1 Diagnosis and treatment planning for Endo-Perio Lesions. ‘Shab. Introduction Tissues of dental pulp and periodontium are inter-linked from the embryonic stage. The dental papilla (precursor of dental pulp) and the dental sac (precursor of periodontal- ligament)are of a common mesodermal origin. At the late bell stage, epithelial root sheath seperates the dental papilla and dental follicle = precursor of dental pulp and periodontal structures respectively except at the base, the future apical foremen. Therefore, it is natural to expect that any part of periodontium can get affected by pulpal inflammation and vice- versa. Effect of periodiontal tissue disease on pulp was first described in 1918 by Turner and Drew.' They demonstrated that pyorrheoa, i.e. suppurative periodontitis, induced changes in the pulp such as fibrosis, calcification and cystic degeneration. In a study on 85 periodontally involved extracted teeth, Seltzer et al? found 94% of the teeth had some degree of pulpal involvement in the form of inflamma- tion, atrophy or complete nacrosis. Similar findings were reported by Sinnai and Soltanof* and Sharp* However, there were others © ® 7 who believed that disease of periodontal structures have no or minimal influence on the status of Pulp. They argued that even in severe peri- odontal destruction, the pulp of the involved ‘éional Professor Department of Dental Sugary AIMS New Deli 110029, study on 75 white rats documented this. fact. They also found that effect of pulp disease always resulted in inflammation of periodontal structures but changes in the pulp due to Periodontal disease was either proliferation or resorption, very rarely was inflammation and nacrosis observed. Langeland et all, in their experimental study on extracted periodontally involved human teeth, observed that calcification in the Pulp was more prevalent than any conspicu- ous inflammation. It was also seen that as long as the main canal - the major pathway of circulation - is not seriously involved, the entire pulp does not succumb. EFFECT OF PULP ON PERIODONTAL TISSUES : Pulp communicates with periodontal ligament Via the apical foramen, auxillary and furcation canals and dentinal tubules. (Diagram-|). In addition, certain pathological conditions cre- ate abnormal communications between the pulp and periodontal ligament structures like dental caries, attrition, abrasion and erosion, fracture of crown or root, internal and external Toot resorptions and iatrogenic perforations. (Diagram-I!). The first indication of periodontal involvement as a sequelae to a pulp involved, generally a non-vital tooth, is the thickening of Periodontal ligament space at the apical end Toxins, liberated by dead puilpal tissue and bacteria cause inflammation in the apical12 Anatomic Relationship Bstwocn Pulp & Periodontal Ligament. + Denina Tubues, Apical Foramen Diagram + periodontal ligament and microscopic resorp- tion of adjucent alveolar bone and apical cementum. If the irtanat, i.e., the toxic ma- terial is not removed from the pulp space, a definite peri-apical radioluscency is seen due to formation of either abscess, granuloma or a cyst. In acute condition, the acute inflamma- tion in periodontal ligament space in the apical region causes extrusion of tooth in its socket and severe tenderness to purcussion and mobility of the tooth, Sometimes even before the apical luscency, furcation luscency is seen in mutti-rooted pulp involved tooth (Fig. 1). This is due to the presence of accessory canals in furcation area. The inflammation progressing from coronal to apical end, it volves the furcal area much before the apical area. Furcal bone being thinner than: the apical bone resorbs faster. Incidence of furcal canals is reported by different workers rang- ing from 2% to 59% "**, Thus, combined lesions involving both the periodontal and pulpal organs are found much more frequently in posterior teeth than in anterior teeth.'? Furcation luscency is typically found in pulp involved deciduous molars due to presence of large number of furcation canals. Even if Diagram 2 Fig 1: Pulp death under large restoration has resulted in furcal and apical bone loss. Furcal radioluscency is one of the intial signs of pulp disease andresults due to presence of accessory canals/ permeability of the dentin in the floor of the pulp chamber. auxillary canals were not present, the in- creased permeability of the floor of the pulp chember in an infected molar leads to free passage of toxic material from the pulp to the adjucent furcal bone."* eee eases nE run oy ness nner nlrsEN Jen eee abs Sep entey eee ees renee |EFFECT OF PERIODONTAL TISSUES ON PULP: It is a common observation that teeth become hypersensitive after periodontal proceedures like flap operation, gingivectomy, curettage or even after deep scaling. Another common observation is that with gingival recession and lengthening of clinical crowns, due to ageing or otherwise, teeth also become hypersensi- tive. These phenomenons explain the influ- ence of periodontal diseases on the status of pulp. When periodontal disease extends apicallly the cementum is nacrosed or during periodontal procedures the cementum is re- moved, the dentin or an incidental lateral canal may be exposed. Dentin itself, with its open dentinal tubules can provide multiple channels of communications and can irritate the pulp. If less than 2 mm. of dentin remains, after scaling or root planing, as might occure ‘on mesiodistal aspect of mandibular anteriors, pulpal changes would occure. Thus, frequent Periodontal procedures of long duration can “cause pulpal pain. Certain drugs, - specially caustic agents used for chemical cautery of inflammed gingival tissue can also cause pulp damage via the dentinal tubules, If the lateral canal is exposed, it may provide pathway between the oral fluids and pulp. In addition, laceration or severing of lateral blood vessels can cause focal areas of coagulation nacrosis in the pulp. Another pathway for periodontal inflamma- tion to reach the pulp are the furcation canals. Ribach and Mitchell’® have shown that imflammation of periodontal ligament can af- fect the dental pulp via lateral canals. Re- cently, a condition termed as burrowing cer- vical resorption has been attributed to chronic periodontal inflammation’. The resorption occures in the cervical area of the root involv- ing root dentin but resisted by predentin and odontoblasts lining the pulp space. (Fig. 2), Treatment of such lesions requires good 13 Fig. 2 : Burrowing cervical resorption - the case shows a large area ofthe resorption in the cervical ha of the roct. Note the intact walls ofthe root canal passing through the resorption defect. endodontic treatment, followed by surgical exposure of the resporption defect, its’ cau- terization with trichlor acetic acid and eventual obturation with glass-ionomer cement.” DIAGNOSIS Pulpal and periodontal diseases have many common clinical symptoms like swelling of gingiva, pus discharge, pocket formation, fistu- lous tract, tenderness to purcussion and tooth mobility. Radiographically also, itis sometimes ifficult to diagnose the exact etiology of the pathological condition. However, certain clini- calfeatures help to distinguish between lesions of endodontic and periodontal origin. (Table I) Trope et al"* found greater percentage of spirochetes in discharge from the draining sinus in lesions of periodontal origin com- pared to the lesions of endodontic origin. This fact can be used to diagnose lesions of periodontal origin from that of endodontic origin by using dark field microscopy which is easy, fast, economical and reliable.14 Endo-perio lesions are classified differ- ently by different workers. Classification crite- ria include etiological factors, anatomical path- ways, clinical manifestations, and treatment stretegies. under endo-perio lesions, the list becomes far too long. Each of the conditions listed merits indepth inquiry into the etiological factors, clinical TABLE- | Endodontic Origin 1. Pulp non-vita Sharp throbbing pain 3. Swalling in and extending beyond the 4. Tracing the fistulous tract leads to apical region or in the region or in the region of a lateral canal 5. The fistulous tract is narrow and tortuous 6. Mobily in an acute stage_ involving multiple teeth limited to an isolated tooth 7. Bone oss involving costal and furcal | bone ited oan lit and Pullock's classification'® is one of the earliest classification given for endo-perio lesion. Grossman® has used this classifica- tion, which is based on treatment needs of the lesion. According to this classification, endo- perio lesions can be classified into 3 types. Type 1. Requiring endodontic treatment only. Type 2. Requiring periodontal treatment only. Tyep 3. Requiring combined endo-perio treat- ment procedures. According to this classificatiobn, type-1 lesions include practically every endodontic situation including fracture, external and inter- nal resorptions, perforations, replantation, transplantation, and endodontic implants. Though technically correct, as every endodontic lesion communicates with peri- odontal structures, for practical categorization Periodontic Origin 1. Pulp vital except in advanced lesion. 2. Dul, chronic pain, 3. Swelling generally confined toattached mucosa 4, Tracing leads to mid root 5. Due to extensive loss of periodontal structures he fistula is wide in i cervical area and can easily be probed. 6. Generalized mobilty 7. Generalised crestal bone loss either horizontal or vertcle, techniques for management, prognosis and causes for failure, This could dilute the focus on specific lesions described traditionally as Type-1 endo-perio lesions having periodontal, manifestations clinically like discharing sinus, discharge through gingival sulcus, swelling, inflammation of gingiva and mobility. Simon, Glick and Frank® in 1972 gave a classification of endo-perio lesions, based on etiological factors and spread through ana- tomical pathways. They categorised these lesions into five types. Type-|_ Primary endodontic lesions Type-ll_ Primary endodontic lesions with secondary periodontial involvement. Type-lil_ Primary periodontial lesions. Type-lV Primary periodontal lesions with secondary endodontic involvement. Type-V True combined lesions.Weine* in 1982 classified endo-perio lesions into 4 types based on clinical presentation of cases and offered treatment strategies for each. Type-l__Primary endodontic lesions mimicking periodontal disease. Type-ll_ Endodontic lesion in a periodontally involved tooth, Type-tIl__ Primary periodontal lesion requiring endodontic traetment for healing, Type-IV Primary periodontallesion secondarily involving the pulp. The main difference between Simon et al's classification and Weine’s classification is their description of Cl.I! cases. Simon et al describe Cl.ll as primarily endodontic lesions secondarily involving the periodontal tissues due to non-treatment of the involved teeth. But Weine describes Cl.ll lesions as those having endodontic problem in already existing periodontitis. Stock® in 1988 modified Simon et a's classification and omitted CI.V of the classification. He argued that both Cl.ll and class IV lesions in advanced stages can become combined lesions and therefore a seperate class to describe these lesions was not necessary. The diagnostic criteria and treatment phi- losophies for various classes of endo-perio lesion is described Cl.I : Primarily lesions of endodontic origin. (Diagram Ill) 15 Diagram = The teeth typically exhibit symptoms sug- gestive of periodontal lesion like mobility, bone loss in furcal and crestal area, deep Pocket, tenderness to purcussion, chronic draining sinus tract, purulent exudate from gingival sulcus and foul taste Fig.3 For differential diagnosis, patient may not have any periodontal disease in other areas of the mouth. The other feature present may be presence of either a large carious lesion or previous restoration close to the pulp. Fig. 3: Endodontal lesion mimicking a periodontal condition, “The patient had purulent discharge from the gingival sulcus Note crestal bone destruction on the mesial aspect. Conser- vative endodontic treatment alone resuited in complete resolution of the lesion,16 Diagram - IV Upon endodontic treatment these lesions heal rapidly and dramatically unlike periodontal lesions. Fig. 4 (a) : Advanced periodontal destruction in 11 and 12 resulted in pulp involvement of 12, which was tender with ‘grade 2 mobilty. 11 was found to be vital chu (Diagram IV) Lesion primarily of endodontic origin with secondary involvement of periodontal tis- sues or endodontic lesion occuring in periodontally involved tooth. The criteria for diagnosis of C’.II lesions is, that the patient does have periodontal disease in other areas of mouth. If pulp death occures in a tooth already involved in periodontal disease, a Cl.Il lesion develops Generally, in advanced periodontal destruction where more than 2/3rd of alveolar bone loss has occured, pulp demage is invariably found (Fig 4(a) and (b)] the classic example is mandibular anterior teeth. Therefore, it is a wise treatment strat- egy to treat such teeth endodontically, before any periodal prosthesis-like splint is con- structed which would add further insult to the already demaged pulp, Alternatively, if a per- sistent sinus tract draining through the gingi- val salcus is left untreated for long time, it could become an infrabony pocket. Therefore, lenght of time the lesion has persisted in a Fig. 4(b): Endodontic reatmentin 12andflap surgery on 11, 12,21 and22was carried outwhich resulledin considerable improvermentof the symptoms. The case is under follow-upFig. 5 : Class I lesion resulting trom traumatic oblique fracture of the root in middle 1/314. susceptible environment also decides the type of lesion and its management. One of the sunusal conditions in Cl.II lesion is a case of verticle fracture of the root. In root fracture, either accidental or iatrogenic, unnatural, very large communication between pulp and peri- odontal ligament space occures, (Fig.5 and 6) Such cases usually present with diffuse radioluscency around the entire root giving a halo appearence. Prognosis for class II lesions depend on the type and quality of treatment given. Usually both endodontic and periodontal treatment would be required. Periodontal treatment may involve simple procedure such as deep curettage or a full flap surgery. The prognosis for endodontic lesion is superior to that for periodontal lesions. Ingle & Beveridge stated that prognosis of primary periodontal lesions is not as favourable as primary endodontic lesions. Also, it has been seen that bone loss due to endodontic lesion is reversible but irreversible due to periodontal Fig. 6 : Iatrogenic verticl root fracture due to over-zealous instrumentation of the canal, A class Illesion with hopeless: prognosis, esion.* Peri-apical lesion, once healed, does not recur. But periodontal lesion may recur after healing, if proper home-care and maintainence therapy is not followed.” Cll: Primarily periodontal lesion requiring endodontic treatment for periodontal healing.(Diagram-V) Diagram - V18 Fig. 7 (a) : A class Il endo-periodontal lesion. Extensive alveolar destructionbetween 15 and16andmoderate vertcle alveolar boneloss cistalto 16. The case prasentedwithdeep periodontal pockets distal to 15 and 16 and a smallinva-oral sinus on palate, Both teeth were caries tree, Vitaly tested positive for both 15 and 16, CLIII are the lesions of primary periodontal origin but may require endodontic treatment (Fig.7) and sometimes even root amputation to gain periodontal healing, even if no pulp demage is present initially (Fig. 8) Typical example is, severe periodontal defect involving a single root in a multi-rooted tooth. The typical case wil have generalized periodontal disease, sometimes, multiple teeth missing. In such cases abetrent occlusal forces on a single tooth could cause extensive alveolar bone loss around a single root. cliv: Primarily periodontal lesion secondarily involving the pulp (Diagram V1) (Fig. 9) In this type, periodontal lesion is the only or predominant problem secondarily causing endodontic lesion. This overlaps the situa- tions occuring in Cl-ll cases. These lesions present the most difficult diagnostic problem. The symptoms may mimick those arising out of pulpal or peri-apical disease - ike sensitivity to temperature changes, tenderness to purcussion, mobility and swelling. On initiation ‘of endodontic treatment some of these symp- toms also regress to a certain extent, mislead- Fig. 7(b) : Conservative endodontic treatment using calcium hydroxide was done on 16 followed by flap surgery and curettage. Note short root-canal filing due to calcific barrier formation in the apial third. Note Improved alveolar bone condition on distal aspect of 16. Clinically, the sinus had healed and mobilty of 15 had reduced, ing the clinician that an endodontic problem is the cause. For differential diagnosis, presence of gener- alized periodontal disease, failure of probing gutta-purcha point to reach the apex, and presence of pulp vitality are all signs of a periodontal lesion. Unlike class-I lesions which show dramatic improvement with endodontic treatment, class-IV lesions will show no im- provement and will actually deteriorate unless periodontal treatment is also instituted (Fig. 10).Occasionelly, such involvement is seen associated with radicular abnormilities like verticle development groove or an invagi- nation (Fig. 11)It usually starts in central fossa of the crown and run apically for varying distances. The direct communication between oral fluids and deeper structures through these anomalous tracts provide for initiation and sustainence of periodontal disease, which19 Fig, 8 (a) : Extensive alveolar bone destruction around the mesial root of 46, Note the cariously exposed 45 with normal peri-apical condition. gradually involve the pulp. The prognosis for such lesion is poor. Prognosis after combined root-canal therapy and periodontal flap with recontouring of gingival margin, to bring the entire defect at supra-crestal level is uncer- tain. Fig, Primarily a periodontal lesion secondarily involving the pulp - a class IV lesion, Note the deep packet communi cation with the perif-apical area and extrusion of I Endodontic treatment followed by periodontal flap surgery and splinting with the adjucent teeth is the recommended treatment, which was carried out n this case. However, the [prognosis is guarded in such cases. Use of Bone chips or hydroxy apatite implants ofthe defect ay help toimprove the prognosis, Fig (b) : Endodontic reatmentin 45 and 46 andaadisection of the mesial root af 46 was done. The six months follow-up X-ray showing the bone filingin in the mesial root socket, Diagram - Vi20 er Fig. 10 (a) Aninteresting case of class IV endo periodontal lesion of 46 showing a large internal resorption like defect and difuse peri-apical luscency involving the furcal and crastal bone. Note widening of periodontal ligament space along the entire mesial root lenght. Pationt was advised tendodontic treatment and radisection of the distal root However, patientrefused surgery butinsistedon endodontic treatment Fig. 10 (b): Conservative endodontic treatmentwith calcium hydroxide improved the per-apical environment f ha Fig. 10 (c) : One year follow-up X-ray showing extensive destruction of distal alveolar bone. Since the resorpation ddafectin the mid-road was in direct communication with oral fluids (defect being supra alveolar) the periodontal pocket vas self-sustaining, Probably, surgical exposure and seal ing of the defect would have prevented this complication However, patiant had refused surgery at the start of the tueatment and had accepted the outcome, whatever that might be. Fig. 14 (a) This case was referred for apicectomy after ‘endodontic therapy in 11 an 12, Besides a large peri-apical radioluscency, root anomaly was noticed in elation to 11. It appeared as an extra root. Careful probing on lingual side revealed a fine groove traversing upwards from the cingu- lum. The condition seemed untreatable and extraction of 11 was advised. Fig, 11 (b) - Extracted tooth showing a deep groove almost dividing the root upto two third ofthe root-lenght.Where ever endodontic treatment is indicated alongwith periodontal therapy, the best sequence of treatment is that endodontic treatment should precede periodontal therapy. It has been shown that if the toxic materials from the root-canal is removed, reattachment of soft tissues after periodontal surgery is improved.*. Also, ifthe pulp content is removed before periodontal treatment, the problem of sensitivity, sometimes severe and persistant, observed after periodontal treatment, can be avoided. Periodontal treatment may involve flap operation, hemisection, radisection or bicuspidization. The indication for each depend on the type of case presentation. If one of the roots of a multi-rooted tooth is involved in extensive periodontal destruction, the choice of treatment is hemisection and removal of half of the tooth with the diseased root or radisection of the affected root and recontouring of the crown. However, if only furcation area show extensive destruction or _.is perforated by iatrogenic reasons, and both “the roots are healthy and treatable endodontically, then bicuspidization and recontouring of furcal area is the treatment of choice. The common restorative option after all these surgical procedure is to provide cast metal restoration and splinting with adjucent teeth. References : 1. Tumer JH and Drew AH. Experimental inquiy ntp bacte- Tiology of pyorthea. Proc. R. Soc. Med. (Odontol) 1919; 12:104, 2. Seltzer S, Bender IB and Zioutz M. The inter-relationship (of pulp and periodontal disease, Oral Surg, 1963; 16:1474. 3. Sinai IH and Soltanoff W. The transmission of pathologic ‘changes between the pulp and periodontal strutures, Oral Surg. 1973; 96.568. 4, Sharp RE. The relationship of the pulp and the periodontium Periodont Abstr. 1977; 25: 130-142. 5. Borgenholtz G and Lindhe J. Effect of experimentally Jnduced marginal periodontitis and periodontal scaling on the dental pulp. J. Clin. Periodontol, 1978; 5:59, 241 6 Heller AB et al. Oral Surg, 1977; 44:099. 7.CzarueckiRtand Schilder H. Ahistological evalution of the human pulp in teeth with varying degress of periodontal ‘diseases, J. Endod, 1979; 4:242, ‘8 Checker FM. Dent. Clin. North Am, 1974; 18:451 ‘8 Langeland K., Rodrigues, H and Dowden W. Perodontal disease, bacteria and pulpal histopathology. Oral Surg) of the romaing, 136 teeth exhibited two mesial canals -Type- Nin 84% and Type-Il in 16%, Two teeth hada single middle ‘canal and one had a ‘C’ shapped canal. 1974; 37:257-270. 10. Kickhan DB, J.Am. Dent, Assoc, 1975;91:353, 11.Shobha R et al. Oral Surg, 1974; 38:294, 12, Vertucci FJ and Wiliams RG, Oral Surg, 1974; 38308, 13, Bender IB and Seltzer S. The effect of diseases of the periodontium on the human pulp. Presented at the Conter- fence on Biology of the Human Pulp. Memphis, September. 1970. 14, Moss SJ, Addesiston M and Goldsmith E.D. Histologic study of pulpal floor of deciduous molars. J. Amer. Dent ‘Assoc. 1965;70:372, 15, Rubach WC and Mitchell DF. Periodontal disease, ‘accessory canals and pulp pathosis. J. Periodontal. 1965; 26:34 16. Messing JJ and Stock CJR. Colour Atlats of Endodontics 1988 Wolfe Medical Publications Ltd, London. pp.242. 17. Editor's note on Shah N and Kohli A. Burrowing cervical resorption, Eaitor's note. Austr-Endod N. 1992; 18: 22-23, 18.Trope M et al Dark field microscopy as a diagnostic aid in differentiating exudates from endodontic and periodontal ‘abscesses. J. Endod. 1988; 14:35, 19. Oliet & Pollock Bull Phila Dent. Sec. 1968; 34:12 20. Grossman's classification - In Endodontic- practica 11th (0d. by Louis | Grossman, Seymour, Oliet and Carlos E. Del Rio, 1988. Verghese Publishing House, India. 21.Simon JHS, Glick DH and Frank AL. The relationship of ‘endodontic periodontic lesions. J. Period, 1972; 43:202. 22. Weine FS. Endodontic periodontal problem in Endodontic ‘Therapy 31d Ed, 1982; C.V. Mosby Co; Toronto pp.503, 223 Stock CJ. The Endo-perio lesions : in A colour Alias of Endodontics by Messing JJ and Stock CJR. 1988, Wolte Medical Publications Ltd, Singapore pp.225, 24.Ingle JI and Beveridge EE. Endodontic 2nd Ed Philadeophia. Lea and Febiger, 1976. 25.Harrington GW. The perio-endo question, Differential agnosis. Dent. Clin, N.Amer. 1979; 23:673-50. 26. PeiimutterS. etal. Effectof endodontic status ofthe tooth in experimental periodontal reattachment in baboons : A preliminary investigation, Oral Surg, 1987;63:232,