10. Periodontic-Endodontic continnum.pptx

Endo perio lesions

1. Endodontic-Periodontic Lesions: Pathogenesis, Diagnosis, and Treatment Considerations Presented by Dr Anjali Chambole pg II year

2. CONTENTS Introduction History Pulpal Disease Communication Between Dental Pulp And Periodontium Anatomical Communication Routes: Classification Of Pathways Of Communication Between Pulp And Periodontium Etiologic Factors Biologic Effects Of Pulpal Infection On Periodontal Tissues Biologic Effects Of Periodontal Infection On The Dental Pulp Classification Diagnosis And Prognosis Treatment Considerations Effect Of Endodontic Pathosis On Development Of Retrograde Peri-implantitis Summery

3. INTRODUCTION Endo-periodontal lesion is a pathologic communication between the pulpal and periodontal tissues at a given tooth that may occur in an acute or a chronic form The term "endo- perio " lesion has been proposed to describe the destructive lesions resulting from inflammatory products found in varying degrees in both the periodontial and pulpal tissues. The periodontium and dental pulp are inter-linked from embryonic stage. The dental pulp originates from dental papilla and the periodontal ligament originates from dental sac, both of which have a common mesodermal origin. In the late bell stage of tooth formation, the dental sac and dental papilla are separated from each other by epithelial root sheath except at the future apical foramen. At apical foramen, the dental pulp and periodontal ligament communicate with each other.

4. History Turner & Drew(1919) 1st described effect of periodontal disease on pulp Simring and Goldberg in 1964 The relationship between the periodontium and the pulp was first discovered by Simon 1972 : Classification based on etiology. diagnosis, treatment and prognosis Weine 1982 : Based on clinical presentation strategies for each

5. PULPAL DISEASE ETIOLOGIC FACTORS (1) Instrumentation during periodontal, restorative, or prosthetic dentistry; (2) the progression of dental caries; and (3) direct, local trauma such as tooth fracture Of these, dental caries is the most common cause of pulpal disease. studies based on culturing suggest that a mean of five bacterial strains may be cultured from infected root canals. The organisms cultured are predominantly gram-negative anaerobes. As the infective process proceeds, the proportion of strict anaerobic-to-facultative organisms and the total number of bacteria increase

6. COMMUNICATION BETWEEN DENTAL PULP AND PERIODONTIUM During tooth development the dental pulp and periodontium communicate with each other at apical foramen . It is the primary route of communication between the pulp and the periodontium. Along with apical foramen, periodontium communicates with pulp tissues through many Canals or pathways known as the lateral or accessory canals. It is estimated that 30-40% of all teeth have lateral or accessory canals and the majority of them are found in the apical third of the root. One study investigated 1,140 extracted teeth and it was found that 27.4% exhibited accessory canals

7. Dentinal tubules: At the cervical area of the root surface, approximately 15,000 dentinal tubules per square millimeter are present". These tubules may get exposed due to various reasons such as periodontal disease, scaling, root planning, surgical procedures, developmental grooves, and gap joint at the cementoenamel junction. Because of the exposure of these dentinal tubules, there are chances of communication between the periodontium and the pulp chamber. Clinically, this dentinal exposure results in dentinal hypersensitivity

8. ANATOMICAL COMMUNICATION ROUTES: Most common anatomical communication route between pulp and periodontium is palatogingival groove . This developmental groove is commonly found in maxillary lateral incisors. Kogon's investigations show that the groove can be found in cingulum, followed by lateral fossa, cementoenamel junction, and root in decreasing order. He also found that most common location is in the midpalatal area of lingual surface followed by distal and then mesial. Its prevalence ranges from 1.01% to 8.5% independent of the sex. The chances of communication between the pulp chamber and periodontium vary according to the depth of the groove. Deeper the groove more are the chances of endo- perio communication.

9. VERTICAL ROOT FRACTURES: A tooth fracture in which the fracture line is oriented along the long axis of the tooth is called as a vertical fracture. The clinical features of vertical root fracture are mobility of the involved teeth, pain on biting, pain on selective loading of the cusps, discomfort periodontal defect, radiographic bone destruction, and abscess formation.

10. CLASSIFICATION OF PATHWAYS OF COMMUNICATION BETWEEN PULP AND PERIODONTIUM Developmental origin Apical foramen Accessory canals and lateral canals Congenital absence of cementum exposing the dent tubules at the cervical region of teeth Permeability of cementum Developmental grooves Enamel projection and enamel pearls

11. Pathological origin Empty spaces on the root created by the destruction sharpey's fibers . Vertical fractures. Idiopathic resorption-internal and external. Loss of cementum due to external irritants. Iatrogenic origin Exposure of dentinal tubules following root planing. Accidental lateral perforation during endodontic procedure. Root fracture due to endodontic procedure

12. Role of microorganisms in endo- perio lesions One study showed that the bacterial profile of both endodontic lesions as well as in teeth with chronic apical periodontitis and chronic adult periodontitis consisted of Actinobacillus actinomycetemcomitans , Bacteroides forsythus , Eikenella corrodens , Fusobacterium nucleatum , Porphyromonas gingivalis , Prevotella intermedia and Treponema denticola . A study was done for qualitative and semi-quantitative evaluation of bacteria in endo-periodontal lesions using polymerase chain reaction (PCR) and DNA-DNA hybridi - zation . Possible associations of six bacteria ( Parvimonas micra, Fusobacterium nucleatum , Campylobacter rectus, Eubacterium nodatum , Eikenella corrodens and Capno- cytophaga sputigena ), belonging to 'orange' and 'green' complexes were evaluated in endo-periodontal lesions.

13. Kurihara et al. (1995) examined the 200 samples of root canal content and the deepest portion of the periodontal pocket by analyzing their microbiological and immunologic aspects. They observed a significant difference in the microflora of the root canal and periodontal pocket. While the periodontal pocket exhibited a great variety of species, the root canal was limited to Gram-positive coccus, including Peptostreptococcus and Streptococcus, or Gram- positive rods, such as Actinomyces and Rothia .

14. It is well established that the main cause of the periodontal lesions and dental caries is the presence of the bacterial plaque, formed by aerobic and anaerobic microorganisms. These inflammatory lesions cause localized edema and a resulting increase in intra- pulpal pressure and cell death. Increased damage associated with an inflammatory exudate cause the local collapse of the venous part of the local microvasculature. This causes local tissue hypoxia and anoxia resulting in localized necrosis, the chemical mediators of which cause further localized edema, completing the cycle. The inflammatory response then progresses to the periodontal ligament at apical foramen and at the opening of the accessory canals. This results in ’’ retrograde periodontitis’’ BIOLOGIC EFFECTS OF PULPAL INFECTION ON PERIODONTAL TISSUES

15. Bacterial by-products relevant to pulpitis include lactic acid, ammonia, urea, lipopolysaccharide (LPS), and lipoteichoic acid (LTA) Dental pulp capable of managing numerous microbial insults because of extensive intrapulpal lymphatic system.

16. Pulpal inflammatory response induced through various mechanisms by various microbial challenges.

17. With the continuous spread of inflammation, there is localized periodontal destruction associated with various signs and symptoms including, periodontal pocket formation, purulent inflammatory exudates, angular bone loss, swelling and bleeding of the gingival tissues and increased tooth mobility.

18. Abscess formation results from continuous periodontal inflammation, which spreads through the periodontium. The abscess may-drain through a fistula or via the periodontal ligament, with ligament and adjacent bone destruction, which can involve the entire root length

19. BIOLOGIC EFFECTS OF PERIODONTAL INFECTION ON THE DENTAL PULP Periodontal pocket formation along the root surface causes attachment loss. The inflammatory response in the periodontium can involve dental pulp. However, the effect of periodontal disease on the pulp is not as clear-cut as the effect of pulpal disease on the periodontium. The initial effect of periodontal inflammation on the pulp may be degenerative. Fibrosis, calcifications, and collagen resorption have been reported in the pulps of teeth with the long-standing periodontal disease. The progression of periodontal pocket results in the involvement of the root surface. With due course of tin deepened periodontal pocket may result in the involvement of the apical foramen causing pulpal damage. The spread inflammation into the pulp results in "retrograde pulpitis ‘’

20. The root surface is covered by cementum and an intact cementum layer is important for the protection of the pulp from pathogenic agents produced by the plaque bacteria. Certain periodontal procedures like : Rigorous scaling and root planning removes cementum, exposing dentinal tubules. Transport the irritants -exposed tubules may allow bacterial invasion and hence, as a consequence, pulp damage may result. Protection and preservation of dentin surrounding the tooth are also important in preserving the health of the pulp and preventing the ingress of periodontal pathogens.

21. Dentin thickness also contributes to the protection of the pulp. Stanley stated that if a 2-mm thickness of dentin remains between the pulp and an irritating stimulus, little chance of pulpal damage exists. Precautions that can be taken during the course of periodontal therapy - Weine (1) avoid using irritating chemicals on the root surface, (2) minimize the use of ultrasonic scalers when <2 mm of dentin remains, and (3) allow minor pulpal irritations to subside before completing additional procedures.

22. CLASSIFICATION OF PERIODONTAL LESION One of the earliest classifications to classify endo- perio lesions was proposed by Oliet and Pullock (1968) This classification is based on treatment needs and has been used by Grossman. Type I: Requiring endodontic treatment only. Type II: Requiring periodontal treatment only. Type III: requiring combined endo- perio treatment procedures.

23. Weine classified endo- perio lesions into 4 types based on clinical presentation of cases and offered treatment strategies for each type. Type I: Primary endodontic lesions mimicking periodontal disease. Type II: Endodontic lesion in a periodontally involved tooth. Type III: Primary periodontal lesion requiring endodontic treatment for healing. Type IV: Primary periodontal lesion secondarily involving the pulp.

24. The most common classification used to classify endo- perio lesions is Simon's classification. Simon et al. (1972) classified the lesions based on the primary source of infection and its spread through anatomical pathways. \ Type I: Primary endodontic lesions. Type II: Primary endodontic lesions with secondary perio-dontal involvement. Type III: Primary periodontal lesions. Type IV: Primary periodontal lesions with secondary endo- dontic involvement. Type V: True combined lesions.

25. SIMON'S CLASSIFICATION OF ENDO-PERIO LESIONS.

26. AAP 1999 CLASSIFICATION Periodontitis Associated with Endodontic Disease ( i )endodontic- periodontal lesion (ii) periodontal- endodontic lesion (iii) combined lesion.

27. Thank you

28. Primary periodontal lesion

29. Primary endodntic and secondary periodontal lesion

30. Primary periodontal lesion

31. Primary periodontal lesions with secondary endo- dontic involvement

32. Combined lesion

33. Diagnosis of endo- perio lesions diagnosis of an endo- perio lesion is made with the help of Visual examination, palpation, percussion, radiographic examination, and fistula tracking Visual examination : The involved tooth and its associated gingiva are thoroughly examined for the presence of inflammation, ulcerations or sinus tracts. a draining sinus track is associated with the involved tooth, which should be diagnosed by visual examination. Palpation : The mucosa covering the roots and apices of the involved teeth is palpated by applying firm digital pressure with a finger. Any peri-radicular abnormality can be detected by palpation such as swelling and fluctuant abscess collection in the tissue.

34. Percussion : The vertical and lateral percussion should be done to evaluate the periodontal and periapical tissue condition. Tenderness on lateral percussion is positive in periodontal inflammation on the lateral surface of the tooth whereas tenderness on vertical percussion is positive in apical periodontitis. Tooth mobility : Tooth mobility is an indicator of the integrity of periodontal attachment apparatus. In the case of primary endodontic involvement, hypermobility is usually present, which disappears within a week of initiating endodontic therapy. Tooth mobility resulting due to loss of periodontal support in case of periodontal lesion varies according to the severity of periodontal destruction.

35. Radiographs : important role in the determination of location and pattern of bone loss around the involved teeth. In lesion of endodontic origin, the periapical bone loss is evident. In the case of periodontal disease, the crestal bone loss can be seen which extends apically according to the severity of periodontal disease.

36. Pulp testing : In the endodontic involvement of the tooth, the pulp vitality tests such as cold test, electric test, blood flow tests and cavity test provide valuable information regarding the status of the pulp. These results of tooth vitality test are more accurate in teeth with single canal. in case of teeth with multiple canals, the accuracy of pulp vitality tests reduces in determining the presence or absence of vital tissue in the root canals

37. Fistula tracking : A sinus tract is formed for the drainage of inflammatory exudates. It is formed through the structures of minor resistance and open anywhere on the oral mucosa or facial skin. It can be seen in the buccal vestibule in attached gingiva or alveolar mucosa. A fistula tracking is done by inserting a semi-rigid material like a gutta percha cone from its opening in the buccal vestibule until resistance is met (Figure 78.2). After inserting GP cone, a radiograph is taken which shows the exact location of the source of this inflammatory exudate.

38. Prognosis The prognosis of an endo- perio case to a great extent depends on the periodontal status. If the disease is primarily pulpal and there is minimal periodontal involvement, the prognosis is good or excellent. But, if the disease is primarily periodontal with secondary involvement of pulp, the prognosis depends on the status of the periodontium. Reason being in primary endodontic disease, the lesion completely resolves after root canal debridement and disinfection whereas in primary periodontal disease the prognosis depends on the regeneration of lost periodontal support. Secondly, in primary endodontic disease, the tooth mobility subsides within few days after initiation of the treatment, whereas, in primary periodontal disease the mobility may not subside completely due to loss of periodontal support.

39. TREATMENT CONSIDERATIONS General aspect of treatment planning: The prognosis of the involved tooth should be considered before the commencement of any kind of advanced restorative work to treat an endo- perio lesion. Many factors should be considered while determining the prognosis such as whether there is furcation involvement, which needs to be addressed, whether the tooth is restorable after the lesion has been treated and whether the patient is suitable for a lengthy, costly and invasive treatment. If any of these factors are not in favor of prognosis of the tooth, extraction is the treatment of choice. Another rule of thumb is wherever endodontic treatment is indicated with periodontal therapy: the best sequence of treatment is that endodontic treatment should precede periodontal therapy It has been shown that after debridement and disinfection of the root canal, reattachment of the soft tissue after periodontal therapy is improved

40. Treatment of primary endodontic and secondary periodontal involvement: In the majority of cases, the endodontic treatment precedes the periodontal treatment. When the disease is endodontic in origin and periodontal involvement is secondary, endodontic treatment resolves the periodontal disease in most of the cases. Surgical endodontic therapy is not necessary, even in the presence of large peri-radicular radiolucency and periodontal abscesses. Periodontal treatment may not be required in these cases. Despite extensive endodontic treatment, if primary endodontic lesions persist, the lesion may have secondary periodontal involvement or it may be a true combined lesion..

41. there should be an observation period after debridement and disinfection of the root canal system to assess the periodontal healing. Within a couple of weeks, the periodontal pocket depth should reduce and clinical features of healthy gingiva are observed. All the periodontal interventions such as deep scaling and surgical periodontal therapy should be postponed until the result of the endodontic treatment can be properly evaluated If the endodontic involvement is well established, first the root canal therapy is instituted and after the debridement and disinfection of the root canal, calcium hydroxide paste is filled in the canal. Calcium hydroxide has bactericidal, anti- inflammatory and proteolytic property, inhibiting resorption and favoring repair. It also has an inhibitory effect on contamination of root canals from periodontium via patent accessory canals. The tooth is then observed for next 2-3 months and afterward, if required periodontal therapy should be initiated

42. Treatment of primary periodontal and secondary endodontic involvement: When primary periodontal involvement is there with secondary endodontic involvement, the treatment depends on the clinical presentation of the case. In acute pain which is usually of endodontic origin, root canal debridement and disinfection is initiated first. Simultaneously, periodontal therapy is initiated to eliminate the plaque and calculus, thus reducing bacterial load in the periodontium In the case of primary periodontal involvement and initial endodontic involvement, non-surgical periodontal therapy is initiated with scaling and root planing . The root canal therapy is not indicated unless pulp vitality test results show changes. If pulp pathology is suspected, root canal treatment should be initiated along with periodontal therapy. After completion of the non-surgical periodontal therapy, the surgical phase is initiated. Various procedures which can be performed depending on case to case include gingivectomy, apically displaced flap, new attachment techniques, and hemisection or root resection

43. If endodontic treatment has not been done, after completion of the periodontal therapy, the patient is re-evaluated for possible retrograde endodontic problems. In these cases, the prognosis entirely depends upon the success of periodontal therapy. The pulpal reaction to the early periodontal lesion or periodontal treatment is usually in the form of dentinal hypersensitivity which can be treated purely with the periodontal therapy

44. To overcome healing limitations in endo- perio lesions use of purified growth factor to stimulate patients own cells towards a regenerative response has been tested.  The positive impact of PRF on bone healing could be attributed to the angiogenic, proliferative and differentiating effects on osteoblasts of tissue growth factor β and platelet derived growth factor (TGF-β and PDGF) that are present in PRF in high concentrations. This has resulted in promising results, though some potential risk factors are associated with it. The prognosis of the lesion depends on the severity of the disease, efficacy of the therapy and response of the patient.

45. EFFECTS OF ENDODONTIC PATHOSIS ON DEVELOPMENT OF RETROGRADE PERI-IMPLANTITIS Persistence of endodontic bacteria and inflammatory cells commonly facilitates the development of retrograde peri-implantitis or a radiographically evident periapical lesion at the apex of an osseointegrated implant, accompanied by swelling, pain, tenderness, and sinus tract formation. retrograde periimplantitis can occur as a result of overloading or premature loading on the implant contamination of the external surface of the implant upon placement, the presence of preexisting periapical inflammation, endodontic bacteria, inflammatory cells at, near, or adjacent to the site of implant placement shown to play an important role in the development of this condition

46. scenarios exist in which the interaction between the implant and the adjacent tooth may lead to retrograde peri-implantitis. Under circumstances where complications arise during implant placement, overheating of bone during preparation of the implant osteotomy, placement of the implant too close to the adjacent tooth, or altering of the blood supply of the adjacent tooth during implant surgery, the implant placement itself may result in devitalization of the adjacent tooth and subsequent development of peri-implantitis. The presence of persistent or refractory periapical inflammation presence of existing or recurrent periapical disease from an endodontically treated tooth resulting in contamination of the adjacently placed implant.

47. Brisman and colleagues demonstrated several cases in which implants placed adjacent to asymptomatic, endodontically treated teeth exhibiting no clinical or radiographic signs of periapical disease resulted in peri-implantitis, which resolved with surgical intervention.

48. Certain treatment considerations should be taken First conventional root canal therapy should be performed to resolve underlying symptomatic or radiographic endodontic and periapical disease, and endodontic retreatment should be performed to address failure of endodontic therapy. Delaying the placement of an implant after completion of endodontic treatment on an adjacent tooth or increasing the distance between the implant and the adjacent endodontically treated tooth may reduce the likelihood of peri-implantitis. The use of nonmachined surfaced implants may also decrease the chances of implant failure because machined-surfaced implants placed adjacent to or at the site of previous endodontic infection are more likely to result in the development of retrograde peri-implantitis

49. 5. Implant stability is also an important consideration when planning for treatment of retrograde peri-implantitis. Affected implants exhibiting poor stability require removal of the implant, debridement of granulation tissue within the implant osteotomy site, and either placement of bone graft and subsequent implant or immediate placement of a longer or wide implant

50. Conclusion Endodontic-periodontal lesions commonly present a daignostic and treatment dilemma. Sometimes it becomes really difficult to determine the primary source of infection in a combined lesion, i.e. periodontal or endodontic. However, with careful diagnosis and treatment planning, in most of the cases, the involved tooth/teeth can be saved with a good prognosis. Some cases may require only endodontic therapy or periodontal treatment while others may require a combined approach. The re-evaluation of eno-perio cases is essential find out any remaining infection in endodontic or periodontal region. Periodic necessary treatment should be provided to the patient as indicated.

51. References Newman MG, Takie HH, Klokkevold PR, Carranza FA.  Carranza’s Clinical Periodontology.   10 th edition. Newman MG, Takie HH, Klokkevold PR, Carranza FA.  Carranza’s Clinical Periodontology.   13 th edition. Periobasics : A textbook of Periodontics and Implantology 2 nd Edition (Nitin Saroch ) Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: consensus report of workgroup 2 of the 2017 world workshop on the classification of periodontal and peri-implant diseases andconditions : classification and case definitions for periodontitis. J Periodontol 2018;89(Suppl 1):S173–S182. Parolia, et al.: Endo ‑ perio lesion: A dilemma from 19th until 21st century Journal of Interdisciplinary Dentistry / Jan-Apr 2013 / Vol-3 / Issue-1 Kuoch P, Bonte E. Endoperiodontal Lesions and Chicago’s New Classification of Periodontal and Peri-implant Diseases and Conditions. J Contemp Dent Pract 2020;21(7):798–802.

52. Thank you