Interrelationship between periodontics and endodontics


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Interrelationship between periodontics and endodontics

  2. 2. Overview. Introduction Influence of pathological conditions in the pulp on the periodontium.  Impact of disease condition in the vital pulp.  Impact of pulp necrosis.  Manifestation of endodontic lesions in the marginal periodontium from lateral canals. Impact of endodontic treatment measures on the periodontium.
  3. 3. Overview.  Root perforations  Vertical root fracture  Influence of periodontal disease on the condition of the pulp  Influence of the periodontal treatment measures on the pulp.  Differential diagnostic considerations.  Treatment strategies for combined endodontic and periodontal lesions.  Conclusion.  References.
  4. 4. Introduction. The fact that the periodontium is anatomically interrelated with the dental pulp by virtual of apical foramina and lateral canals creates pathway for exchange of noxious agents between the two tissue compartments when either or both of the tissues are diseased. Consequently, under certain clinical conditions, diseases in one of the tissue compartments may result in pathological condition in the other.
  6. 6. Impact of disease conditions in thevital pulp. Disease process in the dental pulp frequently involve inflammatory changes. Caries, restorative procedures and traumatic injuries are the most common causes. Any loss of hard tissue integrity, exposing dentin or the pulp directly, may allow bacteria and bacterial products elements present in the oral environment to affect the normal condition of the pulp.
  7. 7. Cont. The resulting inflammatory lesion will be confined and directed towards the source of irritation for as long as the inflammatory defense doesn’t collapse and convert into a destructive breakdown of the pulpal tissue. Occasionally, disruption of the apical lamina dura or widening of the periodontal ligament space may be seen in the perodontium.
  8. 8. Cont. In such instances, typical clinical signs of pulpitis, eg spontaneous pain, thermal sensitivity or tenderness to percussion may or may not be present. It is important to realize that as long as the pulp maintains vitality, although inflamed or scarred, it is unlikely to produce irritants that are sufficient to cause pronounced marginal breakdown of the periodontium.
  9. 9. Cont. Consequently no benefit will be gained from extirpation (pulpectomy) as an adjunct to the treatment of teeth for periodontal diseases.
  10. 10. Impact of pulpal necrosis. Contrary to disease conditions in the vital pulp, pulp necrosis is frequently associated with inflammatory involvement of the periodontal tissue. The lesions are most often located at the apex of the tooth. They may also occur at any site where lateral canals exit into the periodontium.
  11. 11. Cont.. Inflammatory processes in the periodontium associated with necrotic dental pulps have, similar to periodontal disease, an infectious etiology. The essential difference between the two disease entities is their respective source of infection. While periodontal disease is maintained by bacterial accumulation in the dento-gingival region, endodontic lesions are directed towards infectious elements released from the
  12. 12. Cont.. Rarely will established endodontic lesions involve the marginal periodontium, unless they are developing close to the bone margin. A potential pathway for infectious elements in root canal in such instances may be lateral canals.
  13. 13. Manifestations of endodonticlesions in the marginalperiodontium from lateral canals. Inflammatory lesions may develop from a root canal infection at the lateral aspect of the root and in furcation regions of multrooted teeth. The lesions may be induced and maintained by bacterial products, which reach the periodontium through lateral canals. Lesions appear to be rare and do not seem to emerge at a rate that corresponds to the frequency with which lateral canals occur in teeth.
  14. 14. Manifestations of acuteendodontic lesions in themarginal periodontium. Endodontic lesions either do not have overt clinical signs or may present with various acute manifestations of root canal infection. The asymptomatic lesions usually assume a limited extension around the apex, while rapid and extensive destruction that may extend marginally along the attachment apparatus may follow acute exacerbations.
  15. 15. Cont.. Exudation and pus formed in the process may drain off in different directions;  pathways along the periodontal ligament space or  following penetration of the alveolar bone at the apical region with drainage in or near the gingival sulcus/pocket warrant particular attention from a differential diagnostic point of view. In addition to deep pocket probing depths, the accompanying bone lesion may mimic that of periodontitis.
  16. 16. Impact of endodontic treatmentmeasures on the periodontium. When breakdown of periodontal tissue is associated with a root-filled tooth, endodontic etiology should be taken into account, particularly if the root filling is of poor quality. Unfilled spaces in endodontically treated root canals can sustain bacterial growth, and infectious products from these may reach the periodontium along the very same pathways as in an untreated tooth with infected pulp.
  17. 17. Cont.. Endodontic re-treatment may be considered as an adjunct to periodontal therapy when a root canal filling is of poor quality and/or displays signs of periapical inflammation because of the potential that bacterial elements may become disseminated to the periodontium along dentinal tubules exposed by periodontal instrumentation.
  18. 18. Cont.. Periodontal inflammatory lesions may also result from mechanical as well as chemical irritation initiated by root canal treatment. However, medicaments for irrigation and disinfection as well as materials for filling used in modern endodontics are comparatively well tolerated by connective tissues of the periodontium, even if, during treatment, they are forced into the periodontal ligament.
  19. 19. Root perforations. During endodontic treatment, instrumentation can accidentally result in perforation of the root and wounding of the periodontal ligament. Perforations can be made through the lateral walls of the root or through the pulpal floor in multi-rooted teeth.
  20. 20. Root perforation.
  21. 21. Diagram.
  22. 22. Cont.. The clinical course from then depends largely on the extent the wound site becomes infected. If the perforation is more apical along the root, a wound site infection process may first lead to an acute pain condition, including abscess formation and drainage of pus, followed by further loss of fibrous attachment and periodontal pocketing.
  23. 23. Cont.. If an iatrogenic root perforation occurs during instrumentation of root canals, filling of the artificial canal to the periodontium should be carried out without delay to prevent granulation tissue formation and wound site infection.
  24. 24. Cont.. Outcome of treatment depends on how well the wound site can be sealed. The closer the perforation is to the marginal gingiva, the greater the likelihood of proliferation of sulcular epithelium to the perforation site.
  25. 25. Vertical root fractures. Clinical symptoms that are typical of tooth associated infections such as endondontic lesions and plaque-induced periodontitis may also appear at teeth with vertical root fractures.
  26. 26. Cont.. A vertical root fracture is defined as a fracture of a root that is longitudinally oriented at a more or less oblique angle relative to the long axis of the tooth. A vertical root fracture can extend the entire length of a root and then involve the gingival sulcus/pocket area. It may also be incomplete and confined to either coronal or apical ends.
  27. 27. Cont..
  28. 28. Clinical expression. Clinical signs and symptoms associated with vertical root fractures vary hugely. there may be pronounced pain symptoms and abscess formation because of active bacterial growth in the fracture space. In other instances, clinical symptoms may be limited to tenderness on mastication, mild pain, and dull discomfort.
  29. 29. Cont.. A strong indication of a vertical root fracture is sinus tracts occurring at both buccal and lingual/palatal sites. In other instances, a narrow, local deepening of a periodontal pocket in an area not typical for periodontal disease may be the only clinical finding.
  30. 30. Cont.. The diagnosis of a vertical root fracture is often difficult to ascertain because the fracture is usually not readily detectable by clinical inspection unless there is a clear separation of the root fragments. To give a radiographic appearance of the fracture in the absence of separation, the central X-ray beam has to be parallel to the fracture plane.
  31. 31.  A variety of diagnostic procedures should therefore be considered. clinical examination should include measures to make fracture lines visible by application of disclosing solutions, the use of fiber-optic light, inspection by a surgical microscope or endoscope, or by raising a surgical flap.
  32. 32. Treatment consideration. Vertical root fractures that involve the gingival sulcus/pocket area usually have a hopeless prognosis due to continuous bacterial invasion of the fracture space from the oral environment. While there are reports of successful management of fractured teeth by re-attaching the fragments with bonding resin or laser fusing after extraction followed by re- implantation, fractured teeth are normally candidates for extraction.
  33. 33. External root resorption external root resorptions, usually progress without producing clinical symptoms and may therefore go undetected unless observed radiographically. In advanced stages, the surface defect may interfere with the gingival sulcus and thereby initiate an infectious process.
  34. 34. Mechanisms. Two mechanisms are involved in resorption of a hard tissue: (1) a trigger mechanism and (2) a reason for the resorption to continue. Thus, treatment of active root resorption should be directed to eliminate the cause for its continuance.
  35. 35. Cont.. The trigger mechanism in root resorption is a root surface detached from its protective blast cell layer. Detachment may follow any demage to the cementoblastic cell layer. For the resorption to continue, a stimulus is required eg. An infection or a continuous mechanical force such as the one in orthodontic treatment .
  36. 36. Cont.. The treatment of root resorption should be directed towards the cause for the continuance of the resorption, for example removal of infected materials in a root canal or the halt of an orthodontic tooth movement.
  37. 37. diagrams
  38. 38. Clinical presentations. Root resorptions do not cause painful symptoms. Unless a resorptive process is located coronally and is undermining the enamel, giving it a pinkish appearance, the only way to detect and diagnose dental resorption is by means of radiography.
  39. 39.  Only in very late stages, as the resorptive process engages the gingival sulcus, may an infectious process emerge with typical features of a periodontal abscess.
  40. 40. Different forms. There are different forms of external root resorption. The underlying mechanism is understood only for some of them. A genetic link can be seen in certain cases as external root resorptions run in families. There are also instances when only the enamel of an unerupted tooth is resorbed.
  41. 41. Cont.. External resorptions can be caused by precipitation of oxalate crystals in the hard tissues of patients as a result of increased concentration of oxalates in the blood due to kidney failure. Malignant tumors close to a tooth can also cause root resorption
  42. 42. Cont..Root resorption of known etiology are classified as, Surface resorption Replacement resorption associated with ankylosis Inflammatory resorption associated with persistent inflammation in the periodontium adjacent to the resorption site.
  43. 43. Subforms are: • Peripheral inflammatory root resorption (PIRR) • External inflammatory root resorption (EIRR).
  44. 44. Surface resorption. This type of resorption is common, self- limiting, and reversible. In a histologic study of human teeth from individuals varying in age from 16–58 years, only 10% of the teeth showed absence of active resorption or signs of healed resorptions (Henry & Weinman 1951). Resorptions were noted twice as often in older than in young subjects. Another study demonstrated up to 88% of teeth with active or, in most instances, healed
  45. 45. Mechanism. The mechanisms behind surface resorptions are only partly understood. These resorptions are normally initiated in conjunction with a localized injury to the cementoblast cell layer, for example by external trauma or by trauma from occlusion. As clast cells are attracted to the denuded root surface, hard tissue is resorbed for as long as the activating factors are released at the site of injury.
  46. 46. Cont.. The resorptive process then stops within a few days following the disappearance of clast cells along with the defect becoming populated with hard tissue repairing cells leading to cementum repair. The regulating factors governing this process are virtually unknown.
  47. 47. Cont.. Signs of active or healed surface resorptions or both are common in the large majority of teeth of the adult dentition. It is conceivable that minor traumata caused by unintentional biting on hard objects, bruxism, high fillings, etc., cause localized damage to the periodontal ligament and trigger the initiation of this type of resorption.
  48. 48. Cont.. The process is self-limiting and self-healing and no active treatment is required. During orthodontic treatment caution should be exercised and the forces moderated so that the risk of root foreshortening is minimized. When heavy forces are used the involved teeth should be monitored radiographically.
  49. 49. Replacement resorption. This type of resorptive process involves replacement of the dental hard tissues by bone, hence the name. When a surface resorption stops, cells from the periodontal ligament will proliferate and populate the resorbed area. If the surface resorption defect is large, it will take some time before periodontal ligament cells have covered the entire surface.
  50. 50. Cont.. In the interim period osteoblasts from the nearby bone tissue may then arrive first and establish themselves at the resorbed surface. Bone is thus being formed directly upon the dental hard tissue. This results in a fusion between the bone and the tooth substance, which is known as ankylosis. Note that replacement resorption and ankylosis are often erroneously used as synonyms.
  51. 51. Cont.. Clinically, ankylosis is diagnosed by absence of tooth mobility and by a percussion tone that is higher than in a normal tooth. Radiographically, a local disappearance of the periodontal ligament contour may show an initial stage of fusion. However, even in non ankylosed teeth it is not always possible to observe the entire contour of the periodontal ligament.
  52. 52. Cont.. Ankylosis caused by apposition of bone to a root surface is a prerequisite for replacement resorption. The condition may be seen as a form of repair of root surface resorptions. No treatment is available for this condition.
  53. 53. External inflammatoryresorption. The term external inflammatory resorption describes the presence of an inflammatory lesion in the periodontal tissues adjacent to a resorptive process. There are two main forms,  peripheral inflammatory root resorption (PIRR) and  external inflammatory root resorption (EIRR). Both forms are triggered by destruction of cementoblasts and the cementoid.
  54. 54. Cont.. In PIRR, the factor maintaining osteoclast activation is thought to be provided by an inflammatory lesion in the adjacent periodontal tissue. EIRR, on the other hand, receives its stimulus from an infected necrotic pulp.
  55. 55. Cont.. Peripheral inflammatory root resorption (PIRR) and external inflammatory root resorption (EIRR) are two forms of progressive external root resorption associated with persistent inflammation in the periodontal tissues. While the direct cause for progression is not well understood, infectious elements maintaining periodontal inflammation close to a root surface that is not covered by periodontal ligament or epithelium appear to drive PIRR.
  56. 56. Cont.. To remedy the condition it is necessary to remove all resorbing granulation tissue surgically and fill the resorption cavity. In certain cases it may be possible to carry out the treatment from the pulpal side. Regardless of approach, periodontal tissue complications may ensue, including deep pockets and suppuration from such pockets.
  57. 57. Cont.. Treated cases should therefore be monitored by regular clinical/radiographic follow-ups to observe any signs of recurrence and how the periodontal tissue copes. In advanced cases extraction is the only reasonable treatment option.
  59. 59. … The formation of bacterial plaque on detached root surfaces following periodontal disease has the potential to induce pathologic changes in the pulp along the very same pathways as endodontic infection can affect the periodontium in the opposite direction.
  60. 60. Cont… Thus, bacterial products and substances released by the inflammatory process in the periodontium may gain access to the pulp via,  Exposed lateral canals and  apical foramina as well as dentinal tubules.
  61. 61. … A clear cut relationship between progressive periodontal disease and pulpal involvement , however, does not invariably exist. In fact, while inflammatory alterations as well as localized necrosis of pulp tissue have been observed adjacent to lateral canals in teeth exposed by periodontal disease, a number of clinical studies have failed to confirm a direct correlation between periodontal disease and pulp tissue changes .
  62. 62. … It seems that periodontal disease rarely jeopardizes the vital functions of the pulp. Breakdown of the pulp doesn’t occur until the periodontal disease process has reached a terminal state ie. When bacterial plaque involves the main apical foramina. As long as the blood supply through the apical foramen remains intact, the pulp is capable of withstanding injurious elements released by the lesion in the periodontium.
  63. 63. Influence of periodontaltreatment measures on the pulp. Scaling and root planing. Root dentin hypersensitivity.
  64. 64. Differential diagnosticconsiderations. Recognition of pulp vitality is essential for differential diagnosis and for the selection of primary measures for treatment of inflammatory lesions in the marginal and apical periodontium. Deep restorations, dental trauma, endodontic treatment, previous pulp capping, etc, are factors to consider when assessing the need for endodontic Rx.
  65. 65. Cont.. Location, form and extension of radiolucencies as well as clinical symptoms of pain, tenderness, abscess formation, increased probing depth, etc, may not always distinguish a periodontal lesion from an endodontic lesion.
  66. 66. Rx strategies for combinedendodontic and periodontallesions. Rx of combined endodontic and periodontic lesions doesn’t differ from the treatment given when the two disorders occur separately.
  67. 67. Treatment strategies.
  68. 68. CONCLUSION. It should be understood that periodontaldisease may be responsible for the entire lossof the supporting apparatus around a toothand may in addition be the cause of thebreakdown of the pulpal tissue. In such cases endodontic treatment will notcontribute to periodontal healing and theproblem will have to be solved by periodontalRx approach.
  69. 69. … When there is doubt as to whether a lesionin the periodontium is of endodontic orperiodontal origin, or both, the treatmentstrategy previously described may be adhered.
  70. 70. References. Lindhe J, Karring T, Lang NP. Clinical periodontology and implant dentistry, 4th. Ed. Munksgaard 2003, Copenhagen.