Endo Perio Lesions : A Seminar

•         Introduction

•         History

•         Pathways of communication between pulp & periodontium.

•         Classification

•         Diagnosis

•         Primary endodontic lesions

•         Primary endodontic lesions with secondary periodontal involvement.

•         Primary periodontal lesions

•         Primary periodontal lesions with secondary endodontic involvement.

•         True combined lesions.

•         Concomitant pulpal & periodontal lesions

•         Differential diagnosis of Endo Perio Lesions

•         Conclusion

•         References

INTRODUCTION

            The relationship between the pulp and the periodontium has been extensively studied; however, queries regarding the diagnosis, prognosis and treatment are raised time and again. The pathways for the spread of bacteria between pulpal and periodontal tissues have been discussed with controversy. Pulpal infection can drain through the periodontal ligament space and give an appearance of periodontal destruction, termed retrograde periodontitis. Similarly, both pulpal and periodontal infections can coexist in the same tooth, termed combined lesions, where the treatment depends on the degree of involvement of the tissues. Both endodontic and periodontal diseases are caused by a mixed anaerobic infection. This seminar is an attempt to provide a rational approach to the perio–endo/endo–perio question in order to scientifically diagnose and treat these lesions with predictable success..

HISTORY

            Turner and Drew first described the effect of periodontal disease on the pulp in 1918 where they demonstrated changes in the pulp as fibrosis, calcification and cystic degeneration.

            The possibility that periodontal diseases might be related to Pulpal diseases was reported by Colyer (1924) and Cahn (1927) who described structures which are currently termed lateral canals.

            Seltzer and Bender (1963) had done a study on 85 periodontally involved extracted teeth. They found that 37% of periodontally involved teeth without caries or restorations had inflammatory Pulpal changes and approximately 10% had totally necrotic pulps.

            Simring and Goldberg (1964) corned the term ‘retrograde periodontitis’ in which pulpal degeneration products and toxic irritants move towards the apical foramen causing periodontal tissue destruction apically and potentially migrate towards the gingival margin.

            Rubach et al (1965) studied 74 extracted teeth with varying degrees of periodontal disease. Pulpitis originating from periodontitis through accessory canals were shown in five cases and that originating from periapical extension in six instances.

            Chacker (1974) proposed two routes by which injurious agents may gain entrance to the dental pulp.

1) Exposed lateral canals allow direct access of microorganism and their toxic products into the pulp.

2) Dentinal tubules exposed by instrumentation during periodontal therapy. Direct microbial damage to the cementum or diseased cementum can serve as a path of entry into the pulp

            Bender et al (1972) and Lanthleme (1976) suggested that the presence of an intact cementum layer is important for the protection of pulp from toxic elements produced by plaque microbiota. Hence PDL disease and periodontal treatment should be regarded as potential causes of pulpitis and pulp necrosis. Long standing PDL disease develop fibrosis and mineralization. Canals associated with PDL disease were reported to be narrower which is supposed to be reparative process rather than inflammatory response.

.           Langeland (1974) and Bergenholtz & Lindhe (1984) concluded that cumulative effect of periodontal disease has a damaging effect on pulp as indicated by presence of pulp calcification, inflammation or resorption but total pulp degeneration occurs only when apical foramen is infected.

Ross & Thompson (1978), Bergenholtz & Nyman (1984) and Jaoui et al (1995) evaluated patients who presented with advanced periodontal disease, received what was considered to be appropriate periodontal treatrnent and received follow-up maintenance care for periods ranging from 4-24 years. There were 1,623 teeth in the combined studies which were treated for advanced periodontal disease and were assumed to have vital pulps at the completion of treatment and the beginning of the recall period. 4% (67 of 1623 teeth) of these required root canal treatment subsequent to periodontal disease, periodontal treatment & follow-up periodontal care.

Sanders et al (1983) reported that after the use of freeze dried bone allografts, 65% of the teeth that did not have root canal treatment showed complete or greater than 50% bone fill in periodontal osseous defects while only 33% of the teeth which had root canal treatment prior to the periodontal surgical procedure had complete or greater than 50% bone fill.

Many studies have demonstrated significant microbiological similarities between infected root canals and advanced periodontitis. {Tanner et al (1982), Kipioti et al (1984), Trope et al (1988) & Kerekes and Olsen (1990)}.

Belk & Gutman (1990); Jansson, Ehnevid, Lindskog & Blomlof (1993 & 1995) in their series of study suggested that a pulpless tooth periapical lesion with a pulpless tooth promotes the initiation of periodontal pocket formation, promotes the progression of periodontal disease and interferes with healing of a periodontal lesion after periodontal treatment. The presumed pathway is primarily through patent dentinal tubules. The clinical consequences suggested are significantly deeper probing depths, more bone loss, impaired periodontal healing following non-surgical periodontal treatment and enhanced progression of periodontal disease.

Jaoui et al (1995) studied patients with advanced periodontal disease for 5-14 years after completion of active periodontal treatment. Of the 571 teeth that did not have root canal treatment only one tooth (0.175%) required root canal treatment over the 5-14 year recall period.

Ehnevid and Jansson (1998) had concluded that an endodontic infection in the mandibular molars was found to be associated with additional attachment loss in the furcation area and may thus be considered to be one of several risk factor influencing the prognosis of molars in perio lesions.

            Petka (2001) & Wang and Glickmann (2002) have suggested that “Periodontal disease”:

1)      Is a direct cause of pulpal atrophy

2)      Is more deleterious to the pulp than both caries and restorations combined, and

3)      Necrosis, periodontal disease and periodontal treatments should be regarded as potential causes of pulpitis and pulp necrosis.

PATHWAYS OF COMMUNICATION BETWEEN THE PULP AND PERIODONTIUM

They may be classified as follows:

1. Developmental

• Apical foramina
• Lateral / Accessory canals
• Dentinal tubules
• Developmental / Lingual groove
• Root anomalies

Apical foramen

•         Most direct route of communication between pulp and periodontium. Bacteria and inflammatory byproducts may exist 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.

•         Hangeland et al reported that the total histological disintegration of pulp occurs only when apical foramen are infected.

Accessory / Lateral canals

•         In the course of root development strands of mesodermal tissue may get trapped and later become lateral and accessory canals.

•         Endo-perio problems were more frequent in posterior teeth - greater number of auxiliary and furcation canals (Bender and Seltzer).

•         Inflammation progressing from  coronal to apical end involves the furcal area much before the apical area.

•         Furcal  bone being thinner -  resorbs faster.

•         Main radiographic indications for presence of lateral canals:

•         Localized thickening of periodontium on lateral surface of root. 

•         Frank lateral lesions.

•         Persistance of narrow probing defects that do not extend to Apical foramina

Dentinal Tubules

•         Smallest dimension at the periphery and the largest dimension at the pulp.

•         Opening of each small tunnel facing the periodontium is sealed with Cementum.

•         Total density of tubules is significantly lower in the apical root region than in mid root and cervical areas.

•         These tubules may be denuded of their cementum coverage as a result of  periodontal disease, surgical procedures  or developmentally

2. Pathological

• Empty spaces created by destroyed Sharpey’s fibers.
• Root fracture following trauma.
• Idiopathic resorption: Internal or external.
• Cemental agenesis or Hypoplasia.

3. Iatrogenic

• Exposures of dentinal tubules following root planing.
• Accidental lateral perforation during endodontic treatment.

CLASSIFICATION OF ENDO-PERIO LESIONS:

1.      BASED ON TREATMENT PROCEDURES (Oliet and Pollock.1968):

1.      Lesions that require endodontic treatment procedures only :

•         Any tooth with a necrotic pulp and apical glaucomatous tissue replacing periodontium and bone, with or without a sinus tract (chronic periapical abscess)

•         Chronic periapical absess with a sinus tract draining thus passing through a section at the attachment apparatus in its entire length alongside the root.

•         Root fractures, longitudinal and horizontal.

•         Root perforations, pathologic and iatrogenic.

•         Teeth with incomplete apical development and inflamed or necrotic pulps, with and without periapical pathosis.

•         Reimplants, intentional or traumatic.

•         Transplants, auto transplants or allotransplants .

•         Teeth requiring hemisection.

•         Intentional endodontic therapy for prosthodontic consideration.

2.      Lesions That Require Periodontal Treatment Procedures Only :

o   Occlusal trauma causing reversible pulpitis

o   Occlusal trauma plus gingival inflammation resulting in pocket formation.

§  Reversible but increased pulpal sensitivity caused by trauma or, possibly, by exposed dentinal tubules.

§  Reversible but increased pulpal sensitivity caused by uncovering lateral or accessory canals existing into the periodontium.

o   Suprabony or infrabony pocket formation treated with over callous root planning and curettage, leading to pulpal sensitivity.

o   Extensive infrabony pocket formation extending beyond the root apex and sometimes coupled with lateral or apical resorption, yet with pulp that responds within normal limits to clinical testing

3.      Lesions that requires combined endodontic- periodontal treatment procedure

·         Any lesion in group I that result in irreversible relations in the attachment apparatus and requires periodontal treatment.

·         Any lesion in group II that results in irreversible relations in pulp tissue and also requires endodontic treatment.

2. BASED ON ETIOLOGY, DIAGNOSIS, PROGNOSIS AND TREATMENT (Simon’s Classification 1972)

a. Primary endodontic lesion

b. Primary periodontal lesion

c. Primary endodontic with secondary periodontal involvement

d. Primary periodontal with secondary endodontic involvement

e. True combined lesions

3.STOCK (1988) MODIFIED SIMON’S 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.

4.            BASED ON CLINICAL PRESENTATION STRATEGIES FOR EACH. (Weine 1982)

Type 1   -  tooth in which symptoms clinically & radiographically simulate periodontal disease but are infact due to pulpal inflammation and/or necrosis.

Type II  -  tooth that has both pulpal and periodontal disease concomitantly.

Type III – tooth that has no pulpal problem but requires endodontic therapy plus root amputation to gain periodontal healing.

Type IV -  tooth that clinically and radiographically simulates pulpal or periapical disease but infact has periodontal disease.

(Main different between Weine’s and Simon’ s classification is their description of class II cases.)

5. BASED ON POSSIBLE PATHOLOGIC RELATIONSHIPS (Guldener and Langeland 1982):

a. Endodontic – periodontal lesions

b. Periodontal – endodontic lesions

c. Combined lesions

6. BASED ON THERAPY (Grossman’s Classification):

a. Teeth that require endodontic therapy alone.

b. Teeth that require periodontal therapy alone

c. Teeth that require endodontic as well as periodontal therapy.

According to Gerald Harrington (1979), a true endo perio lesion is defined by the following criteria –

•      The tooth involved must be pulpless.

•      There must be destruction of the attachment apparatus from the gingival sulcus to either the apex of the tooth or the area of an involved lateral canal.

•      Both root canal therapy & periodontal therapy must be required in order to

  resolve the lesion.

DIAGNOSIS:

1)      History: A thorough dental history of the onset duration and progress of the problem should be taken signs and symptoms relating to present or past pulpal/ periodontal disease, or present/ past treatment for pulpal or periodontal disease, or a history of trauma to the tooth is important.

2)      Duration: It may give the information regarding extent of pulpal and periodontal tissue destruction to be expected.

3)      Pain: Several aspects of pain should be considered as it differentiates between periodontal & pulpal pathosis. These include the type, intensity, frequency, duration, location and activators of pain. Early pulpitis gives pain on cold, which is mild and of a short duration. As pulpitis advances, heat produces pain that is sharper more severe & of a longer duration. As the inflammation increases in intensity the pain becomes more severe, of longer duration, and is felt with either hot or cold. Finally continuous, severe pain may be felt even at room temperature, suggestive of pulpal degeneration & necrosis.

     Pain from chronic periodontal inflammation is not severe. There may be more soreness or itching present. If severe pain does develop with periodontal lesion, the discomfort may be due to an acute periodontal abscess or a degenerating pulp.

4)      Pulp vitality: It is tested to differentiate between pulpal and periodontal pathosis. The results of various tests (EPT, heat & cold tests) must be interpreted with regard to the individual condition of each tooth, particularly the size & type of restoration present, the amount of secondary dentin formation & the results achieved on so-called normal teeth. Inspite of significant research in Endodontics, the ability to accurately assess the pulpal health within the root canal is still difficult. Research is currently underway to improve diagnostic testing with use of Doppler devices, Pulse-oximetry & even MRI.

5)      Percussion sensitivity: Useful sign of inflammation within the periodontal ligament, but it is not a direct indication of pulpal disease.

6)      Suppuration: It can occur either with periodontal or pulpal pathosis. If associated with periodontal disorder, it may be linked with an acute periodontal abscess, a chronic PDL disease or an acute exacerbation of a chronic disorder. Suppuration in association with pulpal pathosis may be seen with either an acute or a chronic condition such as an acute alveolar abscess or a chronic alveolar abscess draining through a fistula.

7)      Periodontal pockets: If a pocket is present and associated with a tooth of altered vitality, the possibility of a pulpal contribution to the problem should be considered. A pocket that has developed because of irritants, usually is treated initially by removing calculus by supragingival and subgingival scaling. However if degeneration of pulp is a principal cause of the pocket, scaling alone will not improve the condition. The pulpal status needs to be investigated & treated appropriately.

8)      Radiographic observations: The shape, location and extension of a bony lesion may help to complete the diagnosis. Signs of crestal bone loss, furcation involvement & periapical pathology should be sought. In case of a large lesion, placing a gutta-percha point into the pocket or sinus tract may be useful in identifying source.

9)      Mobility

10)  Fistula tracking

In addition, following clinical situations can be identified as a narrow sinus tract type of probing associated with a tooth with vital pulp.

·         A sinus tract through PDL of vital tooth, which comes from adjacent pulpless tooth. Pulpless tooth several teeth away associated with advanced periodontal disease.

·         Developmental grooves associated with a narrow sinus tract on probing.

·         Fused roots of posterior teeth: similar to developmental grooves.

·         Incomplete coronal fractures (Cracked tooth) extending into root of a tooth.

·         Crown root fracture.

·         Spontaneous vertical root fracture.

·         Enamel spurs.

·         Impact trauma resulting in a narrow/wide sinus tract on palatal, of max ant teeth.

·         PDL disease associated with very narrow root especially labial/lingual to mandibular anterior tooth.

PRIMARY ENDODONTIC LESION:

Etiology:

Infection from a necrotic pulp drains into the periodontium to produce a periapical abscess. This remains localized, drains coronally through the periodontal membrane and gingival sulcus, or tracks through the alveolar bone to leave a swelling and a sinus opening in the attached gingiva.

Clinical features:

• Patient has persistent pain rather than discomfort.
• Tooth is non-vital, multirooted tooth shows abnormal response indicating that the pulp is degenerating.
• Sinus tract formation through the periodontium and gingival sulcus.
• Some degree of tooth mobility seen.
• Good mesial and distal bone seen.
• Furcation bone loss present (Grade III through & through)
• Narrow pocket formation.
• Swelling in the attached gingiva.
• Soreness to percussion & chewing.
• Tooth exhibits a large restoration.
• H/O pulp capping/pulpotomy.
• Improper previous RCT.

Treatment:

Root canal Treatment

Recall & reassessment

PRIMARY ENDODONTIC LESION WITH SECONDARY PERIODONTAL PROBLEM:

Etiology:

Untreated or inadequately managed endodontic lesion, become a persistent source of infection to the marginal periodontium.

Clinical features:

• Evidence of pulpal inflammation & necrosis seen.
• Gingival inflammation present.
• Increasing probing pocket depth.
• Evidence of generalized periodontal disease seen.
• Pus & calculus present.
• X-ray shows radiolucency and some amount of crestal bone loss.

Treatment:

• Root canal treatment.
• Retreatment.
• Endoexplorative surgery.
• Periodontal treatment.
• Review.

PRIMARY PERIODONTAL LESION:

Etiology:

Periodontal infection, spreads to involve the periapical tissues. This may be associated with a local anatomic defect such as radicular groove on a maxillary lateral incisor.

Clinical features:

• Localized longstanding discomfort.
• Teeth generally vital.
• Generalized bone loss.
• Calculus & plaque present.
• Possible occlusal trauma.
• Soft tissue inflammation.
• Broad based pocket formation.
• Gingivitis & localized deep pockets with pus and bleeding on probing or application of pressure to gingiva.
• X-ray shows localized bone resorption appearing as horizontal, vertical, furcation or apical defects.

Treatment:

Periodontal treatment

PRIMARY PERIODONTAL LESION WITH SECONDARY ENDODONTIC PROBLEM:

Etiology:

Infection spreads from the periodontium to the pulp causing pulpitis & necrosis.

Clinical features:

• Deep pockets seen.
• H/O extensive periodontal treatment.
• Evidence of pain accentuation seen.
• Tooth gives negative response to vitality testing.
• X-ray picture similar to periodontal lesion showing generally more bone loss.

Treatment:

• Root canal treatment.
• Periodontal treatment / surgery.
• Root resection.
• Hemisection.

TRUE COMBINED ENDO-PERIO LESION:

Etiology:

A periodontal infection coalesces with a periapical lesion of pulpal origin. There are two distinct origins.

Clinical features:

•  Broad base pocket formation with communication with periapical lesion of pulpal origin in a narrow channel.
• May be acute / chronic.
• Very high tooth mobility due to minimal periodontal attachment.
• X-ray shows periapical lesion & large infrabony defect with severe bone loss.
• Evaluate for vertical root fracture.

Treatment:

• Root canal treatment.
• Periodontal treatment.
• Root resection.
• Hemisection.

 

CONCOMITANT PULPAL AND PERIODONTAL LESION

An additional classification has been proposed by Belk and Guntmann (1990) for lesions that may be commonly seen clinically & reflect the presence of two separate and distinct entities.

• Both disease states exist but with different causative factors & with no clinical evidence that either a disease states has influenced the other.
• Situation often goes undiagnosed & treatment rendered to only one diseased tissue in the hope other will respond favorably.
• Both disease processes must be treated concomitantly.

DIFFERENTIAL DIAGNOSIS BETWEEN PULPAL AND PERIODONTAL DISEASE:

	PULPAL	PERIODONTAL
Clinical
Cause	Pulp infection	Periodontal infection
Vitality	Non vital	Vital
Restorative	Deep/Extensive	Not related
Plaque/Calculus	Not related	Primary cause
Inflammation	Acute	Chronic
Pockets	Single narrow	Multiple, wide coronally
PH	Often acidic	Usually alkaline
Trauma	Primary/Secondary	Contributing factor
Microbial	Few	Complex
Radiographic
Pattern	Localized	Generalized
Bone loss	Wider apically	Wider coronaly
Periapical	Radiolucent	Not often related
Vertical bone loss	No	Yes
Histopathology
Junctional epithelium	No apical migration	Apical migration
Granulation tissue	Apical (Minimal )	Coronal (larger)
Gingival	Normal	Some recession
Therapy
Treatment	Root canal therapy	Periodontal treatment

CONCLUSION:

Endo perio lesions present challenges to the clinicians in their proper diagnosis, apt treatment and prognosis of the involved teeth. They have a varied pathogenesis which ranges from quite simple to relatively complex. Knowledge of these diseases is essential in coming to the correct diagnosis and proper treatment plan.