approximately 30 sections from that in (B). displaying part of the lateral canal course. but bacteria are absent .
and might act as chemoattractants to polymorphonuclear leukocytes (PMNs) y lesion simply heals because root canal procedures.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.18:267-80. Bacterial pathogenesis and mediators in apical periodon-titis. removing the bacterial content of the main canal Siqueira JF Jr.y Bacteria in the main canal elicit inflammation in the tissue within the lateral canal y Inflammation might extend to the periodontal ligament. Rocas IN. Braz Dent J 2007. ..being sustained by bacterial products (not necessarily bacterial cells)-.
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. or it is already established but still cannot be visible on radiographs. In these cases. 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. also regarded as a wraparound lesion . (2) Separate lateral and apical lesions: if the pathologic process advances without professional intervention. and the development of an apical lesion is just a matter of time. it is possible that the pulp tissue apical to the ramification is still vital. represent different stages (1) Lateral lesion with no apical lesion: as the infection progresses apically.Weine -3 types of lateral lesions that can be radiographically observed. the second condition can progress to this third one. an apical periodontitis lesion can also be visible radiographically.
Canals were obturated after 2 weeks of calcium hydroxide medication.(A)Maxillary first premolar in 16-year-old girl. treated endodontically and restored with a screw-post and composite. Tooth was restored with a cast post and core and a ceramo-metallic crown. Note that no lateral canals appeared injected with obturation materials. . separate radiolucencies. (B) Nonsurgical retreatment. are present--asymptomatic. one apical and one lateral.
(C) Eight-month follow-up. complete healing of the 2 radiolucencies. Considerable bone formation (D) 2 years and 3 months after treatment with the restoration missing. .
Histopathologic and Histobacteriologic Observations .
irritation or infection through root canal regardless of pulp is vital or non-vital.ACUTE APICAL PERIODONTITIS ( Synonyms: Periapical osteitis. HISTOPATHOLOGIC Classification: 1) Acute apical periodontitis ( PMNL) : Primary & secondary 2) Chronic apical periodontitis ( Lymphocytes.True cyst. plasma cells} 3) Cystic lesions . Pocket cyst . Periapical lesions) Is a painful inflammation of periodontium as a result of trauma. macrophages. Apical granuloma /cysts.
other cells present in the pus fluid are dead cells and destructive components released from phagocytes.FISH s ZONES OF INFECTION Zone of stimulation Zone of irritation (granulomatous zone . predominant cell in addition to osteoclasts . leukocytes and macrophages are also seen. The dominant cells are poly morphonuclear neutrophils.The infection is present in the center of inflammation. Zone of necrosis .This zone has histiocytes as the characterized by fibroblasts and osteoblasts Zone of contamination Round cell infiltration is observed in this zone Polymorphonuclear zone.
negative cocci Veillonella Facultative anaerobes Gram.negative cocci Neisseria rods Actinomyces Eubacterium Proprionibacterium Lactobacillus Arachnia rods Porphyromonas Prevotella Fusobacterium Selenomonas Wolinella rods Actinomyces rods Capnocytophaga Eikenella Campylobacter Sundquist 1994. 1997 .positive cocci Streptococcus Enterococcus Gram.Endodontic micro-organisms Obligate anaerobes Gram.positive cocci Peptostreptococcus Streptococcus Gram. Le Goff et al.
Oral Surg 78:522. ecology and pathogenicity of the root canal. Actinomyces sp. Bacteroides 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. Eubacterim lentum Fusobacterium sp. 1994) .BACTERIA Fusobacterium nucleatum Streptococcus sp. Peptostreptococcus sp.* Prevotella intermedia Peptostreptococcus micros Eubacterium alactolyticum Peptostreptococcus anaerobius Lactobacillus sp. Campylobacter sp.
Bacterial Eclology Of The Infected Root Canals is governed by the following factors: 1. 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 . 4. 2. 5. 6. 3. 7.
Nutritional interactions between some common root canal pathogens .
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.macrophages & monocytes Activates complement alternate pathway.Actinomycetem comitans Gram negative bacteria Product Leukotoxins Effect Inhibition of neutrophils. Ammonia .Microbial products & their effects Microbe A.Propionic acids.
2. . 3. 1. Evading a specific immune response and 4. EVADING A PHAGOCYTIC ATTACK can be accomplished by Per-turbing the inflammatory response. Evading lysis by complement. Preventing phagocytosis or 4. Preventing opsonization. Killing the phagocyte. 3. Overcoming the nutrient limitations in the tissue. Evading the professional leukocytes.STRATEGIES FOR EXTRA CELLULAR SURVIVAL 1. 2.
EVADING A PHAGOCYTIC ATTACK can be accomplished by Per-turbing the inflammatory response. Preventing opsonization. 1. 3. 2. Preventing phagocytosis or 4. Killing the phagocyte. .
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. Journal of Dental Research (2007). Silva TA et al. 86: 306 319. . Chemokines in oral inflammatory diseases: apical periodontitis and periodontal disease.
in turn. Oral Surg Oral Med Oral Pathol 1971.32:126-34. 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. . necrotic. 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.y After pulp exposure to caries. y the increase in tissue pressure. pulp tissue compartments are sequentially subjected to bacterial aggression and become inflamed. Physiology of the human dental pulp. force fluid back into lymphatics and capillaries in the nearby uninflamed tissue.
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. and bone loss is visible on the mesial aspect of the distal root. (A)the carious lesion appeared proximal to the pulp chamber. which shows extensive calcification. Clinically the mandibular second molar showed a buccal amalgam restoration and a large distal carious lesion. A small radiolucency is present on the mesial root apex.
(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. Empty spaces in the pulp tissue are shrinkage artifacts . Inflamed connective tissue is present from this point to an apical direction. Note resorptive defects in dentin. (C) Area where the lateral canal joins the main canal.
Section passing through a lateral canal (arrows) Pulp necrosis reached the level of the entrance of lateral canals and apical ramifications. B) Distobuccal root of a maxillary molar extracted with an apical periodontitis lesion attached.(A. 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 .
with the lumen completely filled by a bacterial biofilm . Second ramification is present on the opposite root canal wall (arrow). B). G) Section taken approximately 60 sections distant from that shown in (A.(F.
y necrotic tissue and bacterial colonization are located only at the entrance of the ramification. y elimination of the bacterial biofilm in the ramification is virtually impossible with the substances and techniques currently available . irrigating solutions might have a chance to remove the disintegrated tissue.clinical implications In the first condition. In the second condition.
Lateral canal is present (B) Detail of the main canal with the lateral canal entrance.(A)Section passing through the main canal of a maxillary incisor with necrotic pulp. 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.3: 149-71. Endod Dent Traumatol 1987. 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.
(B)Section passing through the main canal. displaying a lateral canal that connects the main canal and the lesion . Note the apical root canal clogged with a bacterial biofilm (C) Section taken approximately 80 sections distant from that shown in (A).(A)Root apex of a maxillary second premolar extracted with an apical periodontitis lesion.
also clogged with a dense bacterial biofilm.(D) bacterial content of the lateral canal (E) Section taken 30 sections after that shown in (D). Empty spaces are shrinkage artifacts . passing through the foramen of the lateral canal.
y reached the main apical foramen. but inflammation of the adjacent pulp tissue was minimal. the corresponding microcirculation was severed. . however. when the subgingival biofilm y reached a lateral canal. the whole pulp became necrotic.In cases with periodontal disease.
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. (A) lateral canal in the distal root ending in the interradicular area where bone loss is visible . Radiograph showed small apical radiolucencies on both roots.
(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
Transition from necrotic to vital tissue Mesial canal. . where the main circulation had not been significantly affected by the periodontal pocket biofilm.(H) Higher magnification of lateral canal indicated by arrow in (G). 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). with its lumen filled with bacteria (I) Section passing through the mesial root apex.
y In cases with long-standing pulp necrosis and complex internal anatomy--necrotic tissue and bacteria in ramifications remained untouched.forcing obturation material into this vital tissue might give rise to physical damage and chemical toxicity that result in unnecessary inflammation . y vital cases-.Teeth Subjected to Endodontic Treatment Procedures y Chemomechanical preparation --partially removed necrotic tissue from the entrance of ramifications.
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. .e. in the mountain pass A microorganism still remains hiding which has to Be destroyed either by host cells or thorough debridement. However. Host defense mechanisms and good biomechanical Preparation. the lateral canal i.
and Ultrasonic Activation on the Penetration of Sodium Hypochlorite into Simulated Lateral Canals: An In Vitro Study . *Traditional needle irrigation alone. J Endod 2009.Cesar de Gregorio.Graph showing the mean number of lateral canals successfully penetrated by the irrigant before and after sonic activation. Sonic. Effect of EDTA.35:891 895 .
Charles H.32:93 98 .J Endod 2006. StuartEnterococcus faecalis: Its Role in Root Canal Treatment Failure and Current Concepts in Retreatment.
Flow rates were similar for all sealers. McMichen et al (2003) did a comparative study of selected physical properties of four root canal sealers. Apexit.e. system .FLOW AUTHOR Tagger et al (2003) STUDY studied the interaction between sealers (i. 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. Roth s sealer showed least flow. But.AH Plus. AH 26. Lacey and coworkers (2005) Tested the rheologic properties of Tubli-Seal had a thinner film Apexit.Tubliseal EWT. Roth s 801. AH Plus also had the greatest film thickness. AH Plus had the greatest stability in solution. Grossman's thickness and lower viscosity and sealer. Tubli-Seal. and Ketac-Endo in a capillary better flow than the other sealers.
GuttaFlow. Diaket. Even after 28 days of storage in water. AH26. AH 26. although Sealapex and Ketac-Endo showed a marked weight loss. Roekoseal. RoekoSeal. and Diaket showed less than 3% weight loss. RoekoSeal. Sealapex. Resin based sealers showed less solubility than ZOE based Kerr Pulp sealer. Ketac-Endo. CONCLUSION Most sealers were of low solubility. EndoRez root canal sealers) investigated and compared with Kerr Pulp Canal sealer(ZOE based sealer). Apexit. AHPlus. and Diaket.SOLUBILITY AUTHOR Schafer and Zandbiglari ( 2003) STUDY Studied the solubility of root canal sealers in water. AH Plus. Genco et al (2008) In this study solubility properties of resin based sealers (Epiphany. The sealers examined were AH 26. AH Plus. .
AH 26 and Ketac endo were the sealers evaluated.LEAKAGE AUTHOR Pommel et al (2003) STUDY efficacy of four types of sealers in obtaining an impervious apical seal.Sealapex to guttapercha. Diaket. and Endo Rez CONCLUSION Sealapex displayed higher apical leakage than the other sealers. . and Ketac Endo. compared the shear bond strength to dentine with AH Plus. and leakage than the other two Endo Rez using a computerized fluid sealers. Sealapex. Evaluated the bond strength of 3 sealers i. No statistically significant difference was found between AH 26.AH26. showed AH 26 had a significantly stronger bond to gutta-percha than Sealapex and Roth s sealer AH Plus was superior to both. Pulp Canal Sealer. 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. filtration meter.e Roth s sealer. Pulp Canal Sealer.
and RC Sealer. Canals were allowed more leakage than laterally compacted with gutta-percha Pulp Canal Sealer. an epoxy resin-based sealer. RC Sealer and Rocanal all showed similar apical leakage at every time period . AH Plus. Apical leakage decreased gradually for all sealers from 7 to 21 days. with either Pulp Canal sealer and Sealapex sealer. and AH Plus.studied It was found that Sealapex in a fluid transport model. Seala-pex a calcium hydroxide-based sealer. Cobankara et al (2006) The sealers tested were Rocanal a zinc oxide-eugenol powder-liquid system. an adhesive resin sealer. Sealapex demonstrated poor apical sealing than the other sealers.AUTHOR STUDY CONCLUSION Verdes et al (2006) The sealing ability of sealers .
Epiphany. but no difference among the sealer groups at 4 and 12 week time periods. Guttaflow and Roekoseal compared with Apexit .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. AH plus . Guttaflow and Apexit showed better resistance to bacterial leakage than the other sealers. EndoREZ. Orstavik et al (2009) Evaluated the ex vivo coronal bacterial leakage of Epiphany. .
Kaplan et al(1999) Evaluated the antimicrobial activity of different root canal sealers Apexit. Leonardo et al (2000) antimicrobial activity of four All sealers and pastes presented in vitro root canal sealers (AH plus. Sealapex had low antibacterial activity. Canal). two calcium hydroxide pastes (Calen and Calasept). and a zinc oxide paste against bacterial strains. antimicrobial activity for all bacter-ial strains Sealapex. . Procosol and Ketac Endo. and Fill after a 24-hour incubation period at 37°C. Ketac-Endo.ANTIBACTERIAL ACTIVITY AUTHOR STUDY CONCLUSION found that zinc oxide-eugenol sealers inhibited all the bacteria tested in their study.organisms at all the time intervals studied. Siqueira and Evaluated the antibacterial Gonsalves efficacy of ZnO and Sealapex (1996) using the agar diffusion test.AH plus.AH26. Overall the sealers containing eugenol and formaldehyde proved to be most effective against the micro.
antibacterial activity of Fill Canal (zinc oxide based sealer). and Grossman s sealer were effective in reducing the number of cultiva-ble cells of E. Sealapex. All of the freshly mixed sealers showed complete inhibition of bacterial growth. CONCLUSION MCS. Sealapex and Apexit. Sealapex.]. (agar diffusion method) antibacterial activity study of four root canal sealers: AH Plus. were less effective in this short. faecalis. Similar results were obtained after 24 hours. Apexit). . Calcium hydroxide based sealers. Sipert et al (2005) Pizzo et al (2006) Fill Canal demonstrated large zones of inhibition against all bacteria tested. Endomethasone and Pulp Canal Sealer.term experiment. AH Plus. The direct contact test was performed.AUTHOR Kayaoglu et al (2005) STUDY short-term antibacterial activity of root canal sealers toward E. AH Plus. Grossman's. faecalis suspensions exposed to freshly mixed sealers (direct contact test for 30mins) (MCS [Medidenta International. Inc. Apexit.
y Therefore.Root Canal-Treated Teeth y Ramification contents and adjacent periodontal tissues after obturation is left relatively undisturbed by chemomechanical procedures. 4 possible situations arise vital or necrotic tissue into which the filling material was forced or not .
Classic spectrum of filling techniques. 2 24 .from (A) paste only (least desirable). emphasizing the desirability of minimum sealer volume. to (D) thermoplastic compaction. 12. and (C) cold lateral condensation. Methods of filling root canals: principles and practices JOHN WHITWORTH Endodontic Topics 2005. through (B) single cones with paste.
A lateral canal is visible .a lateral canal with some obturation material at its entrance. (C) Section passing approximately at center of the canal. Radiograph showed normal periradicular conditions.Mandibular premolar with previously vital pulp. (B)Clearing of tooth -. (A)Patient presented after 5 years with loss of coronal restoration and an oblique fracture. Note that no lateral canals appear in the postoperative radiograph.
irrigation. This is because tissue vitality and relative normality are maintained by the periodontal ligament blood circulation.(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. but the bulk of the tissue in the ramification remainedundisturbed and uninflamed in the absence of bacteria. . some hyperemic vessels.obturation). 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.
(A)Mandibular premolar with necrotic pulp. (B) After 11 years. Tissue is present intermixed with the obturation material . the injected lateral canal can be seen (inset). After clearing. the injected lateral canal is no longer visible. Postoperative radiograph showed a lateral canal revealed by filling material. and periradicular conditions are normal. (C) the lateral canal is not actually filled.
(D) upper arrow in (C). Accumulation of inflammatory cells (E)lower arrow in (C). Mononuclear inflammatory cells in a tissue engulfed by obturation material .
34:1124-9. 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. Siqueira JF Jr. J Endod 2008. Failure of the endodontic treatment. tissue fluids. retreatment. or surgery y were found to contain bacteria along their entire extent. y regardless of the presence or not of filling material injected therein. all of which can hamper the pH-dependent antimicrobial effects of calcium hydroxide Ricucci D. and organic matter.In some cases of failure after treatment. . Apical actinomycosis as a continuum of intraradicular and extraradicular infection: case report and critical review on its involvement with treat-ment failure.
Root filling had been exposed for long time to the oral environment. (C) Section passing through main canal and part of lateral canal . (B) After clearing. A lateral lesion remained attached to the root. apparently empty. can be observed centering the lesion. a lateral canal.(A)Maxillary incisor of a 56-year-old man extracted 16 years after endodontic treatment.
((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
(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.
1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
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