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Authors: Dr. Vinisha Pandey, Dr. Vipin Kumar

Abstract

There is no escape from at least one thing in this world and that, whether you like it or not, is a relationship. Just as each one of us is born into a relationship, the tooth too develops and erupts into one…… and that, of course, is the relationship with its surrounding periodontal tissues.
No relationship is a bed of roses. The delicate balance between the pulp and the periodontium can easily get disrupted by an affair with disease. The role of the astitute clinician is to serve as the proverbial ‘peacemaker’ who finds out and eliminates the intruder and helps to reconcile and restore the harmony between the two tissues. This he can do only by accurate diagnosis and effective treatment planning. Only then can these two tissues- the pulp and the periodontium –hope to live together happily ever after!

Introduction

The relationship between periodontium and pulp was first discovered by Simring and Goldberg in 19641. The perio – endo lesion is used to describe lesions due to inflammatory products found in varying degrees in both periodontium and the pulpal tissues.
The periodontium and the pulpal have embryonic, anatomic and functional interrelationship2. They are ectomesenchymal in origin, from which the cells proliferate to form the dental papilla and follicle, which are the precursors of the periodontium and the pulp respectively. The embryonic development gives rise to anatomical connections which remain throughout the life of the tooth 3. Pathways are developed that provide means by which pathological agents pass between the pulp and the periodontium, thereby creating the perio – endo lesion4. Three main avenues for communication are:-
  1. Dentinal tubules.
  2. Lateral and accessory canals and
  3. The apical foramen 5
The tooth, its pulp and its supporting structures should be viewed as a biologic unit. The inter relationship of these structures influence each other during health, function and disease. Because the vitality of the tooth depends on the ability to function and not on the viability of the pulp, the health of the supporting structures is of prime importance 6. The inter relationship between periodontal and endodontic diseases has aroused much speculation, confusion and controversy. Pulpal and periodontal problems are responsible for more than 50% of tooth mortality7. Periodontal disease is a slow progressing disease that may have an atrophic effect on the dental pulp. Periodontal treatments such as deep toot planing, usage of localized medicaments and gum injury or wounding may accelerate pulpal inflammation and provoke the inter related disease process 7,8. The structures of the periodontium are affected adversely by three vectors:- Disease initiated marginally through the gingival crevice, Disease of endodontic origin manifested by endodontic lesions at root apices and anywhere else along the root surface where root canal system exist into attachment apparatus, and excessive occlusal forces acting independently or in conjunction with existing periodontal or endodontic disease. If a combined Endodontic and periodontal problem exists, a combined therapy is required for the health of the attachment apparatus 9. The clinical course of the disease involving the pulpo-periodontal complex is dictated by the bacterial aetiology and thereby the treatment plan is decided. Other factors such as patient co-operation restorability and economics will influence the treatment decisions. However the primary goal of all treatment efforts must be to rid the patient of the infection 10.

PATHWAYS OF COMMUNICATION

Pulpal and periodontal tissues are closely related and the disease transmission between these two lesions has been demonstrated by many studies which showed significant microbiological similarities between infected root canals and advanced periodontitis15,16,17,18 (Tanner et al, 1982; Kipioti et al, 1984; Trope et al, 1988; Kerekes and Olsan, 1990).
Other than these microbial findings, similarities in the composition of cellular infiltrates also suggest the existence of communication between the pulp and periodontal tissues (Bergenholtz et al, 1983). Thus these findings infer that cross-contamination between the pulp and the periodontal tissue is possible.
There are two forms of possible pathways for bacteria and their products connecting the two tissues:
  • Anatomical
  • Non physiological10


I. ANATOMICAL PATHWAYS
These can be further divided into two groups
  • Vascular
  • Tubular

Vascular Pathway - The pulp and periodontium are derived from the highly vascular mesenchymal tissues of the tooth germ. The blood supply maintains a connection between these tissues via the apical foramen and lateral canals throughout the development of the tooth

Apical foramen - The apical foramen is the principal and the most direct route of communication between the periodontium and pulp. The apical foramen decreases in size as the proliferation of the Hertwig’s root sheath continues. The blood supply of the periodontium is derived from the inferior and superior alveolar arteries and reaches the periodontal ligament from three sources:-
  1. Apical vessels
  2. Penetrating vessels from the alveolar bone
  3. Anastamosing vessels from the gingiva19

In all single-rooted teeth the blood supply of the individual periodontal ligament is greatest in the gingival third and least in the middle third20. In multirooted teeth, the supply is similar in the middle and apical thirds. Although periodontal disease has been shown to have a cumulative damaging effect on the pulp tissue, total disintegration of the pulp is only a certainity if bacterial plaque involves the main apical foramina, compromising the vascular supply 21.
Following necrosis of the pulp, various bacterial products like enzymes, metabolites, antigens etc, reach the periodontium through the apical foramen, initiating and perpetuating an inflammatory response there. This results in destruction of periodontal tissue fibers and resorption of adjacent alveolar bone. External resorption of cementum can occur concurrently.

Lateral canals - In addition to these main avenues of communication, there is a multitude of branches connecting the main root canal system with the periodontal ligament. These root canal ramifications were first described some 100 years ago by Preiswerk (1901), Fisher in 1907 and have since been subdivided into furcated, collateral, lateral, secondary, accessory, intercanal and reticular canals by DeDeus 1975, as well as furcation canals by Vertucci and Williams in 1974.
Now this is termed as ‘accessory canal’ for any ramification that connects the root canal system to the periodontal ligament10. As the root develops, ectomesenchymal channels get incorporated, either due to dentine formation around existing blood vessels or breaks in the continuity of the Hertwig’s root sheath, to become accessory or lateral canals4. The majority of accessory canals are found in the apical part of the root and lateral canals in the molar furcation regions. Although these canal ramifications are most frequently found in the apical third of the root (17%) and least at the base of the root (1.6%), the body of the root has the second highest percentage (8.8%)22.
Another important region is the molar furcation area since most regenerative procedures are performed at these locations. According to early studies in molars, 59% patent lateral or accessory canals were present in the coronal and middle thirds of the roots23 and more than one canal was found at trifurcation and bifurcation areas24.
The glossary of American Association of Endodontics (Cohen, 1984) makes the distinction that lateral canals run perpendicular to the main canal whereas accessory canals branch off and run parallel to the main canal25. Bender, Seltzer and their research associates7 stated that periodontal endodontic combination problems were much more frequent in posterior teeth particularly in molars, than in anterior teeth because of the greater number of auxillary and furcation canals present in molars. The percentage of lateral canals in the furcation is 46% in first molars26 and 50 to 60% in any multirooted teeth23.
Lateral canals normally harbor connective tissue and vessels which connect the circulating system of the pulp with that of the periodontal ligament. In some instances the lateral or accessory canal is obliterated by calcification, but patent communications of varying sizes (10 - 250m) may remain in many cases.
Radiographically, it is seldom possible to identify lateral canals unless they have been filled with a contrasting root filling material following endodontic therapy. The radiographic indications of the presence of lateral canals before obturation are:
  1. Localized thickening of periodontal ligament on the lateral root surface and
  2. A frank lateral lesion.

It is important that the dentist recognizes and be familiar with canal ramifications and variations. The ideal treatment of periodontal pocket formation associated with untreated accessory root canals is total debridement and total obturation of the root canal system9.

Tubular pathway – comprises of dentinal tubules which contain cytoplasmic extensions, the odontoblastic process that extends from the odontoblast at the pulpal dentin border to dentino-enamel junction or cemento-dentinal junction. They also contain tissue fluid and nerve fibers.



II. NON PHYSIOLOGICAL PATHWAYS

Iatrogenic root canal perforations are serious complications during dental treatment by powered rotatory instruments. Improper manipulation of endodontic instruments can also lead to a perforation of the root10.
The second group of artificial pathways between periodontal and pulpal tissues are vertical root fractures, caused by trauma which occurs in both vital and non-vital teeth. Vertical root fractures can be a continuation of coronal fractures as in ‘cracked tooth syndrome’. Incidence of root fractures is more in roots that were filled with lateral condensation technique and teeth restored with intra canal posts10.

ETIOLOGIC FACTORS CONTRIBUTING TO PERIO-ENDO LESIONS
Etiologic factors contributing to perio-endo lesions are:-

A. Live Pathogens
They include bacteria, fungi and viruses. These pathogens and their by products affect the periodontium and they need to be eliminated during root canal treatment.

a. Bacteria The periapical tissues become involved when bacteria invade the pulp, causing either partial or total necrosis. Apical periodontitis, an inflammatory process around the apex of a tooth root, is primarily a sequel to microbial infection of the pulp. Authors suggested that endodontic infection in molars associated with periodontal disease may enhance periodontitis progression by spreading pathogens through accessory canals and dentinal tubules. Rupf.S et al detected Actinobacillus actinomycetemcomitans, Tannerella forsythus, Eikenella corrodens, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia and Treponema denticola in all endodontic samples as well as in teeth with chronic apical periodontitis and chronic periodontitis.
Spirochetes are another type of microorganisms associated with both endodontic and periodontal diseases. Recent studies demonstrated that the spirochete species most frequently found in root canals are Treponema denticola and Treponema maltophilum. Treponema denticola posess an array of virulence factors associated with periodontal disease and may also participate in the pathogenesis of periradicular disease. Treponema maltophilum has also been frequently isolated from patients with rapidly progressing forms of periodontitis.

b. Fungi (Yeasts) Yeast colonization associated with radicular pathosis has been demonstrated in untreated root caries, dentinal tubules, failing root canal treatments, apices of teeth with asymptomatic apical periodontitis and in periapical tissues. Colonization of candida albicans and other species like Candida glabrata, Candida guillermondii and Candida incospicia and Rodotorula mucilaginosa were detected in root canal, which can penetrate into dentinal tubules. It has been hypothesized that the reduction of specific strains of bacteria in the root canal during endodontic treatment may allow fungal overgrowth in the low nutrient environment.
Fungi may gain access from oral cavity during treatment as a result of poor asepsis. It has been found that approximately 20% of chronic periodontitis patients harbor subgingival yeast, mostly Candida albicans.

c. Viruses There is increasing evidence to suggest that viruses play an important role in both endodontic and periodontal diseases. Gingival herpes virus were associated with increased occurrence of subgingival P. gingivalis, T. forsythus, P.intermedia, Prevotella nigrescens, T. denticola and A. actinomycetemcomitans suggesting that they may play a role in promoting overgrowth of pathogenic periodontal bacteria.
Recent studies by Sabeti et al suggested that human Cytomegalovirus and Epstein Barr virus play a role in the pathogenesis of symptomatic periapical lesions; which can in turn give rise to cytokines and chemokines which has the potential to induce local immunosuppression or tissue destruction.

B. Non-Living Etiologic Agents
Depending on their origin and nature, non living etiologic agents can be either:-
  1. Extrinsic
  2. Intrinsic

a) Extrinsic agents

Foreign bodies are frequently found to be associated with inflammation of the periradicular tissues. These include substances such as dentin and cementum chips, amalgam, root canal filling materials, cellulose fibers from absorbent paper points, gingival retraction cords, leguminous foods and calculus like deposits. A foreign body response may occur to any of these substances and the clinical reaction may be acute or chronic.

b) Intrinsic Agents

a. Cholesterol - The presence of cholesterol crystals in apical periodontitis is a common histopathologic finding which will be dissolved and washed away, leaving behind spaces as cholesterol clefts. They are released by disintegrating erythrocytes of stagnant blood vessels within any periapical lesion, lymphocytes, plasma cells and macrophages, which die in great numbers and disintegrate in chronic periapical lesions. Cholesterol crystals can also induce a typical foreign body reaction.

b. Russell Bodies – These can be found in most inflamed tissues throughout the body including the periradicular tissues. These are small, spherical accumulations of an eosinophilic substance found within or near plasma cells and other lymphoid cells. Recently, large intracellular and extra cellular Russell bodies were found in inflammatory pulpal tissue of carious primary teeth.

c. Rushton Hyaline bodies - They are keratinous in nature, of hematogenous origin and a specialized secretory product of odontogenic epithelium or degenerated red blood cells, found in some odontogenic cyst.

d. Epithelium - Epithelial cell rests of Malassez is found along with lateral and apical periodontal ligament. In many periapical lesions, epithelium is not present and if they persist, they may respond to the stimulus by proliferating to wall off the irritants coming through the apical foramen. The epithelium is surrounded by chronic inflammation and is termed an epitheliated granuloma. The term ‘bay’ cyst has been introduced for 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. Whereas, a ‘true cyst is the completion of the epithelial proliferative lesion.
It is a three-dimensional epithelium-lined cavity with no communication between lumen and the canal system. True cysts must be surgically removed, but bay cysts that communicate with the root canal may heal with non surgical root canal therapy.

e. Charcot – Leyden Crystals (CLC) - They are naturally occurring hexagonal bipyramidal crystals derived from the intracellular granules of eosinophils and basophils. Recent findings support the theory that activated macrophages have a role in the formation of CLC. The presence of CLC can be detected within a periapical lesion that failed to resolve after conventional endodontic treatment.

C. Contributing factors

a. Poor endodontic treatment can result in periradicular lesions.

b. Poor restorations can result in canal re-contamination by microorganisms.

c. Trauma - Trauma to teeth and alveolar bone may involve the pulp and the periodontal ligament. Treatment of traumatic dental injuries varies depending on the type of injury and it will determine pulpal and periodontal ligament healing prognosis. Clinically root fractures may often present mobility of the involved teeth as well as pain on biting. Often, a periodontal defect or a sinus tract is associated with the fractured root. Treatment includes repositioning of the coronal segment and stabilization by splinting for periods of up to 12 weeks, enhance pulpal and periodontal repair.

d. Resorptions - Root resorption is a condition associated with either a physiologic or a pathologic process resulting in a loss of dentine, cementum and/or bone. It may be initiated in the periodontium and affect initially the external surfaces of the tooth (external resorption) or may start within the pulp space (internal resorption). If left untreated, both can progress to involve the adjacent structures. External root resorption may be divided into three main categories:-
  1. Progressive inflammatory resorption, which is caused by stimuli such as pulpal infection and sulcular infection. Practically all teeth with apical periodontitis will exhibit a certain degree of inflammatory root resorption. Removal of the inflamed pulpal tissue and obturation of the root canal system is the treatment of choice.
  2. Invasive root resorption also known as invasive cervical resorption where invasion of the cervical region of the root is predominated by fibrovascular tissue derived from the periodontal ligament. The process progressively resolves cementum, enamel and dentin and later may involve the pulp space. Secondary bacterial invasion into the pulp or periodontal ligament space will cause an inflammation of the tissues accompanied with pain.
  3. Replacement resorption or ankylosis occurs following extensive necrosis of the periodontal ligament with formation of bone on the denuded area of the root surface. This condition is most often seen as a complication of luxation injuries and certain periodontal procedures.

Root perforations may result from extensive carious lesions, resorption or from operator error occurring during root canal instrumentation or post preparation. Treatment prognosis of root perforations depends on the size, location, time of diagnosis and treatment, degree of periodontal damage as well as the sealing ability and biocompatibility of the repair material.
f. Developmental malformations -
Teeth with developmental malformations like invagination or a vertical developmental groove which begin in the central fossa of maxillary central and lateral incisor crossing over the cingulum and continuing apically down can lead to untreatable periodontal condition

PATHOGENESIS OF PERIO-ENDO LESION

The formation of bacterial plaque on denuded root surfaces following periodontal disease has the potential to induce pathologic changes in the pulp through lateral or accessory canals. This process, the reverse of the effects of a necrotic pulp on the periodontal ligament, has been referred to as retrograde pulpitis.
The effect of periodontal lesions on the pulp can result in atrophic and other degenerative changes like reduction in the number of pulp cells, dystrophic mineralization, fibrosis, reparative dentin formation, inflammation and resorption.

Atrophic Changes

The pulp tissue of a periodontally involved tooth has cells which are small and have more collagen depositions, than normal. Following impaired nutrition, the pulp cells slowly degenerate. The death of cell is so gradual that morphologic evidence sometimes appears to be lacking. The cause of these atrophic changes in the disruption of blood flow through the lateral canals, which leads to localized areas of coagulation necrosis in the pulp. These areas are eventually walled off from the rest of the healthy pulp tissue by collagen and dystrophic mineralization.
With slowly advancing periodontal disease, cementum deposition may act to obliterate lateral canals before pulpal irritation occurs. This may explain why not all periodontally involved teeth demonstrate pulpal atrophy and canal narrowing. Pressure atrophy may also occur because of the mobility of these periodontally involved teeth.

Inflammatory Changes

The causative agents of periodontal disease are found in the sulcus and are continually challenged by host defenses. The response to bacteria is immunologic or inflammatory and periodontium is replaced with granulomatous tissue infiltrated with defensive cells. In contrast, necrotic pulp is not accessible to host defenses and contains very potent irritants that cause pathologic changes. When periodontal disease extends from the gingival sulcus towards the apex, the inflammatory products attack the elements of periodontal ligament and surrounding alveolar bone.
A clear cut relationship between progressive periodontal disease and pulpal involvement, however, does not invariably exist. The most common periodontal lesion produced by the pulp disease is the localized apical granuloma. It is produced by the diffusion of bacterial products through the root apex, with the formation of vascular granulation tissue. Subsequently, resorption of alveolar bone and occasionally of the root itself may occur.

Resorption

Resorption of the sides of the roots is frequently found adjacent to the granulation tissue overlying the roots. When the periodontal lesions are deep, resorption may also be found within the root canals, often opposite lateral canals, and at the apical foramen.
Since this resorptive process extends into the dentin peripherally towards the pulp, and the activating factors are produced from the periodontal lesion, a name which reflects the etiology of this phenomenon, peripheral inflammatory root resorption (PIRR), was proposed (Gold and Hasselgren, 1992).

Effects of Periodontal Treatment Procedures on the Dental Pulp

1. Scaling and root planing -
It not only removes the bacterial deposits but also improper root planing procedure can remove cementum and superficial parts of dentin. Therefore, dentinal tubules will be exposed and normally left unprotected to the oral environment. Subsequent microbial colonization of the exposed root dentin may result in bacterial invasion of the dentinal tubules. As a consequence, inflammatory lesions may develop in the pulp. The initial symptom is sharp pain of rapid onset that disappears once the stimulus is removed. The condition is termed dentine hypersensitivity. The increase in pain intensity may have one or both of the following two explanations. Firstly, the smear layer formed on the root surface by the scaling procedures will be dissolved within a few days. This in turn will increase the hydraulic conductance of the involved dentinal tubules and decrease the peripheral resistance to fluid flow across dentin. Thereby pain sensations are more readily evoked. Secondly, open dentinal tubules serve as pathways for diffusive transport of bacterial elements in the oral cavity to the pulp, which is likely to cause a localized inflammatory pulpal response. An essential component of increasing root sensitivity that patient’s experience after an instrumentation procedure in periodontal therapy is likely to be related to a peripheral sensitization of pulpal nociceptors due to release of inflammatory mediators.
2. Acid etching
Acid etching by using citric acid during periodontal soft tissue reattachment therapy helps to remove bacterial endotoxin and anaerobic bacteria and to expose collagen bundles to serve as a matrix for new connective tissue attachment to cementum. Though beneficial in the treatment of periodontal disease, citric acid removes the smear layer, an important pulp protector. Coton and Siegel reported that citric acid when applied to freshly cut dentine has a toxic effect on the human dental pulp. Kitchings et al concluded that the mechanical procedures are more responsible for pulpal changes than the application of citric acid for 3 minutes.

REFERENCES
 
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  6. Chen SY, Wang HL, Glickman G N. The influence of endodontic treatment upon periodontal wound healing. J Clin Periodontol 1997: 24: 449.
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