Abstract
Lesions of pulpal and periodontal origin may perpetuate from either the infections of dental pulp or periodontium or alveolar bone. This review focuses on interdisciplinary diagnostic approach towards lesions of periodontal or endodontic origin.
Keywords: Endodontic lesions, periodontal lesions, periapical lesions, pulpo-periodontal
INTRODUCTION
The relationship between periodontal and pulpal disease was first described by Simring and Goldberg in 1964.[1] Since then this term has been used to describe lesions due to inflammatory products found in varying degrees in both the periodontium and pulpal tissues.
The differential diagnosis of perio endo lesions has become increasingly important as the demand for complicated restorative work has grown.[1] Neither periodontal nor endodontic treatment can be considered in isolation, clinically, as they are closely related and this treatment must influence the diagnosis and treatment.[2] The controversy concerning the effect of periodontal disease pulp ranges between those who believe that pulpitis or pulp necrosis or both can occur as a result of periodontal inflammation to those who state categorically that pulpal changes are independent of the status of the periodontium.
CLASSIFICATION OF PERIO-ENDO LESIONS
There are four types of perio-endo lesions and they are classified[1] due to pathogenesis:
Endodontic lesions- an inflammatory process in the periodontal tissues resulting from noxious agents present in the root canal system of the tooth [Figure 1a and b]
Periodontal lesions-an inflammatory process in the pulpal tissues resulting from accumulation of dental plaque on the external root surfaces [Figure 2a and b]
True-combined lesions- both an endodontic and periodontal lesion developing independently and progressing concurrently which meet and merge at a point along the root surface [Figure 3a and b]
Iatrogenic lesions- usually endodontic lesions produced as a result of treatment modalities
Figure 1a and b.

Endodontic lesion
Figure 2a and b.

Periodontic lesion
Figure 3a and b.

True-combined lesion
Etiopathogenic anatomic considerations dentinal tubules
Exposed dentinal tubules in area of denuded cementum may serve as communication pathways between the pulp and periodontal ligament.[3] The exposure of dentinal tubules may occur due to developmental defects, disease, or periodontal procedures; these tubules may be denuded of their cementum coverage as a result of periodontal disease, surgical procedures or developmentally when the cementum and enamel do not meet at the cemento-enamel junction (CEJ) thus leaving areas of exposed dentin.[3]
Lateral and 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.[3] Accessory canals in the furcation of molars may also be a direct pathway of communication between the pulp and periodontium.[4] The presence of patent accessory canals is a potential pathway for the spread of bacterial and toxic byproducts, resulting in a direct inflammatory process in the periodontal ligament.[5]
Apical foramen
The apex is also a portal of entry of inflammation byproducts from deep periodontal pockets to the pulp. Pulp inflammation or pulp necrosis extends into the periapical tissues causing a local inflammatory response accompanied with bone and root resorption [Figure 4].[5]
Figure 4.

Diagrammatic representation of anatomical considerations
Pathogenesis
Live pathogens
Bacteria:-Various studies show that the bacteria associated with pulpal and periodontal disease of the same tooth i.e. Actinobacillus actinomycetemcomitans, Tannerella forsythensis, Eikenella corrodens, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia and Treponema denticola.[6] These pathogens were found in both endodontic and periodontal samples. Even the role of oral spirochetes in both perio endo lesions has been well documented. It may be concluded that periodontal pathogens often accompany endodontic infections and support the idea that endodontic-periodontal interrelationships are a critical pathway for both diseases.
Fungi (yeasts) and Viruses: -The presence and prevalence of fungi associated with endodontic disease is well documented in cases of failing root canal treatment, apices of teeth, asymptomatic periodontitis. Majority of the fungi recovered were Candida albicans.[7] Among the predisposing factors for the fungal infection are immunocomprising diseases such as cancer, intra canal medicaments, local and systemic antibiotics, unsuccessful endodontic therapy.
Among the viruses in patients in periodontal disease, Herpes simplex virus is frequently detected in G.C.F. and periodontal lesions. Human cytomegalo virus and E-B virus type1 has also been found.[7]
So there is a need for further stress and importance to use aseptic periodontal and endodontic techniques to maintain the integrity of periodontal and dental hard tissues
Non living etiologic agents
Extrinsic agents
Foreign bodies
Intrinsic agents
Cholesterol
Russell bodies
Rushton hyaline bodies
Charcot – Leyden crystals
Epithelium
Contributing factors
Poor endodontic treatment
Poor restorations
Trauma
Resorptions
External root resorption
Internal root resorption
Developmental malformations
Perforations
Vertical crown and root fracture
Differential diagnosis
Primary endodontic disease
Primary periodontal disease
Combined disease
Primary endodontic with secondary periodontal involvement
Primary periodontal with secondary endodontic involvement
True combined disease
Clinical diagnostic procedures
Visual examination
Palpation
Percussion
Mobility
Radiographs
Pulp vitality test
Blood flow test
Pocket probing
Crack tooth testing
Fistula tracking
Selective anesthetic test
Initial considerations
The prognosis of the tooth should be considered carefully. Considerations include whether there is a functional need for the tooth, whether the tooth is restorable after the lesion is treated, and patient suitability for lengthy, costly, invasive treatment with a need for high patient motivation.[8]
Endodontic lesions
For primary endodontic lesions conventional endodontic therapy alone will resolve the lesion.[1] A review four to six months post-operatively should show healing of the periodontal pocket and bony repair. If primary endodontic lesions persist despite extensive endodontic treatment the lesion may have secondary periodontal involvement or be a true-combined lesion. Primary endodontic lesions with secondary periodontal involvement will not resolve with endodontic treatment alone.[1] The prognosis for primary endodontic lesions is good but worsens in the advanced stages of secondary involvement.[2]
Periodontal lesions
Primary periodontal lesions are treated by hygiene phase therapy in the first instance. Subsequently, poor restorations and developmental grooves involved in the lesion are removed. Early stage periodontal lesions with secondary endodontic involvement, where it may be limited to reversible pulpal hypersensitivity, may be treated by periodontal therapy only. The prognosis of periodontal lesions is poorer than endodontic lesion and is dependent on the apical extension of the lesion.[9]
True-combined lesions
True-combined lesions are treated initially as for primary endodontic lesions with secondary periodontal involvement. The prognosis of a true-combined perio-endo lesion is often poor or even hopeless. The prognosis of an affected tooth can also be improved by increasing bone support by bone grafting and guided tissue regeneration[10]
Iatrogenic lesions
Iatrogenic lesions are also treated in the same way as primary endodontic lesions. Success depends on access to the apical portion of the root canal to enable a seal to be placed. Teeth with lesions caused by vertical root fractures have a hopeless prognosis.[2] Lesions with over-filled root canals can be resolved by periradicular surgery.
CONCLUSION
A perio-endo lesion can have a varied prognosis. Correct diagnosis is important to plan the treatment. This enables the suitable treatment plan; prolonged and unnecessary treatment can be avoided.
Footnotes
Source of Support: Nil.
Conflict of Interest: None declared.
REFERENCES
- 1.Endodontic by John I Ingle. :638–60. [Google Scholar]
- 2.Rotstein I, Simon JH. Diagnosis, prognosis and decision-making in the treatment of combined periodontal-endodontic lesions. Periodontology 2000. 2004;34:165–203. doi: 10.1046/j.0906-6713.2003.003431.x. [DOI] [PubMed] [Google Scholar]
- 3.Ten Cate AR. 4th ed. Mosby; 1994. Oral histology-development, structure and function. [Google Scholar]
- 4.Ammons WF, Jr, Harrington GW. The Periodontic- Endodontic Continuum. Carranza Clinical Periodontology. (9th ed) :840–50. [Google Scholar]
- 5.Pathways of the Pulp, by Stefen Cohen. :651–65. [Google Scholar]
- 6.Jenkins WM, Allan CJ. Guide to periodontics. Wright. (3rd ed) 1994:146–52. [Google Scholar]
- 7.Simon JH, Glick DH, Frank AL. The relationship of endodontic-periodontal lesions. J Periodontal. 1972;43:202–8. doi: 10.1902/jop.1972.43.4.202. [DOI] [PubMed] [Google Scholar]
- 8.Solomon C, Chalfin H, Kellert M, Weseley P. The endodontic-periodontal lesion: a rational approach to treatment. J Am Dent Assoc. 1995;126:473–9. doi: 10.14219/jada.archive.1995.0210. [DOI] [PubMed] [Google Scholar]
- 9.Lindhe J. Clinical periodontology and implant dentistry. Munksgaard. 1997;296:318–51. [Google Scholar]
- 10.Tseng CC, Harn WM, Chen YH, Huang CC, Yuan K, Huang PH. A new approach to the treatment of true-combined endodontic-periodontic lesions by the guided tissue regeneration technique. J Endodontology. 1996;22:693–6. doi: 10.1016/S0099-2399(96)80067-7. [DOI] [PubMed] [Google Scholar]
