1. Endo-perio lesions from a different perspective
1st International Online Dental Congress
Endo-perio lesions from a different perspective
Dr. Hany Mohamed Aly Ahmed
B.D.S. – H.D.D. (Endo) – M.Sc.D conv. Ph.D. (Endo)
Senior lecturer of Endodontics, School of Dental Sciences, USM.
Co-organizing chairperson of the first online Endodontic congress.

2. Introduction
The pulp and periodontal inter-relationships, as well as their contribution in the aetiology of some endodontic and periodontal diseases, have been widely investigated.
Literature demonstrates many challenges because of the wide variability in the normal anatomical and pathological communication pathways between the pulp and periodontal tissues.

4. The apical foramen and accessory canals (including lateral and furcation canals) are the most anatomical communication pathways between the pulp and periodontal tissues which serve for vascular, lymphatic, neural and connective tissue communications.
furcation canal
(Ahmed, 2009, 2012, Vertucci 2005)

5. Exposed cervical dentin, where cementum and enamel do not meet at CEJ, can provide tubular communications through patent dentinal tubules (DT). In addition, DT exposure because of physiological root resorption in deciduous molar teeth may play a role in facilitating toxin diffusion.
(Ahmed, 2012)

6. Wassermann et al (1941) proved that the cementum is permeable, and there is a significant amount of minerals transported through the cemento-dentinal junction. In addition, the cellular cementum is able to provide canaliculi communication through the cytoplasmic processes of cementocytes which might be contiguous in some areas with the dentinal tubules.

7. Sharpey’s fibers, which can have an uncalcified central core in the cellular cementum, occasionally create fibrinous communications into the dentin periphery. The breakdown of Sharpey’s fibers would leave a sieve-like surface full of micro-channels that facilitate the invasion of microorganisms and/or their toxins to the underlying dentin.
(Hiatt 1977)
(Dongari et al., 1988)
(Sgupbach et al., 1990)

8. COMMENTARY
It is difficult to interpret the contribution of such minor anatomical landmarks in clinical practice; however, it may give an explanation for some cases when the operator cannot find any etiological factor for the endo-perio lesion, or at least, it shows that the pathogenesis of endo-perio lesions is a complex process that may arise from a number of major and minor pathways.

9. In spite of the good thermal insulating property of dentin, experimental studies have reported the considerable thermal conductivity of radicular dentin and cementum complex during different endodontic procedures that might endanger the periodontal tissues.
(Lipski, 2005)
(Hashem, 2007)

10. The bridge is not the only communication pathway between the two towers!.

11. b) The accessory canals gradually decrease in number.
It is also relevant to note that these anatomical communications are subject to a lot of “dynamic changes” from early root formation and passing through different physiological age change mechanisms. With age:
a) The apical foramen decreases in diameter, and its deviation from the root long axis is increased because of cementum apposition.
b) The accessory canals gradually decrease in number.
c) The radicular dentin becomes less permeable because of the formation of sclerotic dentin.
d) Additionally, the cementum is supposed to become less permeable with age.
(Kuttler, 1955, Stein 1990, Nanci 2008, Kakoli et al., 2009)

12. Severe types of Palato-gingival grooves
Direct
Severe types of Palato-gingival grooves
(Lara et al 2000)

13. Facial radicular grooves
Direct
Facial radicular grooves
(Kerezoudis et al 2003)

14. Extended radicular grooves due to teeth gemination or fusion
Direct
Extended radicular grooves due to teeth gemination or fusion
(Aryanpour et al 2002)

15. Direct
Other causes such as radicular dens invaginatus, structural defects in cellular cementum and dentin dysplasia type I.
radicular dens invaginatus
(Pandey & Pandey 2005)

16. Direct
Disease
Including progressive external root resorption due to infection that can expose the pulp, root perforation due to caries, progressive internal root resorption which may perforate to the external root surface.
Clinically, there is a communication between the internal root resorption and the oral cavity

17. Direct
Trauma
Including non-iatrogenic root fractures such as vertical root fracture resulted from cracked non-endodontically treated teeth, horizontal root fracture due to trauma, trauma induced root resorption, and cemental tears.
HRF
cemental tears
(Cvek et al 2004, Stewart & McClanahan 2006)

18. Direct
Iatrogenic
Iatrogenic causes include root fracture due to procedural errors, accidental perforations, and exposed dentinal tubules due to cemental defects caused by improper hand and ultrasonic scaling.
(Caputo et al 2014)

19. Indirect
There is a possible contribution of accessory disto-lingual roots in the presence of localized periodontal destruction in mandibular molar teeth and this occasion may accelerate the pulp involvement through accessory canals or the apical foramen.
(Huang et al 2007, Sachdeva & Phadnaik 2012)

20. Indirect
Enamel pearls which may cause of plaque accumulation and subsequent periodontal disease in areas showing high incidence of accessory root canals.
(Tabari et al 2011)

21. Indirect
a) Mandibular second molar with a severe periodontal affection and mobility. b) After extraction, a deep radicular groove is identified between the fused mesial and distal roots. c-e) SEM analysis of the radicular groove area revealed multiple accessory canals (white arrows) located near the groove. In addition, some intermittent invaginations have been identified at some areas of the radicular groove (yellow arrows).

22. DYNAMIC IN NATURE
Some pathological communications may reveal different histological patterns according to the healing tissue response. Teeth exhibiting horizontal root fractures can show pulp and periodontal communications through a uniting callus of hard tissue or by the interposition of bone and/or connective tissue or through granulation tissue.
(Heithersay & Kahler 2013)

23. SUMMARY

24. The complexity of these normal anatomical and pathological variations provides a well protected environment to the invading microorganisms.
Microorganisms
(Peters and Peters, 2006, Chivatxaranukul et al., 2008)

25. Classifications of endo-perio lesions
A review of the literature identifies many suggested classifications for endo-perio lesions. Most of these classifications are based on:
Aetiological factors and pathological patterns
Treatment strategies and prognosis.
Aetiological factors, pathological patterns and treatment strategies on the whole.

26. Aetiological factors and pathological patterns:
Simon et al 1972 (most popular)
Class I: Primary endodontic lesion. Class II: Primary periodontal lesion.
Endodontic therapy is only required
Periodontal therapy is only required

27. Aetiological factors and pathological patterns:
Simon et al 1972 (most popular)
Class III: Primary endodontic disease with secondary periodontal involvement.
Endodontic therapy followed by periodontal therapy are required except for few emergency indications or severe calculus. 2 1

28. Aetiological factors and pathological patterns:
Simon et al 1972 (most popular)
Class IV: Primary periodontal disease with secondary endodontic involvement.
Endodontic therapy followed by periodontal therapy are required except for few emergency indications or severe calculus. 1 2

29. Endodontic and periodontal therapies are required
Aetiological factors and pathological patterns:
Simon et al 1972 (most popular)
Class V: True combined lesion. X
Endodontic and periodontal therapies are required Y

30. Aetiological factors and pathological patterns:
Guldener 1985
Weine 1984
Torabinejad & Trope 1996
Rotstein & Simon 2004
Abbott & Salgado 2009
Foce 2011
Pathological patterns and treatment strategies
Oliet & Pollock 1961
Geurtsen 1985
Aetiological factors, pathological patterns and treatment strategies on the whole:
Hiatt 1977

31. DO WE NEED A NEW CLASSIFICATION FOR ENDO-PERIO LESIONS?!!

32. Class I: Synchronous endo-perio lesions
This class refers to the clinical identification of a simultaneous involvement of both the pulp and periodontal tissues by the same aetiological factor. This can be caused by certain traumatic injuries including avulsion and intrusion.

34. Class II: Pulpal lesions with subsequent periodontal involvement
a) Localized pathological pattern
This pattern includes the periodontal rarefaction as a result of pulpal disease. This periodontal involvement can be closed (no communication with the oral cavity) or opened (communication with the oral cavity either by a sinus tract or fistula) with no calculus formation, or opened with the formation of plaque and calculus. The treatment of the latter would require both endodontic and periodontal treatment.
Periodontal affection with a sinus tract formation can be the fate of pulpal necrosis caused by caries.

35. Class II: Pulpal lesions with subsequent periodontal involvement
b) Unilaterally Distributed pathological pattern
Another pattern can be identified in patients with non-functioning sides because of the presence of an untreated endodontically affected tooth with previous history of pain while chewing. If the offending tooth is left untreated, plaque accumulation, calculus formation, and loss of periodontal attachment may proceed to involve the affected and neighbouring mandibular and maxillary teeth at the same non-functioning side.

36. Class II: Pulpal lesions with subsequent periodontal involvement
Uni. Distributed pattern:
Badly decayed mandibular 1st molar with pain on percussion. c, d) Gingival inflammation and calculus formation of mandibular and maxillary posterior teeth were identified at the same side. e) On the contrary, the gingival and periodontal tissues were healthy in the non affected side.

37. Class III: Periodontal lesions with subsequent pulpal involvement
a,b) Severe chronic periodontitis of a non carious and non cracked maxillary 1st molar with severe and continuous pain.  c) RCT resulted in relief of symptoms. Post-operative radiograph shows three patent accessory canals filled with the root canal sealer.

38. Class IV: Independent endo-perio lesions

39. Class V: Iatrogenic endo-perio lesions
Orthodontic treatment could be suspected as an etiological factor for simultaneous pulp and periodontal affections.

40. Class V: Iatrogenic endo-perio lesions

41. Class VI: Advanced endo-perio lesions
Yellow arrow
White arrow

42. Class VI: Advanced endo-perio lesions
Yellow arrow
White arrow

43. Class VII: Indefinite endo-perio lesions
a) A maxillary 1st molar with severe chronic periodontitis and mobility. b, c) After extraction and root sectioning, an unprepared isthmus (black arrow) and a missed 2nd mesio-buccal canal were identified. The role of this missed anatomy in accelerating the progression of the related periodontal disease would be suspected (yellow arrows) but not considered as a definitive etiological factor.

44. THANK YOU!!