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Healing of large periapical lesions following calcium hydroxide endodontic therapy : Two case reports and review of literature “Thomas SB *‘Al Kandari AR and **Abdul Rahem AA ABSTRACT ‘Two cases of large periapical lesions are presented. The lesions were treated by conservative endodontic therapy, following which the lesions showed complete resolution. These results suggest that the largeness of a lesion does not mandate its surgical removal and that even cyst-like lesions heal following conservative therapy. Key words ~ Periapical lesions, calcium hydro: Introduction Trauma to a tooth can damage the pulp when the crown and root are not fractured. Pulp may survive depending on the severity of the trauma and the type of inflammatory reactioin that follows. Due to trauma, a vascular pulp may degenerate into vascular necrosis. The necrotic material then seeps out of the portals of exit of the root canal system and into the supporting vascular attachment apparatus, generating lesions of endodontic origin. Based on histological findings, a chronic periapical lesion may be diagnosed as a granuloma or cyst. In the past, large periapical lesions were managed by endodontic treatment followed by surgical excision. This was particularly true for periapical cysts. However with the advancement of endodontics and a better understanding of the periapical tissues, even these cyst like lesions can be treated by conservative method. ‘Two cases of periapical lesions that were Endodontist ‘Amiri Dental Centre Head of Department of Endodontics and Amiri Dental Centre, Ministry of Public Health, Kuwait Endodontst Adan Dental Centre, Ministry of Public Health, Kuwalt 32 le. successfully treated by nonsurgical endodontic therapy are presented. These cases emphasize the fact that every effort should be made to treat such lesions irrespective of size by conservative method. Case Reports Case 1 ‘22-year-old woman was referred to the clinic for the treatment of a gradually increasing swelling on the palate of 4 weeks duration Previous history revealed an accident and trauma to the left maxillary lateral incisor 15 years ago. It was left untreated for many years. Examination revealed a tender, soft fluctuant swelling that extended from the anterior aspect of the palate to the region of the distal aspect of the first molar. The lateral incisor was discoloured and nonvital on thermal and electric pulp testing. Periapical radiograph revealed a wide-open apex and resorption in relation to the lateral incisor (Fig. 1a.) For immediate drainage of the swelling, the lateral incisor was opened which led to draining of suppurative fluid. The swelling was compressed and more fluid flowed out. The canal was thoroughly irrigated with sodium hypochlorite and provisional restoration was Thomas SB et al ial Fig. 1: (a) Periapical lesion associated with maxillary leftincisors, Fig. Fig. 1: (@) Atthe end of 12 months. Fig 1 used to seal the access cavity, Patient was prescribed antibiotics. The patient was recalled the next day and the same procedure was carried out. Intracanal calcium hydroxide [Ca (OH),] dressing was placed and a provisional restoration was used to seal the cavity (Fig. 1b). The patient was recalled at 2 weeks interval for a month and the Ca (OH), dressing was changed. After a month, the swelling had completely subsided. The patient was reviewed every month. At the end of 9 months, radiograph revealed a slight decrease in the size of radiolucency but no apical closure (Fig. 1¢) root canal treatment was completed (b)Placement of intracanal ‘calcium hydroxide dressing. 1c) Remarkable decrease in size of lesion and apical closure at the end of 2% years. 33 Calcium hydroxide therapy... Fig. 1 :(¢) Decrease in size of lesion at the end of 8 months. for the central incisor which had tested negative for vitality, Radiograph revealed a slight decrease in the size of the lesion but no apical closure (Fig. 1d). The lateral incisor was. opened and throughly cleaned and Ca(OH), was reintroduced into the canal and sealed with a temporary restoration The patient however did not keep her appointments regularly and this delayed the treatment. She returned to the clinic after 2% years with a complaint of pain in the lower left third molar area. A radiograph taken at this time tevealed a marked difference in the size of the lesion and formation of an apical barrier (Fig. 1€).The patient was recalled for root canal filing but did not show up for her appointment. Case 2 A twenty-five year old man was referred for treatment of palatal swelling in relation to the maxillary left central, lateral incisor and cannie area. He had severe pain in the area three days before he reported for treatment. The patient give the history of a fall at the playground five years ago. Examination revealed a soft, slightly tender swelling in the palate just behind the incisor and canine area. The maxillary incisors and canine were non-vital and periapical fadiolucency extended from the maxillary left central incisor to the mesial aspect of the canine (fig. 2a). When the root canals of the non-vital teeth were opened, straw coloured fluid flowed out. On compression of the palatal swelling, more fluid was expressed through the canals. The canals were debrided with sodium hypochlorite and calcium hydroxide paste was placed in the canals. The access cavities were \ Fig. 2 : (a) Periapical lesion in the ‘maxillary left incisors and canine. — Fig. 2 : (¢) Obturation completed after 4 weeks. im | if Fig. 2 : (b) Placement of intracanal Calcium hydroxide dressing, (a) Complete resolution alter 2 years. Endodontology, Vol. 12, 2000 sealed with temporary restoration (fig. 2b) Patient was prescribed antibiotics. The patient was recalled weekly for a month and similar treatment was carried out. Four weeks later, the canals were dried and obturated with gutta percha (fig. 2c). The palatal swelling had completely subsided. The patient was reviewed every three months for 24 months after completion of endodontic therapy. All the end of 24 months, there was complete resolution of the periapical lesion (fig. 24) Discussion The precise mechanism involved in the formation of periapical lesions is not fully understood. It is generally agreed that if the pulp becomes necrotic, its environment becomes suitable to allow microorganisms to multiply and release various toxins into the periapical tissues, initiating an inflammatory reaction and leading to the formation of the periapical lesion"?, Studies were carried out to examine the role of bacteria in the formation of periapical lesions** and it was found to be present in the root canals associated with the lesions**. The endodontic flora consists of rods, spirochetes, cocci and filamentous forms’. However only a few periapical lesions have shown the presence of bacteria within the body of the lesion**. One study* even demonstrated the absence of bacterial colonies in eighteen periapical lesions examined, except —_ for occasional isolated intracellular bacteria which was believed to be bacteria phagocytosed by macrophage like cells. Thomas SB et al . oe The histogenesis of the periapical cyst is uncertain but remnants of the epithelial cell rests could possibly be the source of the epithelium in cyst lining and various factors may contribute to the growth of the cysts. The inflammation in the periapical region may stimulate the proliferation of the epithelium, which by acting as a semi-permeable membrane, could draw fluid into the cyst cavity by osmotic pressure’. Bone resorbing factors such as prostaglandins could contribute to further expansion of the cyst. Radiographic and histopathological evaluation of periapical lesions"? showed that cysts are the most common periapical lesions. ‘Among periapical lesions of an area greater than 200mm?, 92% or more were cysts". Thus, larger the periapical lesion, greater the chance for it to be a cyst. In Case 2, the radiographic area of the periapical lesions was more than 200mm. Based on size, presence of cholesterol within the lesion contents and a defined radiographic margin, the lesions was probably a periapical cyst’®. The exact mechanism by which the cysts heal is not fully understood. One concept for treatment of cyst was to treat the involved teeth endodontically and surgically excise the lining". Others suggest that it would heal spontaneously after endodontic therapy. As healing takes place, collagen deposits compress the capillaries supplying the cyst, thereby cutting the blood supply to the epithelial lining. The lining degenerates and is removed by macrophages. Another theory is that if root canal therapy is extended beyond the apical foramen, the inflammatory reaction develops and destroys the cyst lining and converts the lesion into granuloma". When the causative factors are removed, it heals spontaneously. In case I, we see a clinical case of incomplete apical development. The open apex case"* occurs when trauma or decay causes pulp exposure and/or periapical involvement, prior to the completion of root development ‘An open apex refers to the absence of sufficient Calcium hydroxide therapy... root development to provide a conical taper to the canal and is referred to as a “blunderbuss* canal. Calcium hydroxide has been used in endodontic therapy since 1920 when Hermann: first described its use in the treatment of nonvital teeth. Since then Ca (OH), alone or in combination with other drugs have been used to promote apexification. The average time required to achieve apexification is 6 to 24 months”. it has been stated"? that Hertwig's root sheath is not completely destroyed when the pulp becomes nonvital in the developing tooth. Thus apexification procedures stimulate further function of the sheath to continue apical development. Calcium hydroxide kills bacteria because of the effect of hydroxyl ions. These ions are extremely reactive, combining repidly with lipids, proteins and nucleic acids. They cause lipid peroxidation, increasing the bacterial membrane permeability, protein denaturation, inactivating enzymes and DNA damage. These phenonmena cause bacterial death. The caicium ions activate the complement system in the immunologic reaction by activating the calcium dependent ATP-ase which has been associated with hard tissue formation. The calcified material that forms over the apical foramen has been histologically identified as an osteoid (Bonelike) or cementiod (cementum-like) material by investigators who have done apexitication on periapically involved teeth'*, Normal root formation usually does not, occur following apexification. Instead there appears to be a differentiation of adjacent connective tissue cells into specialized cells; there is also deposition of calcified tissue adjacent to the filling material. The calcified material is continuous with the lateral root surfaces. The apex may be partial or complete but consistently has minute communications with the periapical tissues. For this reason apexitication must always be followed by a permanent root canal filling material. One of the most perplexing cases to treat, is the tooth with constant clear or reddish exudate and a large periapical radiolucency"* Calgium hydroxide has been used as an intra canal medicament to attain a clean and dry canal. This is probably due to the pH of the periapical tissues which is acidic in the weeping stage. The pH is converted to a more basic environment by the calcium hydroxide and this in turn activates the alkaline phosphatase which plays an important role in hard tissue formation. Healing is complete when apical periodontal ligament is restored to normat architecture®*. A periapical scar may formas a residual radiolucent lesion. This may be ignored if a continuous periodontal ligament ‘of normal thickness is present around the affected tooth’? The periapical lesions in both the above cases were successfully treated non-surgically This only confirms with the study conducted by Schwarze and Guenay where clinical study was performed on 103 teeth with lesions to evaluate the success rate of surgical and non surgical endodontic therapies. From the data collected, it was concluded that conservative endodontic treatment of periapical lesions revealed high success rate (75%) than surgical treatment (69%). The periapical lesions in both cases were large but resolved after nonsurgical therapy. Periapical tissues have rich blood supply, lymphatic drainage and abundant undifferentiated mesenchymal cells* and there fore, good potential for healing. Thus treatment should be directed at removing the causative factors, References 1, Shear M. Histogenesis of dental cyst: Dent Pract 1963; 19:298-243 2. Pulver WH, Taubman MA, Smith PH, Immune com- ponents in the numan dental periapical lesions. Arch Oral Biol 1978; 23:435.443, 3. Yanagiswa S. Pathologic study of periapical granulo- Endodontology, Vol. 12, 2000 ‘mas: Clinical, histopathologic and immunohistopathologic studies. J Oral Pathol 1980, 9:288-300. 4. Andreasen JO, Rud J: A histobacteriologic study of dental and periapical structures after endodontic surgery. Int J Oral Surg. 1972; 1:272-281. 8, Langeland K, Block RM, Grossman. LI. A histopathologic study of 35 periapical endodontic surgi- cal specimens. J Endod 1977; 6. Stabholz. A, Sela MN: The role of microorganisms in the pathogenesis of periapical issions: Effect of streptococcus mutans and its cellular constituents on the dental pulp and priapical tissues of cats. J. Endod 1983: 9, 171-175. 7. Nair PNR. Light and celectron microscopic studies of root canal flora and periapical lesions: J. Endod 1987: 13:29:39. 8. Walton RE. Ardinand K. Histological evaluation of pres: tence of bacteria in induced periapical lesions in mon- keys. J. Endod 1992; 18:216-221 9. Weisenfed D. in, Scully C (Ed) The mouth and perioral tissues, Oxtord : Heinamann Medical books., 1989:49. 10.Zain RB, Roswali N. Ismail K. Radiographic evalua- tion of lesion sizes of histologically diagnosed periapical cysts and granulomas. Ann Dent 1989: 48:3-5. 11.Grossman LI. Root canal therapy, ed 3. Philadelphia: Lea & Febiger. 1950:99. 12, Bhasker SN: Non surgical resolution of radicular cyst Oral Surg. 1972; 34:458-468, 13.Shafer WG. Hine MK. Levy BM: A textbook of oral pathology, Ed. 3, Saunders 1974:451 14.Stern MH, Mackler BF, Selbst AG: Quantitative analy- sis of cellular composition of human penapical granu- Toma J. Endod 1981; 7:117-122 15.Frank AL. = Therapy for the divergent pulpless tooth by continuous apical formation. J. Am. Dent Assoc. 1966: 72:87. 16.Weine FS, Endodontic Therapy 4th Edition 1989: 626- 640, 17.A bacteriological and histological evaluation of 58 periapical lasions: J. Endod 1992; 18, 182-155, 18.Ham JW. Patterson SS. Mitchel DF : Induced apical closure of immature pulpless teeth in monkeys. Oral Surg, 1972; 33:438, = 19.Klein DJ. Study of endodontically apexitied teeth Endodont Dent Traumatol 1991: 7:112. 20. Torabinejad M Walton RE. Pulp and periapical patnosis. In: Walton RE, Torabinejad M (eds). Principlas and Prac. tice of Endodontics, Philadelphia: Sunders, 1989: 47-48 21.Harty FJ, Endodontics in Clinical Practice, ed 2. Bristol, England, Wright, 1982:195, 22. Gordon T. Effect of Ca (OH), on bovine pulp tissue. J Endo 1985: 11:156-60. 23, Schwarze TH. Guenay H. Endodontics or surgical therapy of periapicat lesions. J. Endod. 1999; 25, 36

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