Anatomic relationship between pulp and periodontium
In case of endodontic lesions, the pathway of inflammation is through the apical foramen, furcation canals, and lateral accessory canals to the periodontium resulting in a 1 ° endodontic lesion, sometimes progressing toward 2 ° periodontal involvement. In case of periodontal lesions, the progression of periodontitis is by way of lateral canal and apex to induce a 2 ° endodontic lesion. True combined and concomitant endodontic-periodontal lesions are a mixture of the two, and it is difficult to differentiate the primary reason and the source.
10.3.1 Apical Foramen
The pulp and periodontal tissues are derived from 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. The apical foramen is the main and most direct route of communication between the periodontium and the pulp. Although periodontal disease can have a damaging effect on the pulp tissue, total disintegration of the pulp is only possible if bacterial plaque involves the apical foramen, thus, compromising the vascular supply. Following the total necrosis of the pulp, various bacterial products like enzymes, metabolites, antigens, etc. reach the periodontium through the apical foramen, initiating an inflammatory response.
Pulp exposures, periodontitis, and caries lesions are of significant importance in the development of periodontal-endodontic lesions. If these lesions are not well treated and the canals are not disinfected and sealed completely, it may account for the progression of the lesion or even for the endodontic reinfection [12–14].
10.3.2 Lateral Canals
In addition to the apical foramen, there are a number of branches connecting the main root canal with the periodontal ligament. These root canal ramifications were first described nearly 100 years ago and are known as “accessory canals.” As the root develops, ectomesenchymal channels get incorporated, either due to the dentin formation around existing blood vessels or breaks in the continuity of the Hertwig’s root sheath, to become lateral or accessory canals [15]. The term accessory canal is nowadays used to describe any ramification that connects the root canal system to the periodontal ligament [11].
Lateral canals contain connective tissue and vessels which connect the circulating system of the pulp with that of the periodontal ligament. The radiographic indications of the presence of lateral canals are localized thickening of periodontal ligament on the lateral root surface or a frank lateral lesion. The majority of the accessory canals are found in the apical part of the root and lateral canals in the molar furcation region. The percentage of these lateral canals and their frequency on the root surface are as follows: apical third 17%, coronal third 1.6%, and body of the root 8.8% [16]. According to Bender et al., the periodontal endodontic problems were much more frequent in the molars than in the anterior teeth because of the greater number of accessory canals present in the molars.
10.3.3 Dentinal Tubules
(a, b) Dentinal tubules under SEM (Scanning Electron Microscope). (These pictures were taken from the study of Prof Mehmet Omer Gorduysus, pictures were taken in Middle East Technical University, Ankara-Turkey). On the left side, the clean dentinal tubules are seen. Tubules as hollow tubes are very unique pathways between periodontium and pulpal tissues. The cementum does not cover the dentin in the cervical area all the time, and the exposed tubules allow microorganisms and noxious stimuli into the canals. On the right side (b), the smear layer and microorganisms around the dentinal tubules are visible
According to Adriaens et al. [5], the bacteria coming from the periodontal pockets may contaminate the pulp through the dentinal tubules that would be exposed during root planning and scaling, serving as a microorganism reservoir resulting in the recolonization of the treated root surface. In contradiction to this, some studies [18, 19] have stated that because even with the removal of the cementum during the periodontal therapy in the vital teeth, the pulp tissue is protected against the harmful agents through forming reparative dentin. Moreover, the dentinal fluids move toward the exterior surface, thereby reducing the diffusion of the harmful products of the bacteria on the exposed dentin.
10.4 Nonphysiological/Pathologic Pathways
Pathologic pathways between pulp and periodontium
Another way of communication between periodontal and pulpal tissues is vertical root fractures caused by trauma which can occur in both vital and non-vital teeth. The incidence of root fractures is more in the roots that are filled with lateral condensation technique and the teeth restored with intracanal posts [11]. They serve as a bridge for pulp contamination. If the periodontium had a previous inflammation, it may lead to dissemination of the inflammation which can result in pulp necrosis [21].
Mandibular right lateral tooth represents developmental abnormality and related that in the X-ray periapical radiolucency. This is an example for endo-perio lesion-related developmental defects and malformations (from the archive of Prof. Mehmet Omer Gorduysus, author of the chapter)
(a–c) Following the root canal therapy, surgery, and restoration (from the archive of Prof Mehmet Omer Gorduysus, author of the chapter)
In the middle third of the root (tooth 22), an internal resorption was observed radiographically which is communicated to periodontium. Patient had endodontic and periodontal clinical symptoms. The root canal was calcified at the apical third of the tooth. (From the archive of Prof Mehmet Omer Gorduysus, author of the chapter)
The resorption area was obturated with injectable gutta-percha (Obtura II) and followed up. (From the archive of Prof Mehmet Omer Gorduysus, author of the chapter)
Wide-open apex and related infections, coronal leakage and unsuccessful coronal restorations, extrusion kind or rapid orthodontic movements, deep restorations, secondary caries, bone loss of the tooth supporting area, periodontal pockets, unsuccessful endodontic surgical applications, weak retrograde fillings, flora changes during the dental replantation and transplantation, and sinus tracts (fistula) are all possible pathological pathways. Besides these, extruded gutta-percha or posts beyond the apex also create a chronic irritation as foreign material. Amalgam particles, separated particles of absorbent paper cones and other materials, and calculus are extrinsic irritating factors and may cause pathological pathways between endodontium and periodontium.
10.5 Etiopathogenesis
10.5.1 Effect of Periodontal Lesions on the Pulp
High percentage of pulpal inflammation and degeneration has been reported in periodontally involved teeth than in teeth with no periodontal disease [22]. Research shows that periodontal disease has no effect on the pulp till it involves the apex or the periodontal breakdown has exposed an accessory canal to the oral environment [3, 23].
Microbial agents are the main etiologic factors involved in these lesions. 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. Hence, a deleterious effect of periodontal disease on the pulp can occur and produce pulpitis and is often referred as retrograde pulpitis [1].
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. The explanation for atrophic changes is the disruption of blood flow through the lateral canals, which leads to localized areas of coagulation necrosis in the pulp. These areas are subsequently walled off from the rest of the healthy pulp tissue by collagen and dystrophic mineralization. With slowly advancing periodontal disease, cementum deposition may obliterate lateral canals before pulpal irritation occurs. Hence, this is the reason why not all periodontally involved teeth demonstrate pulpal atrophy and canal narrowing.
The causative agents of periodontal disease are found in the sulcus and are continually challenged by host defenses. An immunologic or inflammatory response is elicited in response to this microbiologic challenge. The speed of the pathogenesis increases generally as the immunity and resistance of the patients becomes lower. Noxious stimuli such as chemicals, rubber dam, broaches, local trauma, brushing style, etc., all may increase the “pathogenesis,” and thus the endo-perio interfacing situations may accelerate. Either physiological or pathological pathways come into function and synergize with the help of predisposing factors. This results in the formation of granulomatous tissue in the periodontium. When periodontal disease extends from the gingival sulcus toward the apex, the inflammatory products attack the periodontal ligament and the surrounding alveolar bone. A clear-cut relationship between progressive periodontal disease and pulpal involvement, however, does not 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 the alveolar bone and occasionally of the root itself may occur [24].
As these inflammatory changes increase in intensity, there is clinical evidence of bone loss, pain, infection, and abscess which increases the tooth mobility and leads to sinus tract and fistula formation. These situations may be categorized as acute or chronic or subacute exacerbations or flare-ups and sometimes may be a part of the clinical observations. Besides the individual factors, the pathogenicity of the microorganisms and the virulence are also important.
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 and at the apical foramen. Since this resorptive process extends into the dentin peripherally toward the pulp, and the activating factors are produced from the periodontal lesion, this known as peripheral inflammatory root resorption (PIRR) was proposed [25].
10.5.1.1 Effects of Periodontal Treatment Procedures on the Dental Pulp
Commonly, the teeth become hypersensitive after periodontal procedures like scaling and root planning, gingivectomy or deep curettage, and lengthening of clinical crowns. This may be due to the influence of the periodontal diseases on the status of the pulp. When the periodontal disease extends apically, the cementum gets necrosed or removed, and the dentin or a lateral canal may get exposed. Dentinal tubules get exposed as a result and act as a channel of communication thus irritating the pulp. Root planning and scaling may result in the rupture of the vessels and destruction of the neurovascular bundle in the lateral canals, provoking a reduction of the blood supply and consequently leading to pulp alterations. If less than 2 mm of dentin remains after procedures like scaling and root planning (especially in mandibular anteriors), pulpal changes would occur in the teeth. Thus frequent periodontal procedures of long duration may cause pulpal pain.
The increase in intensity of pain may be explained by one or both of the following two reasons. Firstly, the smear layer formed on the root surface by the scaling procedures will be dissolved within a few days. This, in turn, will 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 [4].
Drugs/chemical agents used for the cauterization of inflamed gingival tissues can also cause damage to the dental pulp via the exposed dentinal tubules.
Root conditioning using citric acid, though beneficial in the treatment of periodontal disease, unfortunately also removes the smear layer, an important pulp protector. Cotton and Siegel reported that citric acid, when applied to freshly cut dentin, has a toxic effect on the human dental pulp [26]. However, several other studies have concluded that pulpal changes after the application of citric acid does not show any significant changes in the pulp [27, 28].
10.6 Pulpal Diseases and the Periodontium
10.6.1 Effects of Endodontic Infection on the Periodontium
It has been demonstrated that intra pulpal infection tends to promote epithelial down growth along a denuded dentin surface. An endodontic infection if untreated is a local modifying risk factor for periodontitis by way of the apex and lateral or accessory canals.
Necrosis of the pulp can result in rapid and widespread destruction of periodontium, the production of radiolucency at the apex of the tooth, in the furcation or at various points along the root. It has been demonstrated that periodontal treatment of teeth with pulpal necrosis and periapical radiolucency resulted in impaired periodontal healing [26]. Retrograde periodontitis caused by pulpal disease is a common cause of severe, localized destruction of periodontal tissues and manifests as periodontal pocket formation, purulent inflammatory exudates, angular bone loss, swelling and bleeding of the gingival tissues, and increased tooth mobility. Therefore, it is essential that pulpal infections be treated first, before undertaking periodontal procedures.
10.7 Classification
- 1.
Primary endodontic lesion
- 2.
Primary periodontal lesion
- 3.
Primary endodontic lesion with secondary periodontal involvement
- 4.
Primary periodontal lesion with secondary endodontic involvement
- 5.
True combined lesion
Diagrammatic representation of endo-perio lesions based on the classification by Simon JH, Glick DH, Frank JL [29]
10.8 Primary Endodontic Lesions
An acute exacerbation of a chronic apical lesion on a tooth with a necrotic pulp may drain coronally through the periodontal ligament into the gingival sulcus [10]. Dental pulp with inflammatory changes is the essential and main reason. Most common causes are traumatic injuries, caries, and restorative procedures.
The necrotic pulp may drain through the apical foramen, lateral canal, or through the accessory canals at the furcal area. This condition may clinically mimic the presence of a periodontal abscess. In reality, however, it would be a sinus tract originating from the pulp that opens into the periodontal ligament. The pocket that forms is narrow and has little or no local factors. Radiographs with gutta-percha cone tracing the sinus tract will point toward the origin of the lesion. Root canal treatment is the treatment of choice. Prognosis is excellent with complete and rapid resolution of the lesion in most cases.
10.9 Primary Periodontal Lesions
Periodontium is the essential and main cause of the process. These lesions are primarily related to the accumulation of plaque and calculus. Pockets may be deep and wide [10]. In this process, chronic periodontitis progresses apically along the root surface. In most cases, pulpal tests indicate a clinically normal pulpal reaction. The prognosis depends on the efficacy of periodontal treatment [10].
10.9.1 Combined Lesions
10.9.1.1 Primary Endodontic Lesions with Secondary Periodontal Involvement
Untreated endodontic lesion results in destruction of periapical alveolar bone and in multirooted teeth bone in the interradicular area. Later drainage into gingival sulcus, plaque and calculus follow path of tract leading to periodontal involvement.
10.9.1.2 Periodontal Lesions with Secondary Endodontic İnvolvement
The apical progression of a periodontal pocket continues till the apical tissues are involved. The pulp may become necrotic as a result of infection entering via lateral canals or the apical foramen. Prognosis is better in molar teeth than in single-rooted teeth [30]. Although the pulp is exposed to bacteria via patent dentinal tubules, it is quite capable of repair and healing. Production of reparative dentin and reduced canal diameter may result, but pulp tissue remains relatively unaffected. Unless periodontal disease has progressed to involve the tooth apex, the effect of periodontal disease on the pulp is negligible.
As mentioned earlier, the treatment of periodontal disease can also lead to secondary endodontic involvement. It is possible for a blood vessel within a lateral canal to be severed by a curette and for the microorganisms to be pushed into the area during treatment, resulting in pulp inflammation and necrosis [10].
10.9.1.3 True Combined Lesions
True combined endodontic periodontal disease occurs less frequently than other endodontic-periodontal problems. It is formed when an endodontic lesion progressing coronally joins an infected periodontal pocket progressing apically [29]. These lesions occur independently of each other and are indistinguishable. The two lesions can either merge or exist separately. Merged lesions form by ongoing marginal attachment loss or by exacerbations of apical periodontitis.
The degree of attachment loss in this type of lesion is invariably large, and the prognosis is questionable. This is particularly true in single-rooted teeth. In molar teeth, root resection can be an alternative treatment. The radiographic appearance of combined endodontic periodontal disease may be similar to that of a vertically fractured tooth.
Features of endo-perio lesions
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