ENDODONTIC- PERIODONTAL INTERRELATIONSHIP AND CONTROVERSIES CONTENTS Introduction Pathways of communication between the dental pulp and the

periodontium Developmental Origin Pathological Origin Iatrogenic Origin Classification of ENDO-PERIO lesions Etiological factors Live pathogens :Bacteria, Fungi, Viruses Non living agents: Extrinsic agents Intrinsic agentsContributing factors

Primary Endodontic lesions Primary Periodontal lesion

Combined diseases Primary periodontal lesion with secondary endodontic involvement Primary endodontic lesion with secondary periodontal involvement True combined lesion Clinical diagnostic procedures Effect of pulpal disease and endodontic procedures on the periodontium Effect of Periodontal disease and procedures on pulp Clinical manifestations of endodontic and periodontic lesion Differential diagnosis Controversies Summary and conclusion References

INTRODUCTION Pulpal and Periodontal tissues have close embryonic, anatomic and functional inter relationships.
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 Tissues of dental pulp and periodontium are inter linked from the embryonic stage. The dental papilla and the dental sac are of a common mesodermal origin. In 1964, Simring and Goldeberg first described the relationship between Endo and Perio. The interrelationship between periodontal and endodontic disease has aroused much speculation, confusion and controversy. Pulpal and periodontal problems are responsible for more than 50% of tooth mortality today. Diagnosis is often difficult since these diseases have been studied primarily as separate entities and each primary disease may mimic clinical characteristics of the other disease. Deleterious effect of pulp disease on the periodontium are well documented, the converse effects of periodontal disease on pulp remains unclear. As long as the main canal / Apical foramen is not involved the entire pulp does not succumb. Anatomic considerations

Pathways of communications between pulp and periodontium can be

Physiological
-Developmental

Non physiological
- Pathologic - Iatrogenic Pathways of Developmental Origin: Apical foramen, Accessory canals/lateral canals Congenital absence of cementum exposing DT. Permeability of cementum, Developmental grooves Pathways of Pathological Origin: Empty spaces on root created by Sharpeys fibers Root # following trauma
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 Idiopathic resorption- Internal and external Loss of cementum due to external irritants.
Pathways of Iatrogenic Origin: Exposure of DT following root planning Accidental lateral perforation - endodontic procedures Root fractures - endodontic procedures.

COMMUNICATION LINKS COMMUNICATION LINKS

Apical foramina Major connections between periodontal and pulpal tissues, and direct route of communication. Bacteria 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. Pulpal inflammation or pulp necrosis extends into the periapical tissues causing a local inflammatory response accompanied by bone and root resorption. Endodontics - aim to eliminate intraradicular etiologic factors , leading to healing of the periapical tissues. Lateral and accessory canals Present anywhere along the root. 30-40% apical third of the root. DeDeus (1975) -17% apical third, 9% middle third, and <2% in the coronal third. Prevalence of PDL disease associated with LC is relatives low. Kirkham (1975) studied 1,000 human teeth with extensive PDL disease and found only 2% had LC located in a PDL pocket. Accessory canals in the furcation .The prevalence may vary from 23% to 76% . Seltzer et al. (1963) reported that pulpal inflammation may cause an inflammatory reaction in the interradicular PDL tissues. Dentinal tubules Exposed dentinal tubules in areas of denuded cementum may serve as communication pathways between the pulp and periodontal ligament.
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 Exposure may occur due to developmental defects, disease, or periodontal procedures. In the root, DT extend from the pulp to the DCJ. (1 to 3 m in dia) The diameter of the tubules decreases with age or as a response to a continuous low grade stimulus by the apposition of highly mineralized peritubular dentin. The number of DT varies. 8,000 at the DCJ 57,000 at the pulpal end 15,000 - cervical area of the root / sq mm. SEM studies have demonstrated that dentin exposure at the CEJ occurs in 18% of teeth in general and in 25% of anterior teeth in particular . Furthermore, the same tooth may have different CEJ characteristics with dentin exposure on one side while the other sides are covered with cementum. This area becomes important in assessing the progression of endodontic pathogens, as well as the effect of root scaling and planing on cementum integrity, and bleaching-induced root resorption following the use of 30% hydrogen peroxide Other areas of dentinal communication may be through developmental grooves, both palatogingival and apical.
CLASSIFICATION Earliest classification Oliet and Pollock. (1968) Based on etiology by Simon (1972) Type 1 - Primary endodontic lesions Type 2 - Primary endodontic lesions with secondary periodontal involvement. Type 3 Primary periodontal lesions Type 4 Primary periodontal lesions with secondary endodontic involvement. Type 5 True combined lesions.

CLASSIFICATION OF PULPO PERIODONTAL DISEASE

Weine in 1982 - based on clinical presentation strategies for each.

Type II - Endodontic lesion in a periodontally involved tooth. Type III Primary periodontal lesion requiring endodontic treatment for healing. Type IV - Primary periodontal lesion secondarily involving the pulp.

Based on treatment plan, Grossman classification (1988). Type 1 Requiring endodontic treatment only. Type II Requiring periodontal treatment only. Type III Requiring combined endo-perio treatment
Stock (1988) modified Simons classification. Omitted Class V of the classification. He argued that both Class II and Class IV lesions in advanced stages can become combined lesions and therefore a separate class to describe these lesions was not necessary. ETIOLOGICAL FACTORS Live pathogens: Bacteria Fungi (Yeasts) Viruses Bacteria Endodontic disease is caused by bacteria (Rogas 2001) The periapical tissues become involved when bacteria invade the pulp, causing either partial or total necrosis. The relationship between the presence of bacteria and pulpal and periapical diseases was demonstrated by Kakehashi et al in a classic work (1965)

In that study, pulps of normal rats - exposed to the oral environment. Consequently, pulp necrosis ensued, followed by periapical inflammation and lesion formation. However, when the same procedure was performed on germ-free rats- pulps remained vital and relatively non-inflamed, and the exposure sites were repaired by dentin.
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 The study demonstrated that without bacteria and their products periapical lesions of endodontic origin do not occur. Moller et al (1981) confirmed these findings in monkeys. Blomlof et al. (1992) created defects on root surfaces of intentionally extracted monkey teeth with either open or mature apices. The canals were either infected or filled with calcium hydroxide and replanted back in their sockets. After 20 wks, marginal epithelial downgrowth was found on the denuded dentin surface of the infected teeth. Jansson et al. (1993) concluded that pathogens in necrotic root canals may stimulate epithelial downgrowth along denuded dentin surfaces with marginal communication and thus augment periodontal disease. Jansson & Ehnevid (1998) investigated the effect of endodontic infection on periodontal probing depth and the presence of furcation involvement in mandibular molars. They found that endodontic infection in mandibular molars was associated with more attachment loss in the furca. These authors suggested that endodontic infection in molars associated with periodontal disease may enhance periodontitis progression by spreading pathogens through accessory canals and dentinal tubules. Proteolytic bacteria predominate in the RC flora, which changes over time to a more anaerobic microbiota Rupf et al. (2000) studied the profiles of PDL pathogens in pulpal and PDL diseases associated with the same tooth. Specific PCR methods were used to detect Aa, Tf, E corrodens, F nucleatum, P g, P i, and Td. These pathogen were found in all endodontic samples and the same pathogens were found in teeth with chronic apical Periodontitis and chronic adult periodontitis They concluded that periodontal pathogens often accompany endodontic infections and supported the idea that endodontic-periodontal interrelationships are a critical pathway for both diseases.

Spirochetes :
T. denticola and T . Maltophilum.
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 Virulence factor of Td includes chymotrypsin -like protease complex, extracellular or membrane-associated proteolytic and hydrolytic enzymes, and metabolites. It possesses an array of virulence factors associated with PDL disease and may also participate in the pathogenesis of peri radicular disease T. maltophilum is a small, motile treponeme. Although the virulence factors of this microorganism have not yet been fully studied. This has also been frequently isolated from patients with RPP. FUNGI : Candida albicans. It has been detected in 21 % of infected RC using 18S rRNA directed speciesspecific primers. It also showed the ability to colonize canal walls and penetrate into DT. Other species- Candida glabrata, Candida guillermondii, and Candida incospicia were also detected. Predisposing factors affecting the colonization of this process are immunocompromising diseases such as cancer, certain intracanal medicaments, local and systemic antibiotics and previous unsuccessful endodontic therapy It has been hypothesized that the reduction of specific strains of bacteria in the RC during endodontic treatment may allow fungal overgrowth in the low nutrient environment Another possibility is that fungi may gain access from the oral cavity during treatment as a result of poor asepsis. It has been found that approximately 20% of chronic periodontitis patients also harbor subgingival yeasts .As in endodontic infections, C albicans was also, the most common species of fungi isolated Egnan MW (2002) demonstrated that the presence of fungi in root canals is directly associated with their presence in saliva . These findings further stress the importance of using -aseptic endodontic and periodontal techniques, -maintaining the integrity of dental hard tissues, and covering the tooth crown as soon as practical with a well-sealed permanent restoration in order to prevent coronal leakage.
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 VIRUSES There is increasing evidence to suggest that viruses plays an important role in both endo-perio disease.
HSV is frequently detected in GCF and periodontal lesions HCMV was found in about 65% of PDL pocket and 85% in gingival biopsies. EBV-1 was detected in more than 40% of pocket (Slots et al 2000). Sabeti et al (2001) suggested that HCMV and EB virus play a role in the pathogenesis of symptomatic periapical lesions. Non-living etiologic agents (Depending on their origin and nature ) Extrinsic agents: Foreign Bodies. Treatment failure may be explained by the presence of certain foreign substances in situ. Such as dentin and cementum chips, amalgam, RC filling materials, cellulose fibers from absorbent paper points, gingival retraction cords, leguminous food and calculus

A foreign body response may occur to any of these substances and the clinical reaction may be either acute or chronic. Therefore such conditions maybe either symptomatic or asymptomatic. Treatment: Mechanical or surgical removal of the foreign body. Intrinsic agents Cholesterol Russell bodies Rushton bodies Charcot-Leyden crystals Cholesterol Presence of cholesterol in apical periodontitis is a common H/P finding. These crystals induce a typical foreign body reaction. With time-dissolve/washed away leaving behind clefts Origin: disintegrating erythrocytes of stagnant blood vessels within periapical lesion, lymphocytes, plasma cells which die in great numbers and disintegrate in chronic periapical lesions or by the circulating plasma lipids.
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 Accumulation of cholesterol crystals in inflamed periapical tissues suggested to be one of the causes of failure of endodontic therapy.
Russell bodies Found in most inflamed tissues throughout the body including the peri radicular tissues. Small spherical accumulations of an eosinophilic substance found within or near plasma cells and other lymphoid cells.

It is hypothesized that Russell bodies are caused by the synthesis of excessive amounts of normal secretory protein in certain plasma cells engaged in active synthesis of immunoglobulins. However the prevalence of Russell bodies, the mechanisms of their production, and their exact role in pulpal inflammation have not Yet fully elucidated. Rushton bodies The presence of Rushton hyaline bodies (RHB) is a, feature unique to some odontogenic cysts. Their frequency varies from 2.6% to 9.5%. RHB usually appear within either the epithelial lining or the cyst lumen . They have a variety of morphologic forms including linear (straight or curved), irregular, rounded and polycyclic structures, or they may, appear granular. The exact nature of RHB is not fully understood. It is suggested that they are keratinous in nature, of hematogenous origin, a specialized secretory product of odontogenic epithelium , or degenerated RBCs Charcot-Leyden crystals (CLC) Are naturally occurring hexagonal bipyramidal crystals derived from intracellular granules of eosinophils and basophils. Often associated with increased numbers of peripheral blood or tissue eosinophils in parasitic, allergic, neoplastic and inflammatory disease. Activated macrophages were reported to have an important role in the formation of CLC in several disease processes. The presence of CLC can be detected within a periapical lesion that failed to resolve after conventional endodontic treatment. Although the pathologic role is still unknown, they may he associated with some cases of treatment failures.
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Epithelium (epithelial rests of Malassez)

Normal components of the lateral and apical periodontal ligament Fish net like three-dimensional,interconnected network. In many periapical lessons epithelium is not present and therefore is presumed to have been destroyed .If the rests remain, they may respond to a stimulus by proliferating to wall of the irritants coming through the apical foramen. The epithelium is surrounded by chronic inflammation and is termed an epitheliated granuloma. If this lesion is not treated, the epithelium continues to proliferate in response to the bacteria and inflammatory products from the apical foramen. The term "bay" cyst has been introduced for the microscopic representation of this situation. This is a chronic inflammatory lesion that has epithelium lining surrounding the lumen, but the lumen has a direct communication with the root canal system through the foramen. "True" cyst : It is a three-dimensional, epithelium-lined cavity with no communication between the lumen and the canal system . When periapical lesions are studied in relation to the root canal a clear distinction between these two entities should be made. This distinction between a bay and a true cyst is important from the standpoint of healing It may be that true cysts must be surgically removed, but bay cysts that communicated with the root canal may heal with nonsurgical root canal therapy. The formation of a cyst and its progression from a bay cyst to a true cyst occurs over time. Valderhaug (1973) in a study done in monkeys, showed no cyst formation until at least 6 months after the canal contents became necrotic. Thus the longer a lesion is present, the greater the chance of becoming a true cyst. However, the incidence of true cysts is probably less than 10% .

CONTRIBUTING FACTORS
Poor Endodontic treatment Poor restoration

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Trauma Resorption Perforations Development malformations Cracked tooth syndrome

COMMUNICATION LINKS
Poor endodontic treatment
Correct endodontic procedures and techniques are key factors for treatment success. Unfortunately, poor endodontic treatments are often associated with peri radicular inflammation. Poor endodontic treatment allows canal reinfection, which leads to treatment failure. Endodontic failures can be treated by either orthograde or retrograde retreatment with good success. In recent years, retreatment techniques have improved dramatically due to use of the operating microscope and development of new armamentarium

Poor restorations

Coronal leakage is an important cause of failure of endodontic treatment. Coronal restorations are the primary barrier against coronal leakage and bacterial contamination of endodontic treatment. Therefore it is essential that the root canal systems be protected by good endodontic obturation and well sealed coronal restorations. Root canals may become recontaminated by microorganism due to delay in placement of a coronal restoration and fracture of the coronal restoration

In an in vitro study, they found that packing excess G.P and sealer over the floor of the pulp chamber, after completion of root canal filling, did not seal the root canals. It was therefore recommended that excess of G.P. filling should be removed to the level of the canal orifices and that the floor of the pulp chamber be protected with the well sealed restorative material. (Saunder et al ) IEJ 1990. However, even popular permanent restorative materials may not always prevent coronal leakage. Cemented full crowns as well as dentin-bonded crowns also showed leakage
Trauma
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 Trauma to teeth and alveolar bone may involve the pulp and the periodontal ligament. Both tissues can be affected - directly or indirectly.
Trauma can be classified as: (Bakland LK 2002) Enamel fractures Crown fractures with/ without pulp involvement Crown fractures with pulp involvement Crown-root fracture Root fracture, Luxation and Avulsion.

- Treatment of traumatic dental injuries varies depending on the type of injury and it will determine pulpal and periodontal ligament healing prognosis Enamel fracture involves enamel only: chipping and incomplete fractures or cracks. Treatment : grinding and smoothing the rough edges or restoration of missing enamel structure. In cases where only the enamel is involved, the pulp usually maintains its vitality and the prognosis is good.

Crown fracture without pulp involvement is an uncomplicated fracture that involves enamel and dentin without pulp exposure. Treatment : conservative restoration with composite resin or reattachment of separated fragments. Crown fracture with pulp involvement is a complicated fracture with exposure of the pulp. The extent of the # helps to determine the necessary pulpal and restorative treatments A small fracture may indicate vital pulp therapy followed by acid-etched composite restoration. A more extensive fracture may require root canal treatment as well. The stage of tooth maturation is an important factor in choosing between pulpotomy and Pulpectomy. The amount of time elapsed from the injury often affects pulpal prognosis. The sooner the tooth is treated, the better the prognosis. Crown-root fractures are usually oblique and involve both crown and root. They include enamel, dentin, and cementum and may or may not include the pulp
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 Often include molars and premolars, but anterior teeth can also be affected. A cusp fracture that extends subgingivally is a common finding and often presents a diagnostic and clinical challenge Treatment depends on the severity of the fracture and may vary from only removing the fractured tooth segment and restoration to endodontic treatment, periodontal treatment and/or surgical procedures. Root fractures Involve cementum, dentin, and pulp. They may be horizontal or transverse. C/F: mobility, pain on biting. Often, a periodontal defect or a sinus tract is associated with the fractured root. R/F: a root # can only be visualized if the X-ray beam passes through the # line. Horizontal and oblique root # are easier to detect radiographically while the diagnosis of vertical root # is more challenging. Treatment: Repositioning of the coronal segment and stabilization by splitting up to 12 weeks will enhance pulpal and periodontal repair. Teeth with # roots do not necessarily require RCT if healing takes place with no evidence of pulp disease . Luxation (tooth displacement) Injuries such as concussion, subluxation, extrusive luxation, lateral luxation, and intrusive luxation. In concussion : tooth is only sensitive to percussion no radiographic changes, are found. In subluxation :teeth are sensitive to percussion and also have increased mobility. Often sulcular bleeding is present, indicating damage to the periodontal ligament. In both concussion and subluxation radiographic findings are unremarkable and the pulp may respond normally to vitality tests. No treatment is usually required for minor subluxation if mobility is severe stabilization of the tooth is necessary. In extrusive luxations the teeth have been partially displaced from the socket and increased mobility is found. Radiographs also show displacement. The pulp usually does not respond to vitality tests and requires RCT once irreversible pulpitis is diagnosed .The tooth requires repositioning and splinting usually for a 2-3-week period.

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 Lateral luxations the tooth has been displaced away from its long axis. Percussion sensitivity may or may not be present. A metallic sound upon percussion indicates that the root has been forced into the alveolar bone. Treatment includes repositioning and splinting. Lateral luxations that involve bony fractures usually require up to 8-.weeksplinting periods. Intrusive luxations the teeth are forced into their sockets in an axial direction. They have decreased mobility and resemble ankylosis . Treatment depends on root maturity. If the root is not completely formed and have an open apex the tooth may re-erupt. If the tooth is fully developed, active extrusion is indicated. In such cases RCT is indicated since pulp necrosis develops in almost all cases . Avulsion :tooth is totally displaced from its alveolar socket. If the tooth is replanted soon after avulsion, the PDL has a good chance of healing. Extra-alveolar time and the storage media used to transport the tooth are critical factors for successful replantation. Resorptions Condition associated with either a physiologic or a pathologic process resulting in a loss of dentin, cementum and/or bone. Classified: External resorption and Internal resorption. Untreated, ER may invade cementum, dentin and ultimately the pulp space Untreated IR may advance and perforate to the external root surface. External root resorption may be divided into three main categories 1) Progressive inflammatory resorption 2) Invasive resorption (non inflammatory) 3) Replacement resorption (non inflammatory).
Progressive inflammatory resorption Etiology: Pulpal infection and sulcular infection. Occurs following traumatic displacement injuries, tumours, cysts, PDL disease, pulp inflammation and necrosis. Practically all teeth with apical periodontitis exhibit a inflammatory root resorption .This can be located on either the apical or lateral aspects of the root but is more frequent at the apex.
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 During the initial stages the resorption cannot be detected radiographically, however, it is evident in histologic sections. If allowed to progress, the resorptive process may destroy the entire root. If detected and treated early the prognosis is good. Invasive root resorption (invasive cervical resorption) is a relatively uncommon and invasion is predominated by fibro vascular tissue derived from the PDL. The process resorbs cementum, enamel and pulp space. There may be no signs or symptoms unless there is pulpal or periodontal infection. Secondary bacterial invasion into the pulp or PDL space will cause an inflammation of the tissues accompanied with pain. Resorptive defect is only detected by routine radiographic examination. C/F vary from a small defect at the gingival margin to a pink coronal discoloration of the tooth crown. R/F: the lesion varies from well delineated to irregularly bordered radiolucencies. Internal root resorption Etiology: unknown, predisposing factors: orthodontic treatment and intracoronal bleaching with 30%H2O2 Treatment: of the condition presents clinical problems because the resorptive tissue is highly vascular and the resulting hemorrhage may impede visualization and compromise placement of a restoration. Successful treatment relies upon the complete removal or inactivation of the resorptive tissue. In most cases, surgery is necessary to gain access to the resorptive defect. Topical application of 90% aqueous solution of trichloroacetic acid, curettage and sealing of the defect has proved successful in most of the cases. Large defects with advanced stages of condition have poor prognosis.
Replacement resorption or ankylosis Occurs following extensive necrosis of the PDL with formation of bone onto a denuded area of the root surface. Most often seen as a complication of avulsed teeth that have been out of their sockets in dry conditions for several hours. Certain PDL procedures and PDL wound healing have been reported to induce replacement root resorption.
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 Granulation tissue derived from bone or gingival connective tissue may induce root resorption and ankylosis. Ankylosed teeth are incorporated in the alveolar bone and will become part of the normal remodelling process of bone. This is a gradual process and the speed by which the teeth are replaced by bone varies depending mainly on the metabolic rate of the patient. In most cases, it may take years before the root is completely resorbed. Clinically, replacement root resorption is diagnosed by Lack of mobility of the ankylosed teeth. The teeth will also have a Metallic sound-upon percussion, will be in infraocclusion. R/F, absence of a PDL space is evident and the in growth of bone into the root will present a characteristic "moth-eaten" appearance.
Internal root resorption

Occurs as a result of multinucleated giant cell activity. Etiology: Unknown, but appears to be related to chronic pulpal inflammation associated with an infected coronal pulp space. Internal resorption will only take place in the presence of granulation tissue and if the odontoblastic layer and predentin are affected or lost. Causes: usually trauma, bacteria Traumatic factors: mechanical, chemical or thermal. Extreme heat has been suggested as a possible cause for this type of resorption.. Therefore, the clinician must use sufficient irrigating solutions when performing root scaling with ultrasonic devices as well as when using cauterization during surgical procedures. It is usually asymptomatic and diagnosed during a routine radiographic examination. Early diagnosis is critical for the prognosis. R/F: The resorptive defect discloses a distorted outline of the root canal. A round or an oval-shaped enlargement of the root canal space is usually found. Histologically granulation tissue multinucleated giant cells and coronal pulp necrosis are commonly found.
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Root Perforations Communications between the RC system and either periradicular tissues or the oral cavity may often reduce the prognosis of treatment. Etiology: Extensive carious lesions, resorption, or from operator error occurring during RC instrumentation or post preparation Treatment prognosis : depends on the size, location, time of diagnosis and treatment, degree of PDL damage as well as the sealing ability and biocompatibility of the repair material. Treatment success depends mainly on immediate sealing of the perforation and appropriate infection control. Materials : MTA, Super EBA, intermediate restorative material, (Cavit), amalgam. Developmental malformations Fail to respond to treatment when they are directly associated with an invagination or a vertical developmental radicular groove. (failure of the tooth germ to form another root) Maxillary central and lateral incisors, crossing over the cingulum, apically down the root for varying distances.

As long as the epithelial attachment remains intact the periodontium remains healthy. However, once this attachment is breached and the groove becomes contaminated by bacteria, a self-sustaining infrabony pocket can be formed along its entire length. It acts as a nidus for accumulation of bacterial biofilm and an avenue for the progression of PDL disease. Diagnosis: Patient may present symptoms of a periodontal abscess or a variety of asymptomatic endodontic conditions. If the condition is purely periodontal, it can be diagnosed by visually following the groove to the gingival margin and by probing the depth of the pocket, which is usually tubular in form and localized to this one area, as opposed to a more generalized periodontal problem. The tooth will respond to pulp-testing procedures. Bone destruction that vertically follows the groove may be apparent radiographically.

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 If this entity is also associated with an endodontic disease, the patient may present clinically with any of the spectrum of endodontic symptoms. The developmental groove may be visible on the radiograph as a dark vertical line. This condition must be differentiated from a vertical fracture, Treatment: Buring out the groove, placing bone substitutes, and surgical management of the soft tissues and underlying bone. Occasionally, the tooth needs to be extracted due to a poor prognosis.
Differential diagnosis For differential diagnostic procedures the Endo-Perio lesions are best classified as endodontic, periodontal or combined diseases. They can also be classified by treatment depending on whether endodontic, periodontal or combined treatment modalities are necessary. They include: primary endodontic disease, primary periodontal disease, and combined diseases. The combined diseases include: -Primary endodontic disease with secondary periodontal involvement, -Primary periodontal disease with secondary endodontic involvement, and -true combined diseases. Primary endodontic disease An acute exacerbation of a chronic apical lesion on a tooth with a necrotic pulp may drain coronally through the PDL into the gingival sulcus.

This condition may mimic clinically the presence of a periodontal abscess. In reality, it is a sinus tract from pulpal origin that opens through the PDL ar e a . For diagnostic purposes, it is imperative to insert a gutta-percha cone into the sulcus and to take one or more radiographs to determine the origin of the lesion. When the pocket is probed, it is narrow and lacks width. A similar situation occurs where drainage from the apex of a molar tooth extends coronally into the furcation area. This may also occur in the presence of lateral canals extending from a necrotic pulp into the furcation area.

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 Primary endodontic diseases usually heal following RCT. The sinus tract extending into the-gingival sulcus or furcation area disappears at an early stage once the necrotic pulp has been removed and the root canals are well sealed It is important to recognize that failure of any periodontal treatment will occur when the presence of a necrotic pulp has not been diagnosed, and endodontic treatment has not followed.
Primary periodontal disease These lesions are caused primarily, by periodontal pathogens. In this process, chronic periodontitis progresses apically along the root surface.

In most cases, pulp tests indicate a clinically normal pulpal reaction There is frequently accumulation of plaque and calculus and the pockets are wider. The prognosis depends upon the stage of periodontal disease and the efficacy of periodontal treatment. The clinician must also be aware of the radiographic appearance of periodontal disease associated with developmental radicular anomalies . Combined diseases Primary endodontic disease with secondary periodontal involvement If after a period of time a suppurating endodontic disease remains, untreated, it may become secondarily involved with periodontal breakdown. Plaque forms at the gingival margin of the sinus tract and leads to plaqueinduced periodontitis in the area. The tooth requires both endodontic and periodontal treatment If the endodontic treatment is adequate, the prognosis depends on the severity of the plaque-induced periodontitis and the efficacy of periodontal treatment. These lesions may also occur as a result of root perforation during RCT, or where pins or posts have been misplaced during coronal restoration. Symptoms may be acute, with PDL abscess formation associated with pain, swelling, pus or exudate, pocket formation and tooth mobility.

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 A more chronic response may sometimes Occur With out pain, and involves the sudden appearance of a pocket with bleeding on probing or exudation of pus. Root perforation - close to the alveolar crest- raise a flap and repair the defect with appropriate filling material. In deeper perforations, or in the roof of the furcation, immediate repair of the perforation has a better prognosis than management of an infected one. Use of MTA has resulted in cemental healing following immediate repair. Root fractures may also present as primary endodontic lesions with secondary periodontal involvement. These typically occur on root-treated teeth, often with post and crowns. The signs may range from a local deepening of a periodontal pocket to more acute periodontal abscess formation. Root fractures have also become an increasing problem with molar teeth that have been treated by root resection.
Primary periodontal disease with secondary endodontic involvement The apical progression of a PDL pocket mav continue until the apical tissues are involved. In this case the pulp may become necrotic as a result of infection entering via lateral canals or the apical foramen.

In single-rooted teeth-prognosis is usually poor. In molar teeth prognosis may be better since not all the roots may suffer the same loss of supporting tissues, root resection can be considered as a treatment alternative. The effect of the progression of chronic periodontitis on the vitality of the pulp is controversial If the blood supply circulating through the apex is intact, the pulp has good prospects for survival. It has been reported that pulpal changes resulting from periodontal disease are more likely to occur when the apical foramen is involved. In these cases, bacteria originating from the periodontal pocket are the most likely source of root canal infection.

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 A strong correlation between the presence of microorganisms in root canals and their presence in periodontal pockets of advanced periodontitis has been demonstrated. Support for this concept has come from research in which cultured samples obtained from the pulp tissue and radicular dentin of periodontally involved human teeth showed bacterial growth in 87% of the teeth (Adriaens PA 1988) The treatment of periodontal disease can also lead to secondary endodontic involvement. Lateral canals and DT may be opened to the oral environment by scaling and root planing or surgical flap procedures. It is possible for a blood vessel within a lateral canal to be severed by a curette and for microorganisms to be pushed into the area during treatment, resulting in pulp inflammation and necrosis.
True combined disease It occurs less frequently and is formed when an endodontic disease progressing coronally joins with an infected PDL pocket progressing apically.

The degree of attachment loss in this type of lesion is invariably large and the prognosis guarded . This is particularly true in single-rooted teeth. In molar teeth, root resection can be considered as a treatment alternative if not all roots are severely involved. In most cases periapical healing may be anticipated following successful endodontic treatment. The periodontal tissues, however, may not respond well to treatment and will depend on the severity of the combined disease. The radiographic appearance of combined endodontic-periodontal disease may be similar to that of a vertically fractured tooth. A fracture that has invaded the pulp space, with resultant necrosis, may also be labeled a true combined lesion and yet not be amenable to successful treatment If a sinus tract is present, it may be necessary to raise a flap to determine the etiology of the lesion. Visual examination
Clinical diagnostic procedures
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Palpation Percussion Mobility Radiographs Pulp vitality testing: Cold test, electric test, blood flow test, cavity test, restored teeth testing Pocket probing Fistula tracking Cracked tooth testing: Transillumination, wedging, staining. Selective anesthesia test Clinical diagnostic procedures Clinical tests - for obtaining correct diagnosis and differentiating between endodontic and PDL disease. One test is usually not sufficient to obtain a conclusive diagnosis.

Visual examination (Soft tissue) lips, cheeks, oral mucosa, tongue, palate and muscles should be done routinely. The alveolar mucosa and attached gingiva :presence of inflammation, ulcerations, or sinus tracts. sinus tract is associated with a necrotic pulp. Teeth: caries, defective restorations, erosions, abrasions, cracks, fractures, and discolorations.

A discolored permanent tooth - necrotic pulp. A "pink spot" in crown - active internal resorption.

A conclusive diagnosis for pulpal disease cannot be achieved by visual examination alone and must always be accompanied by additional tests. Visual examination - improved by the use of enhanced magnification and illumination with the help of Magnifying loops and the operating microscope These facilitate the location of calculus, caries, coronal and radicular fractures, developmental defects, and areas of denuded dentin mainly at the CEJ. Internal root resorption discolored tooth with necrotic pulp

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Palpation

Palpation- firm digital pressure to the mucosa covering the roots and apices. Index finger pressed against the underlying cortical bone. This will detect the presence of periradicular abnormalities or "hot" zones that produce painful response to digital pressure. A positive response to palpation may indicate active periradicular inflammatory process. It does not indicate whether the inflammatory process is of endodontic or periodontal origin. PALPATION Percussion Tapping on the incisal or occlusal surfaces - blunt instrument - the back end of a mirror handle. The tooth crown is tapped vertically and horizontally. It indicates the presence of a periradicular inflammation that may be either from pulpal or PDL origin. The sensitivity of the proprioceptive fibers in an inflamed PDL will help identify the location of the pain. This test should be done gently, especially in highly sensitive teeth. It should be repeated several times and compared to control teeth PERCUSSION Mobility Performed using two mirror handles on each side of the crown. Pressure is applied in a facial-Lingual direction as well as in a vertical direction and the tooth mobility is scored. Tooth mobility is directly proportional to the integrity of the attachment apparatus or to the extent of inflammation in the PDL ligament In Teeth with extreme mobility: primary cause may be periodontal disease. MOBILITY Fractured roots and recently traumatized teeth often present high mobility. Periradicular abscess of pulpal origin may cause similar mobility. This can only be verified if other tests indicate pulp necrosis or if mobility improves a short time after completion of endodontic therapy.
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 Pressure exerted by an acute apical abscess may cause transient tooth mobility . This may also occur as a result of orthodontic movement and pulp necrosis of previously traumatized teeth
Radiographs Essential for detection of anatomic landmarks and a variety of pathological conditions, for documentation and legal purposes. Aid in detection of carious lesions, extensive or defective restorations, previous RCT, stages of root formation, root fractures, periradicular radiolucencies, thickened PDL and alveolar bone loss.

Radiographic changes will only be detected once the inflammation or bacterial byproducts originating from the dental pulp cause sufficient demineralization of the cortical bone. Often, the initial phases of periradicular bone resorption is confined only to cancellous bone and cannot be detected unless the cortical bone is also affected. Periodontal disease causing alveolar bone loss can be effectively detected by radiographs. For purposes of differential diagnosis, periapical and bitewing radiographs should be taken from several angles. Radiograph is two dimensional picture of a three dimensional object hence clinical signs and symptoms as well as findings from the other clinical tests should always be considered at the time of radiographic evaluation.

RADIOGRAPHS

Pulp vitality testing These tests are designed to assess the response of the pulp to different stimuli.

An abnormal response may indicate degenerative changes in the pulp. In general no response indicates pulp necrosis and moderate transient response indicates normal vital pulp. A quick painful response may often indicate reversible pulpitis and lingering response indicate irreversible pulpitis. Since some of these tests may provoke a painful reaction they should be carefully performed and their nature and importance explained to the patient.
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 When correctly performed and adequately interpreted these tests are reliable in differentiating between pulpal disease and periodontal disease. The most commonly used pulp vitality tests are cold test, electric test, blood flow tests and cavity testing
Cold test This test is performed by applying a cold substance, or agent, to a wellisolated tooth surface. Tooth isolation can be achieved by drying the crown surfaces with cotton rolls, gauze and a very gentle air blast.

Methods: Ice sticks, ethyl chloride, Co2(dry ice), and refrigerants such as dichlorodifluoromethane (DDM). Co2 (-780c) and DDM(-500c)are extremely cold and are only used when the pulp does not respond to less cold agents. Vital pulps - sharp brief pain, does not last more than a few seconds. An intense and prolonged pain response- irreversible pulpitis. Lack of response- pulp necrosis. When adequately performed, this test is reliable in determining whether the pulp has undergone irreversible damage. However, false-positive and false-negative -multiradicular teeth where not all roots are affected or in teeth with calcified root canals.
Electric test An electric stimulus applied using a special pulp tester. Tooth is first cleaned, dried and isolated and a small amount of toothpaste is placed on the electrode of the pulp tester, which is then put into contact with the clean sound tooth surface. Electric current is gradually applied until the patient reports sensation. The purpose - is to stimulate the sensory nerve fibers of the pulp to produce a response. No response- indicates pulp necrosis. A positive response interpreted as either intact vital pulp or partially necrotic pulp. It does not provide any information about the condition of the vascular supply of the pulp.
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VITALITY TESTING While interpreting the results the clinician must take into consideration the various false-positives and false-negatives of this test .

Causes for false-positive responses are partial pulp necrosis, patient anxiety, ineffective isolation, and inadvertent contact with metallic restorations.
False-negative responses are: obliterated root canals, recently traumatized teeth, teeth with immature apices, patient taking drugs that elevate the pain threshold, and poor electrode-tooth contact. Adv: Easy to perform and provides accurate determination of pulp necrosis in adult teeth. Blood flow test It is designed to determine the vitality of the pulp by measuring its blood flow.

Different systems such as dual wavelength spectrophotometry, pulse oximetry, and laser Doppler have been developed to measure either oxyhemoglobin, low concentration of blood or pulsation of the pulp. Sensors are applied to the external surfaces of the crown and the pulp blood flow is recorded and compared to controls. It is non-invasive and painless, are relatively new and are not used routinely. Cavity test Highly reliable in determining the vitality. Consists of creating a cavity in the tooth without anesthesia. Positive response -vital pulp tissue. Negative response - pulp necrosis. If no response is obtained, the cavity is extended into the pulp chamber and endodontic treatment is initiated. Not routinely performed since it may produce pain in cases where the pulp is vital. It should only be limited to cases where all other tests proved inconclusive and a definitive diagnosis of the pulp condition could not be established. Restored teeth testing Testing teeth- extensive coronal restorations is somewhat more challenging.

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 The restoration should be removed to facilitate pulp testing. In cases where restoration removal is not feasible, a small access opening is made through the restoration until sound tooth structure is reached. Cold test and cavity test will give the most reliable results. Access through full gold crowns and porcelain (copious water irrigation) restorations can usually be done without affecting the strength and stability of the restoration. Access repair is done with amalgam, or another permanent filling material.. Pocket probing Important test that should always be performed when attempting to differentiate between endodontic and periodontal disease. A blunt calibrated periodontal probe is used to determine the probing depth and clinical attachment level. It may also be used to track a sinus. A deep solitary pocket in the absence of periodontal disease may indicate the presence of a lesion of endodontic origin or a vertical root fracture. PROBING Periodontal probing can be used as a diagnostic and prognostic aid. For example, the prognosis for a tooth with a necrotic pulp that has developed a sinus tract is excellent following adequate root canal therapy. However, the prognosis of root canal treatment in a tooth with severe periodontal disease is dependent on the success of the periodontal therapy. Therefore, correct identification of the etiology of the disease, whether endodontic, periodontal or combined, will determine the course of treatment and long-term prognosis.
Fistula tracking Endodontic or periodontal disease may sometimes develop a fistulous sinus tract.

Inflammatory exudates may often travel through tissues and structures of minor resistance and open anywhere on the oral mucosa or facial skin.
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 Intraorally, the opening is usually visible on the attached buccal gingiva or in the vestibule Extraorally, the fistula may open anywhere on the face and neck. However, it is most commonly found on the cheek, chin and angle of the mandible, and occasionally also on the floor of the nose . If the etiology is pulpal, it usually responds well to endodontic therapy. Simple visual examination of the sinus does not necessarily indicate the origin of the inflammatory exudate or the tooth involved. Identifying the source of inflammation by tracking the fistula will help the clinician to differentiate between diseases of endodontic and periodontal origin. Fistula tracking is done by inserting a semi rigid radiopaque material into the sinus tract until resistance is met. Commonly used materials include gutta percha cones or presoftened silver cones. A radiograph is then taken that will reveal the course of the sinus tract and the origin of the inflammatory process.

FISTULA TRACKING Cracked tooth testing

Transillumination Designed to aid in the identification of cracks and fractures in the crown

A fiberoptic connected to a high-power light source is used to illuminate the crown and gingival sulcus.

The contrast between the dark shadow of the fracture and the light shadow of the surrounding tissue will clearly reveal the size and orientation of the fracture line. An existing restoration may need to be removed to enhance visibility.
Wedging This technique aids in the identification of vertical crown fractures or crownroot fractures.

Such fractures cause a painful response to the patient at the time of chewing.
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 During the test wedging forces are created as the patient is instructed to chew on a cottonwood stick or other firm material. This test is fairly reliable in identifying a single tooth causing pain during mastication.
Staining Identifies lines of fracture in the crown and root and is often used in conjunction with the wedging test.

The tooth crown is dried and a cotton pellet soaked with Methylene blue dye is swabbed on the occlusal surface of the tooth- the patient is asked to bite on a stick and perform lateral jaw movements This way the dye penetrates well into the zone of the fracture. The dye is then rinsed from the tooth surfaces and visual examination with magnifying loops or the microscope will reveal a distinctive fracture line darkened with dye. Selective anesthesia test Useful when source of pain cannot be attributed to a specific arch. Disappearance of pain following a mandibular block will confirm the source of pain originating from a mandibular tooth. The periodontal ligament injection is often used to narrow down the zone in question, however, it cannot anesthetize a single tooth without affecting adjacent teeth. No conclusive diagnosis differentiating between endodontic and periodontal disease can be made using this type of tests. EFFECT OF PULPAL DISEASE ON THE PERIODONTIUM
Bacteria and toxic irritants in pulp- intrapulpal pressure Vital pulp no changes in the periodontium. Unresolved endo lesion - bone loss , pocket formation and impair wound healing. Endodontic infection - local modifying risk factor if left untreated. Diem et al (2002) reported that all tissues of the periodontium had a potential for regeneration regardless of the status of the pulp. With the proper endodontic treatment, periodontal disease of pulpal origin should heal.

First indication of periodontal involvement due pulp disease - thickening of PDL space at the apical end.
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 Nature and extent of PDL destruction is dependent on several factors -virulence -duration of the disease and -host defense mechanism. In acute cases, inflammation in PDL space in the apical region causes -extrusion of tooth in its socket and -severe tenderness- percussion and -mobility.

EFFECT OF PULPAL DISEASE ON THE PERIODONTIUM

INFLUENCE OF ENDODONTIC PROCEDURES

Endodontic therapy adversely affects periodontal healing. Mechanical preparation, sealers, surgical trauma hinder new bone ,cementum and connective tissue repair. Precautions to be taken when perio therapy to follow endodontic treatment. -Induce less mechanical trauma -Use periodontic friendly irrigants -Use more biocompatible sealers
EFFECT OF PERIODONTITIS ON THE DENTAL PULP

Atrophic changes, Interference of blood supply to lateral/ accessory canals, strangulation of blood vessels, Reduction in pulp cells, Dystrophic calcification, Fibrosis, Reparative dentin, Resorption Strong correlation exists (Seltzer et al 1978) Found inflammatory alterations and localized pulp necrosis adjacent to lateral canals in roots exposed by periodontal disease.

No relationship exists Mazur and Massler(1979) Disclaim relationship of PDL disease as a causative factor in pulpal disease Periodontitis involving apical foramen can lead to pulp necrosis
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 Lange land et al (1974) as long as the blood supply through the apical foramen remains intact, the pulp is usually capable of withstanding physiologic insults induced by periodontal disease. Pulpal reaction is influenced by the stages of PDL disease and also by PDL treatment. EFFECT OF PERIODONTAL PROCEDURES ON PULP Pulpal changes seen in PDL disease were closely related to PDL treatment than to the disease Vigorous SRP removes cementum expose DT transport irritants-pulpal inflammation , severe blood vessels (lateral, furcal canals) and cause necrosis of the dental pulp Presence of an intact cementum layer is important for the protection of the pulp
Precautions during PDL therapy Avoid use of irritating chemicals. Minimise use of ultrasonics & rotary scaling instruments when < 2 mm of dentin thickness remaining PRIMARY ENDODONTIC LESIONS Causes Deep carious lesion Large restoration approximating the pulp, History of a pulpotomy, pulp capping, Poor RCT Symptoms Mobility Localized bone loss Narrow pocket Tenderness to percussion Sinus tract Swelling Diagnosis Radiographs Pulpal vitality test Tracing of sinus tract Periodontal probing Treatment
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Complete resolution is usually anticipated after conventional endodontic therapy. Prognosis Excellent

PRIMARY ENDODONTIC LESIONS WITH SECONDARY PDL INVOLVEMENT Characteristics Long standing pulpal pathosis leads to destruction of PDL apparatus. Accumulation of plaque and calculus results in further apical migration of the attachment.
Diagnosis Radiographs Pulp- Nonvital Periodontal probing (Plaque and calculus, pocket) Treatment Endodontic and Periodontic treatment, With endodontic therapy only part of the lesion can be expected to heal. Ingle and Beveridge: prognosis of primary PDL lesions is not as favorable as primary endodontic lesions. It has been seen bone loss due to endodontic lesion is reversible but irreversible due to periodontal lesion.

Prognosis For endodontic lesion is superior. Periodontal therapy depends on the severity of periodontal involvement, and must receive regular maintenance PRIMARY PERIODONTAL LESIONS
Characteristics Teeth vital Generalized bone loss Calculus/plaque Soft tissue inflammation Broad based pockets, Mobility Periodontal abscess during acute phase
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Diagnosis Visual examination Probing Pulp testing Radiographs Primary Periodontal disease Treatment Periodontal therapy Root amputation Guided tissue regeneration Pulp space therapy (advanced cases) Prognosis Depends on the outcome of periodontal therapy. Depends on the extent of the periodontitis and on patients ability to comply with potential long term treatment and maintenance therapy. PRIMARY PERIODONTAL LESION WITH SECONDARY ENDODONTIC INVOLVEMENT Characteristics Deep periodontal pockets History of extensive periodontal procedures Symptoms Sensitivity to temperature Tenderness to percussion Mobility and Swelling Diagnosis History of disease progression Probing Pulp testing Radiographic changes Treatment Pulp space therapy Periodontal therapy Root amputation Guided tissue regeneration Prognosis
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Depends on continuing periodontal treatment subsequent to endodontic therapy. TRUE COMBINED LESIONS Characteristics Once the pulpal and periodontal lesions coalesce, they may be clinically indistinguishable. Necrotic pulp/ failed Endodontic treatment, plaque, calculus and periodontitis will be present in varying degrees. Diagnosis Probing Radiographs Pulpal testing

True combined endo-perio disease

Is periodontal disease a cause of pulp necrosis? Can a pulpless tooth be the cause of periodontal disease? Answers - utmost clinical importance. The appropriateness of treatment planning hangs in the balance.
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 For e.g. should RCT be carried out prophylactically for a tooth with moderate or advanced PDL disease?
Should a pulpless tooth be retained or should it be removed and replaced with an osseointegrated implant? Many of our clinical impressions related to the dental pulp, and indeed many of our misinterpretations, stem from early histological observations.

Adequate fixation of pulp tissue. The potential for the dental pulp to survive the various challenges presented during the lifetime of a patient is also by and large related to presumptions made in interpretation of histological data. Dental pulp resides in a rather precarious environment. Effectiveness of a tissue's vasculature is key to its adequate function, such physiological observations suggest that the dental pulp has mechanisms which provide a significant capacity for survival. The effects of PDL disease and procedures on the pulp
(Cohen 2002 pathways of pulp) PDL disease is a 'direct cause of pulpal atrophy and necrosis' 'Periodontal disease' is more deleterious to the pulp than both caries and restorations combined.

PDL disease and PDL treatments should be regarded as potential causes of pulpitis and pulpal necrosis. The pathways - DT, LC, and the AF. Demonstration of the, presence of such path- ways is commonly identified as evidence that specific periodontal disease must have some effect on the health of the dental pulp. Contradicting studies

Kirkham (1975) 100 teeth -2% Tagger & Smukler (1979)-root amputation, pulps no inflammatory changes. Haskell et al. (1980) similar study - found no inflammatory cells or very few inflammatory cells Czarnecki & Schilder (1979) performed a histological study of intact, cariesfree teeth and compared the pulps of teeth which were periodontallyinvolved.
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Jaoui et al. (1995) studied patients with advanced PDL disease for 5-14years after completion of active PDL treatment. Of the 571 teeth that did not have RCT at the time of completion of PDL treatment, only one tooth (0.175%) required root canal treatment over the 5- to 14-year recall period. CLINICAL OBSERVATIONS Virgin tooth with pulpal necrosis. Etiology in most cases can be root fracture, trauma, herpes, developmental defects etc Only when the etiology is unknown last resort is to tag PDL disease or PDL procedure as etiology which is very rare.

Adults 35yrs and above- PDL disease and get PDL treatment Advanced periodontal disease would have been identified not only as the likely cause of pulp necrosis but as the only possible cause. From these studies it appears that PDL treatment, as well as PDL disease, has a negligible effect on the dental pulp. In summary, unless PDL disease extends all the way to the tooth apex, the weight of evidence in the literature suggests that the dental pulp is capable of surviving significant insults and that the effect of PDL disease as well as PDL treatment on the dental pulp is negligible. Clinical significance of the relationship between PDL disease and the dental pulp has been greatly exaggerated in historical and much of the current periodontal-endodontic literature. The effects of endodontically involved teeth on periodontal health and healing
Jansson, Ehnevid and Blomlof (1993-1998) Only recently potential effect of tooth with a necrotic pulp has been described as a risk factor: In the initiation and progression of PDL disease, and the resolution of periodontal pockets Evidence: similarity of the microbial flora in root canals and deep periodontal pockets, Pathway- dentinal tubules. Results: deeper probing depths, more bone loss, impaired periodontal healing following nonsurgical periodontal treatment, and enhanced progression of PDL disease. Clinical message, of these studies was that RCT should be completed before PDL therapy.
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CONTRADICTING STUDY One credible human study supports RCT may interfere with the effectiveness of attachment regeneration procedures. Sanders et al. (1983) reported in 1983 that after the use of FDBA 65% of the teeth that did not have RCT showed complete or greater than 50% bone-fill in periodontal osseous defects, while only 33% of the teeth which had RCT prior to the PDL surgical procedure had complete or greater than 50% bone-fill.

In summary, while it has been suggested that a pulpless tooth may represent
an etiological risk factor related to periodontal disease, the comparative risk must be considered negligible based on clinical outcomes. Diagnosis Pulp testing procedures and periodontal probing are critical to accurate diagnosis.

Contour of a defect in the attachment can be identified by careful probing and that the contour is important in determining the appropriate treatment for resolving the lesion For E.g. a draining sinus tract through the PDL space from a periapical lesion or lateral lesion. By careful probing, a break in the integrity of the sulcus is found and can be probed some distance down the root surface. The break is about 1 mm wide and probing a millimeter to either side is within normal limits. It is usually referred to as a narrow sinus tract-type of probing. This type of probing will be associated with a tooth with a necrotic pulp or a tooth which has had root canal treatment a very high percentage of the time. Although it involves the attachment and there is a defect that can be probed, it is strictly an endodontic problem and will resolve after adequate root canal treatment. No periodontal treatment is necessary.
SINUS TRACT WITH VITAL PULP
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 Adjacent pulpless tooth or a pulpless tooth several teeth away Developmental grooves Fused roots of posterior teeth Incomplete coronal fractures (cracked tooth) Crown-root fractures Enamel spurs As with many things in life, there is the general rule and then there are the exceptions. The general rule in this case is that a narrow sinus tract- like probing is commonly associated with a pulpless tooth and the exceptions are as listed above Conclusion Interrelationship between pulpal and periodontal disease have been both confirmed and denied for over 100 years. The most intimate and demonstrable relationship between the two tissues is by means of the vascular system. The similarities between the endodonticperiodontal microflora suggest that cross-infection between the root canal and the periodontal pocket can occur.
An in depth understanding of the mechanisms by which these diseases processes interact ,together with a thorough diagnostic examination, usually will help direct the proper course of treatment.

References

Clinical textbook of Periodontology; Carranza, 9 Edition Pathologic interactions in pulpal and periodontal tissues. J. Clin. Periodontol 2002;29:663-671. Diagnosis, prognosis and decision making in the treatment of combined periodontal endodontic lesions. Periodontology 2000, Vol. 34, 2004, 165 203. Detection of localized tooth related factors that predispose to periodontal infections. Periodontology 2000, Vol. 34, 2004, 136150.

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The influence of endodontic treatment upon periodontal wound healing. J. Clin. Periodontol 1997;24:449-456. Clinical diagnosis and treatment of endodontic and periodontal lesions;. Quintessence International 1993;24:135-139. The periodontal-endodontic controversy Periodontology 2000, Vol. 30, 2002, 123 130. Pathways of pulp Cohen 8th edition

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