Tooth resorption part I - pathogenesis and case series of internal resorption
A 49-year-old female patient undergoing periodontal therapy was referred from the department of Periodontics for management of internal resorption in tooth #8 that was evident on a routine periapical radiograph. The patient's medical history was non-contributory. No episode of pain was reported by the patient in tooth #8. The patient gave a history of trauma to her anterior teeth about 15 years back. On clinical examination, tooth #8 was discoloured and displayed an Ellis class IV fracture. It failed to respond to thermal and electric pulp testing while the adjacent teeth responded within normal limits. Tooth #8 on a periapical radiograph revealed a well delineated oval enlargement of the pulp space in the apical third of the root, which was continuous with the root canal walls []. The diagnosis was inflammatory non perforating internal resorption.\nFollowing access cavity preparation, the canal was negotiated. The root canal system was debrided using stainless steel K- files to a master apical file (MAF) size 40 under 5.25% sodium hypochlorite (NaOCl) irrigation. Since the tooth was nonvital, there was no bleeding evident from the root canal that is typical of active resorptive tissue. However, to facilitate thorough debridement of the resorptive defect ultrasonic activation of NaOCl was carried out. The canal was dried with paper points and calcium hydroxide (Ca(OH)2) paste was placed as an intracanal medicament for 1 week. At the next appointment, the Ca(OH)2 paste was flushed out; the canal was dried and obturated with warm vertical compaction technique using gutta-percha []. The post endodontic restoration was completed at a later date and the patient was referred back to the department of Periodontics.\nThe case report exemplifies inflammatory internal resorption which was probably self-limiting as tooth #8 was nonvital. For internal resorption to progress, the pulp tissue apical to the resorptive lesion must have viable blood supply that provides clastic cells whereas the infected necrotic coronal pulp tissue provides stimulation for those clastic cells.[] Bacteria probably entered the pulp space through the fracture site thus infecting the coronal pulp tissue which served as a stimulus for the resorption process resulting in the damage to the odontoblast layer and predentin. Wedenberg and Lindskog reported that damage to both these layers results in exposure of the underlying mineralized dentin to odontoclasts.[] The resorptive defect that forms is filled with inflammatory connective tissue. Failure to intervene at this stage could result in further progress of the resorption in the defect laterally resulting in a perforation or the resorption may progress apically and the pulp tissue apical to the resorptive defect may undergo necrosis,[] the later consequence being evident in this case. The management of internal resorption is intended to remove all the vital and non vital pulpal remnants and to disinfect and obturate the root canal.[] NaOCl an effective antimicrobial irrigating solution, aids in dissolving necrotic tissue.[] Ultrasonic activation of irrigants has also proved to be an effective method to remove debris lodged in inaccessible resorptive sites.[] However, some amount of debris may still persist within the resorption niche thus necessitating the placement of an intracanal medicament like Ca(OH)2[] that has a pronounced antimicrobial effect due to its alkaline pH.[] Placement of Ca(OH)2 has been recommended for 1 to 2 weeks that provides sufficient time to necrotize the residual pulp tissue.[] The obturation of internal resorption defects can be difficult due to their shape and lack of adequate access. The warm vertical compaction and thermoplasticized gutta-percha techniques have proved beneficial in this regard as they seal the defects satisfactorily.[]