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| INVITED REVIEW |
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| Year : 2013 | Volume
: 3
| Issue : 1 | Page : 2-11 |
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Endo-perio lesion: A dilemma from 19 th until 21 st century
Abhishek Parolia1, Toh Choo Gait2, Isabel C. C.M. Porto3, Kundabala Mala4
1 Faculty of Dentistry, Divison of Oral Clinical Sciences, International Medical University, Kuala Lumpur, Malaysia
2 School of Dentistry, International Medical University, Kuala Lumpur, Malaysia
3 Department of Restorative Dentistry, Cesmac University Center, Maceió, Alagoas, Brazil
4 Department of Conservative Dentistry and Endodontics, Manipal College of Dental Sciences, Manipal University, Mangalore, Karnataka, India
| Date of Web Publication | 25-Oct-2013 |
Correspondence Address:
Abhishek Parolia
Faculty of Dentistry, Divison of Oral Clinical Sciences, International Medical University, Kuala Lumpur, Malaysia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2229-5194.120514
 Abstract | | |
The interrelationship between endodontic and periodontal diseases has been a subject of speculation, confusion and controversy for many years. Pulpal and periodontal problems are responsible for more than 50% of tooth mortality today. An endo-perio lesion can have a varied pathogenesis which ranges from quite simple to relatively complex one. These lesions often present challenges to the clinician as far as diagnosis and prognosis of the involved teeth are concerned. It is very essential to make a correct diagnosis so that the appropriate treatment can be provided. To make a correct diagnosis the clinician should have a thorough understanding and scientific knowledge of these lesions and may need to perform restorative, endoontic or periodontal therapy, either singly or in combination to treat them. Therefore, this presentation will highlight the diagnostic, clinical guidelines and decision-making in the treatment of these lesions from an Endodontist's point of view to achieve the best outcome.
Clinical Relevance to Interdisciplinary Dentistry
- Perio-endo lesions are very complex in nature and can have a varied pathogenesis.
- Treatment decision-making and prognosis depend primarily on the diagnosis of the specific endodontic and/or periodontal diseases.
- To have the best prognosis, clinician should refer the case to various areas of specialization, to perform restorative, endodontic or periodontal therapy, either singly or in combination. Therefore, to achieve the best outcome for these lesions, a multi-disciplinary approach should be involved.
Keywords: Diagnosis, endo-perio lesions, management
How to cite this article:
Parolia A, Gait TC, Porto IC, Mala K. Endo-perio lesion: A dilemma from 19 th until 21 st century. J Interdiscip Dentistry 2013;3:2-11 |
How to cite this URL:
Parolia A, Gait TC, Porto IC, Mala K. Endo-perio lesion: A dilemma from 19 th until 21 st century. J Interdiscip Dentistry [serial online] 2013 [cited 2023 Mar 28];3:2-11. Available from: https://www.jidonline.com/text.asp?2013/3/1/2/120514 |
| Introduction | |  |
The pulp-periodontal interrelationship is a unique one and can consider them as a single continuous system or as one biologic unit in which there are so many paths of communication. The interrelationship of these structures influences each other during health, function and disease. They can get affected individually or combined; when both systems are involved they are called true endo-perio lesions. Endodontic-periodontal problems are responsible for more than 50% of tooth mortality today. [1] They present challenges to the clinician as far as diagnosis and prognosis of the involved teeth are concerned. It is very essential to make a correct diagnosis so that the appropriate treatment can be provided. The relationship between the periodontium and the pulp was first discovered by Simring and Goldberg in 1964. [1] Since then, the term 'perio-endo lesion' has been used to describe lesions due to inflammatory products found in varying degrees in both periodontium and pulpal tissues.
The pulp and periodontium have embryonic, anatomic and functional interrelationship. There are various pathways for the exchange of infectious elements and irritants from the pulp to periodontium or vice versa, leading to the development of endodontic periodontal lesions. [2],[3]
Pathways of developmental origin (anatomical pathways):
- Apical foramen, accessory canals/lateral canals
- Congenital absence of cementum exposing dentinal tubules
- Developmental grooves
Pathways of pathological origin:
- Empty spaces on root created by Sharpey's fibers
- Root fracture following trauma
- Idiopathic root resorption - internal and external
- Loss of cementum due to external irritants.
Pathways of iatrogenic origin:
- Exposure of dentinal tubules following root planning
- Accidental lateral root perforation during endodontic procedures
- Root fractures during endodontic procedures.
The main etiological factors for endo-perio lesions are living (bacteria, fungi and viruses) and nonliving pathogens. Along with these, many contributing factors such as trauma, root resorptions, perforations, and dental malformations also play an important role in the development and progression of such lesions [4],[5] [Figure 1]. The condition of the pulp is an important factor in susceptibility to microbial invasion. A vital pulp is very resistant to microbial invasion. Penetration of the surface of a healthy pulp by oral bacteria is relatively slow or may be blocked entirely. In contrast, a necrotic pulp is rapidly invaded and colonized by bacteria. When the pulp becomes necrotic, inflammatory byproducts of pulpal origin may leach out through these pathways and initiate/trigger an inflammatory vascular response in the periodontium, cause destruction of periodontal tissue fibers, resorption of adjacent alveolar bone and cementum. Nature and extent of periodontal destruction depends on various factors such as virulence of microorganisms, duration of the disease and the host defense mechanism. Similarly, the reverse of the effect of a necrotic pulp on the periodontal ligament, has been referred to as retrograde pulpitis. [5]
Over the past century, the dental literature has consistently reflected a controversy related to the effect of periodontal disease on the dental pulp. It has been found that the pulp has a quite sophisticated vasculature system with a network of capillary beds, precapillary sphincters and arteriovenous shunts, which provides a significant capacity for the pulp to survive. From clinical observations, it is rare to find a virgin tooth (no decay, restorations, fracture, perforation) with evidence of periapical pathosis for which cause for the pulp becoming necrotic cannot be determined. Many studies have demonstrated that periodontal disease or sequelae of periodontal treatment does not affect the pulp. [6],[7],[8] On the other hand, studies have suggested that the effect of periodontal disease on the pulp is atrophic and degenerative in nature including a decrease in number of pulp cells, an increase in dystrophic calcifications, fibrosis, as well as a direct inflammatory affect. [9],[10],[11] Therefore, periodontal disease and periodontal treatments should be regarded as potential causes of pulpitis and pulpal necrosis'. [12] However, It has been advocated that periodontal disease has no effect on the pulp, unless it extends all the way to the tooth apex, the dental pulp is capable of surviving significant insults and that the effect of periodontal disease as well as periodontal treatment on the dental pulp is negligible. [13]
Though there are many conflicting studies abound, Harrington et al. [14] mentioned another parameter which may influence our clinical impressions related to the dental pulp, and indeed many of our misinterpretations, from early histological observations. They explained the importance of adequate fixation of pulp tissue as it has always been, and continues to be, a challenge, and artifacts resulting from inadequate fixation continue to be described as evidence of pathosis. They recommended careful reviewing of the papers published prior to 1975, as well as some written since if their descriptions of perceived pulp pathosis are in fact simply histological artifacts.
Historically the effect of periodontal disease on the dental pulp has been a source of discussion but recently the effect of pulpal necrosis on the initiation and progression of marginal bone loss has been discussed. [13] The potential effect of a tooth with a necrotic pulp or a tooth with previous root canal treatment has been taken into account as a risk factor in the initiation, progression of periodontal disease, and the resolution of periodontal pockets. Many studies have stated that a pulpless tooth with a periapical lesion promotes the initiation of periodontal pocket formation, progression of periodontal disease, and interferes with healing of a periodontal lesion after periodontal treatment. [15],[16],[17] It has also been found that the periapical trauma may occur by over instrumentation during shaping and cleaning of the root canal, extrusion of irrigants, sealer and gutta percha points that may hinder new bone, cementum and connective tissue repair. Therefore, precautions should be taken when periodontal therapy has to be followed by endodontic treatment.
| Classification of Periodontal-Endodontic Lesions | | |
The first classification of endodontic-periodontal lesions based on pathology of origin was proposed by Simon et al. [18] as follows:
- Primary endodontic lesions
- Primary periodontal lesions
- Primary endodontic lesions with secondary periodontal involvement
- Primary periodontal lesions with secondary endodontic involvement
- True combined lesions.
Though Simon et al. have classified these lesions into five types but actually three, four and five can be considered as combined lesions. There have been many classifications suggested by several other authors such as "independent periodontal and endodontic lesions" [19] or "concomitant pulpal and periodontal lesions" [20],[21] to describe endo-perio lesions. In contrast to combined perio-endo lesions, concomitant pulpal and periodontal lesions reflect the presence of two separate and distinct disease states with different causative factors and with no clinical evidence that one disease state has influenced the other. Recently, von Arx and Cochran [22] proposed a clinical treatment classification of perio-endo-furcation lesions based on the role of membrane application in endodontic surgery. Singh [23] classified endo-perio lesions based on the pathogenesis and added the term iatrogenic lesions, usually endodontic lesions produced as a result of treatment modalities. There are many classifications for endo-perio lesions, but for differential diagnostic purposes, the so-called 'endo-perio lesions' are best classified as endodontic, periodontal, or a combined disease. [24] These lesions can also be classified by treatment depending on whether endodontic, periodontal, or combined treatment modalities are needed. All these classifications are mainly based on the theoretic pathways explaining how these radiographic lesions are formed. Therefore, by comprehensive understanding of the pathogenesis and investigations, the clinician can make a sound diagnosis, formulate an appropriate treatment plan and assess the prognosis of these lesions.
| Diagnosis | | |
Nomenclature distinguishes between lesions caused by periodontal pathogens, as seen in chronic periodontitis, and lesions of the apical periodontal tissues associated with endodontic pathology. When the location is distinct and the lesion is discrete, the two are easy to differentiate. When they simultaneously affect the marginal and apical areas of the periodontium, thus making it essential to ascertain their true cause through differential diagnosis. [25] If a patient has been monitored over a period of time diagnosis of primary endodontic disease and primary periodontal disease usually can be easily done; once the lesions progress to their final stage, they usually give similar clinical and radiographic appearance and the differential diagnosis becomes more challenging. For example, a similar in clinical and radiographic features will be seen with both, a growing periapical lesion with secondary involvement of periodontal tissues and a longstanding periodontal lesion that has progressed to the apex.
It is easier to determine the origin of the lesion when a pulp vitality test is positive because this will rule out an endodontic etiology. However, pulp tests may not be always reliable. This consideration is particularly relevant when challenges to pulpal status arise from periodontal diseases such as partial necrosis of a pulp in a multirooted tooth due to long standing periodontal lesions. If pulpal necrosis is associated with inflammatory involvement of the periodontal tissue, it presents a greater diagnostic problem. In this situation, the location of these pulpal lesions is most often at the apex of the tooth, but they may also occur at any site where lateral and furcal canals exit into the periodontium. [26] Therefore, accurate diagnosis can be made by careful history taking, thorough oral hard and soft tissue examination, the use of pulp testing procedures and periodontal probing. [19]
The following steps help in diagnosing the exact lesion [Table 1].
| Treatment and Prognosis of Endo-Perio Lesions | | |
Treatment decision-making and prognosis depend primarily on the diagnosis of the specific endodontic and/or periodontal disease [Table 2]. The main factors to consider are pulp vitality and the type and extent of the periodontal defect.
Primary endodontic lesions
Primary endodontic diseases usually heal following root canal therapy. The outcome of endodontic treatment is influenced by the presence of microorganisms within the root canal system. Good prognosis is to be expected if treatment is carried out properly with a focus on infection control. The sinus tract extending into the gingival sulcus or furcation area disappears at an early stage once the affected pulp has been removed and the root canals well cleaned, shaped, and obturated. In case of tooth with large periapical lesion, orthograde endodontic therapy has been advised instead of surgical endodontic therapy. [27],[28] Placement of intra-canal medicaments such as calcium hydroxide has found to be very effective in the healing of large periapical lesion. Calcium hydroxide works in many ways, [29] chemically it damages the microbial cytoplasmic membrane by the direct action of hydroxyl ions, suppresses enzyme activity, disrupts the cellular metabolism and inhibits deoxyribonucleic acid (DNA) replication by splitting DNA. Physically it acts as a physical barrier that fills the space within the canal and prevents the ingress of bacteria into the root canal system. It also kills the remaining micro-organisms by withholding substrates for growth and limiting space for multiplication. Biologically it encourages the periapical hard tissue healing around teeth with infected canals, inhibits root resorption and stimulates periapical healing after trauma. [30],[31],[32],[33],[34]
Primary periodontal lesions
Primary periodontal disease should only be treated by periodontal therapy. In this case, the prognosis depends on the severity of the periodontal disease, efficacy of periodontal therapy and patient response; however, prognosis of primary periodontal lesions is not as favorable as primary endodontic lesions. Primary periodontal lesions should be treated by hygiene phase therapy in the first instance. Subsequently, poor restorations and developmental grooves that are involved in the lesion must be removed. Periodontal surgery should be performed after the completion of hygiene phase therapy if deemed necessary. Since, the presence of an intact cementum layer is important for the protection of the pulp and vigorous surgical periodontal procedures may remove cementum and expose dentinal tubules, which in turn transport irritants, thereby cause pulpal inflammation and necrosis of the dental pulp. Therefore, clinicians should take precautions during periodontal therapy and avoid the use of irritating chemicals, minimize the use of ultrasonics and rotary scaling instruments when <2 mm of dentin thickness remaining. Judicious use of periodontal surgical intervention is advantageous to treat this lesions. [35]
Primary endodontic with secondary periodontal lesions [Figure 2]
The treatment and prognosis of the tooth with these lesions are different from those of teeth involved with only primary endodontic disease. The prognosis for treatment of primary endodontic disease with secondary periodontal involvement depends primarily on the severity of periodontal involvement. Tooth with these lesions should first be treated with endodontic and simple hygiene phase therapy. In this case, multi-visit endodontics should be practiced and the placement of intracanal medicament was found to be very useful in reducing inflammation and favoring repair. [36] Treatment results should be evaluated in 2-3 months and only then further periodontal treatment should be considered. This sequence of treatment allows sufficient time for initial tissue healing and better assessment of the periodontal condition. [37],[38] It also reduces the potential risk of introducing bacteria and their byproducts during the initial phase of periodontal healing. In this regard, it has been suggested that aggressive removal of the periodontal ligament and underlying cementum during interim endodontic therapy may adversely affect periodontal healing, therefore, should be avoided. [39] But in cases where healing with only endodontic therapy does not occur then both endodontic and periodontal treatments should be carried out since with endodontic treatment alone, only part of the lesion may heal up to the level of the secondary periodontal lesion. If the endodontic treatment is adequate, the prognosis depends on the severity of the marginal periodontal damage and the efficacy of periodontal treatment. Primary endodontic lesions with secondary periodontal involvement may also occur as a result of iatrogenic damage such as root perforation or fracture during root canal treatment or placement of pins or posts. Root perforations are treated according to their aetiology. The outcome of the treatment 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 sealer. It has been recognized that the success of the treatment depends mainly on immediate sealing of the perforation and appropriate infection control. Several materials such as mineral trioxide aggregate, reinforced zinc oxide-eugenol cementglass ionomer cements and Vitremer have been recommended to seal root perforations. [40],[41],[42] 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. Treatment depends on the tooth type, extent, duration and location of fracture, for example, single rooted tooth with lesions caused by vertical root fracture has a hopeless prognosis and should be extracted [43] while molars can be treated by root resection or hemisection. [44] However, many case reports are described in literature where many innovative techniques to treat and retain anterior teeth have been attempted with varying success. Clinician have either removed the fractured segment or attempted to bond the root using a biocompatible material. [45],[46],[47],[48] Therefore, before considering any complex or extensive restructure treatment, the desirability for retention of the tooth root should be carefully weighed up against extraction and replacement with a denture, bridge or implant. | Figure 2: Primary endodontic lesion with secondary periodontal involvement. (a) Clinical picture showing maxillary right first molar with the presence of palatal swelling with 7mm deep periodontal pocket mimicking primary periodontal lesion. (b) Radiograph showing presence of deep coronal restoration and mesial caries approaching the pulp with periapical radiolucency, confirming primary endodontic lesion. (c) Radiograph showing completion of root canal therapy in maxillary molar with periapical healing. (d) Clinical picture showing complete resolution of periodontal pocket
Click here to view |
Primary periodontal secondary endodontic lesion and true combined lesions
Primary periodontal disease with secondary endodontic involvement and true combined endodontic-periodontal diseases require both endodontic and periodontal regenerative procedures. The success rate of the endodontic-periodontal combined lesion without a concomitant regenerative procedure has been reported to a range from 27% to 37%. [49] Combined lesions can be classified into three types, first, tooth with two separate lesions, one endodontic usually periapical and one periodontal with no communication, second, teeth with a single lesion that involves both endodontic and periodontal pathoses and third, teeth with endodontic and periodontal lesions that were once separate but now communicate. True-combined lesions should be treated initially as primary endodontic lesions with secondary periodontal involvement. Prior to surgery, palliative periodontal therapy should be completed and root canal treatment carried out. The prognosis of true combined lesion is often poor or even hopeless, especially when periodontal lesions are chronic and extensive. The prognosis of combined diseases mainly rests with the efficacy of periodontal therapy. [5] Though, root amputation, hemisection or bicuspidization may allow the root configurations to be changed sufficiently for a part of the root structure to be saved, however, the operator need to consider various factors before root resection such as tooth function, root filling, anatomy, restorability, bone support around the healthy root and patient's compliance. A tooth that requires a root to be resected always needs root canal treatment; therefore, the surgery must be planned with care, particularly with respect to the timing of the root treatment. Ideally, the tooth should be root filled prior to surgery. [36] The prognosis of an affected tooth can also be improved by increasing bony support, which can be achieved by bone grafting and guided tissue regeneration (GTR). These advanced treatment options are based on responses to conventional periodontal and endodontic treatment over an extended time period. These regenerative procedures with the aid of the microscope, in the treatment of combined lesions have been found to have a success rate of 77.5%. [50] GTR therapy was first introduced in 1980's since then both human and animal studies have demonstrated various degrees of regeneration of bone and attachment apparatus. [51],[52] GTR therapy has also been implemented in the endodontic surgeries as a concomitant treatment during the management of the endodontic-periodontal lesions. [53],[54],[55],[56] The decisions and treatment strategy for the application of the regenerative procedures are made at various levels such as pre-surgical, post-root canal treatment, intra-surgical, and post-surgical. Factors influencing treatment outcome should also be considered at each level under patient-specific, defect-specific, and healing categories. [57] The pre-surgical assessment includes establishing and verifying the non-vital status of the pulp, the extent and severity of the periodontal destruction, and therapeutic prognosis of the planned regenerative procedure. Once the therapeutic prognosis of the periodontal regenerative procedure is determined to be favorable, then endodontic therapy should be provided. Root canal therapy helps to reduce the mobility of the involved tooth therefore, after a successful root canal therapy; tooth mobility should be further assessed to determine the necessity for splinting. Cortellini et al. [58],[59] have recommended splinting of the mobile tooth before GTR procedure. The intra-surgical assessment should include morphology of the periodontal defect, defect type, material of choice to fill the defect and augment healing, control of patient's oral hygiene, and wound stabilization. [60],[61] Furthermore, long term follow up is mandatory for these lesions. However, advanced diagnostic tests like cone beam computer tomography to check the conditions of the hard tissues, pulse oximetry for evaluate the true vitality, polymerase chain reaction to identify the specific microbes may add value in proper diagnosis. Cases should be well discussed to achieve good prognosis[Figure 3] and [Figure 4]. | Figure 3: Primary endodontic secondary periodontal lesion. (a) Intraoral periapical radiograph showing root canal treated maxillary left first premolar with radiolucency along the root. Clinically, a deep narrow pocket was found on the mesial aspect of the root suggesting the presence of vertical root fracture. (b) Clinical view of the extracted tooth showing two fractured fragments of the tooth
Click here to view |
 | Figure 4: Patient complained of pus discharge from gums in between central incisors. Patient gave a history mild impact trauma on mandibular anterior 10 years ago. (a) Clinical picture showing the presence of sinus opening in between central incisors. (b) Radiograph of mandibular anterior teeth showing the presence of large radiolucency in between central incisors with a wide base at the apex suggesting primary endodontic lesion (both centrals did not respond to vitality tests). (c) Radiograph showing initiation of root canal therapy and placement of calcium hydroxide as an intracanal medicament. (d) Radiograph showing completion of root canal treatment. (e) Radiograph showing healing after 1 year
Click here to view |
| Conclusion | | |
A perio-endo lesion can have a varied pathogenesis which ranges from quite simple to relatively complex one. To make a correct diagnosis the clinician should have a thorough understanding and scientific knowledge of these lesions. Despite the segmentation of dentistry into the various areas of specialization, a clinician needs to perform restorative, endodontic or periodontal therapy, either singly or in combination. Therefore, to achieve the best outcome for these lesions, a multi-disciplinary approach should be involved.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2]
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