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An Insight Into Internal Resorption Hindawi Publishing Corporation ISRN Dentistry Volume 2014, Article ID 759326, 7 pages http://dx.doi.org/10.1155/2014/759326 Review Article An Insight into Internal Resorption Priya Thomas, Rekha Krishna Pillai, Bindhu Pushparajan Ramakrishnan, and Jayanthi Palani Department of Oral and Maxillofacial Pathology, Annoor Dental College & Hospital, Muvattupuzha, Ernakulam District, Kerala 686673, India Correspondence should be addressed to Priya Thomas; [email protected] Received 20 January 2014; Accepted 27 March 2014; Published 12 May 2014 Academic Editors: S.-C. Choi and G. Mount Copyright © 2014 Priya Thomas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Internal resorption, a rare phenomenon, has been a quandary from the standpoints of both its diagnosis and treatment. It is usually asymptomatic and discovered by chance on routine radiographic examinations or by a classic clinical sign, “pink spot” in the crown. This paper emphasizes the etiology and pathophysiologic mechanisms involved in internal root resorption. Prognosis is good for smaller lesions; however, for those with extensive resorption associated with perforation the tooth structure is greatly weakened and the prognosis remains poor. 1. Introduction teeth. Unlike the deciduous teeth, the permanent teeth rarely undergo resorption unless stimulated by a pathological Tooth resorption presents itself either as a physiological process. Pathologic resorption occurs following traumatic or a pathological process occurring internally (pulpally injuries, orthodontic tooth movement, or chronic infections derived) or externally (periodontally derived). According to of the pulp or periodontal structures [1]. If the process is left the Glossary of the American Association of Endodontists, untreated, it will result in the premature loss of the affected resorption is defined as a condition associated with either a teeth [2]. physiologic or a pathologic process resulting in the loss of Internal resorption is noticed in the inner walls of root dentin, cementum, or bone [1]. canal while external resorption is noticed on the root surface External resorption begins from the external or cervical or cervical area. External root resorption exists concurrently surface of the tooth and proceeds inwards and is asso- with resorption of the alveolar bone and the resorptive ciated with factors like periapical pathosis, pressure from processpresentsinasimilarmannertothatofbone. orthodontic treatment, and rapidly growing tumors. Internal resorption (IR) is a rare, insidious, resorptive pathological process, beginning in the pulpal space and extending into 3. Pink Tooth of the surrounding dentin. Its diagnosis and management have Mummery/Internal Resorption been a challenge to dental practitioners. Due to its insidious pathology, internal resorption can progress to a great extent Internal resorption was first reported by Bell in 1830. Pink before its detection. Treatment is by arresting the cellular tooth of Mummery (1920), so called due to the presence of a activity accounting for the resorptive process. pinkdiscolorationonthecrown,isnamedaftertheanatomist Mummery [3]. Internal resorption can be categorized by the type/cause 2. Classification: See Table 1 of resorption as inflammatory, transient, progressive, and replacement [1](seeTable 2). Inflammatory resorption is Resorption is of various types. Physiologic resorption is asso- more likely to commence following damage to the pre- ciated with deciduous dentition resulting in their exfoliation, dentin subsequent to a bacterial infection or trauma [4]. paving the pathway for the eruption of their succedaneous A transient internal resorption is another form of trauma 2 ISRN Dentistry Table 1: Classification based on type of process, location, and the Table 2: Modified Andreasen classification. type and cause. Modified Andreasen classification based on the type of resorption Location in relation Type/cause of (a) Internal inflammatory resorption Type of process to root surface resorption Internal resorption (b) Internal replacement resorption (i) Physiological (i) Inflammatory (c) Transient apical breakdown resorption (i) Internal (ii) Transient (ii) Pathological (ii) External/cervical (iii) Progressive (a) External surface resorption resorption (iv) Replacement (b) External inflammatory resorption External resorption (c) External replacement resorption (d) External cervical resorption (e) Transient apical breakdown induced noninfective, self-limiting root resorption and this will generally follow a luxation injury [5, 6]. Progressive type of internal resorption is stimulated by constant inflammation The literature also cites the association of herpes zoster following infection [7]. Root canal replacement/metaplastic with resorption and the degeneration of odontoblast due to resorption involves subsequent deposition of mineralised systemic viral infection [17]. Solomon et al. [16]reporteda tissue resembling bone or cementum but not dentin [1]. case of internal resorption affecting 21 and 23, with a history Reichart et al. [8] entitled this metaplastic tissue as “reparative of herpes zoster affecting the maxillary branch of the left cementum” or “osteodentin-like material.” trigeminal nerve. The effect on the dental pulp could be The prevalence, etiology, and natural history of internal possibly explained by the virus being attracted to the nerve resorption are uncertain [7] and the associated key molecular endings in the pulp [18]. Ramchandani and Mellor [18]and pathogenesis/events have not been understood completely. Wadden [19]havealsoaccountedcasesofinternalresorption Dentin is lined internally from the pulpal surface by the linked with herpes zoster infection. odontoblastic layer and predentin. The two layers together Genetic factors have also been implicated in the devel- form a barrier and prevent its resorption. Many studies have opment of internal resorption. The link between interleukin- proven that, similar to the osteoclasts, the odontoclasts do (IL-) 1 gene polymorphism and root resorption has been not adhere to or resorb unmineralized matrix [9]. Wedenberg reported in a study of monozygotic twins [20]. andLindskogreportedthatdamagetoboththeselayers result in exposure of the underlying mineralized dentin to odontoclasts making it vulnerable to resorption [9]. The 3.2. Pathophysiology: See Figures 1 and 2. Internal resorption uncommon occurrence of dentin resorption can furthermore usually occurs as a result of a continuous chronic inflam- be explained by the dominance of odontoclast inhibitory matory process. Progress of internal resorption is dependent substances such as OPG (osteoprotegerin) over activators on two things: presence of vital pulp tissue at/below the like RANKL (receptor activator of nuclear factor kappa B resorption area and partially or completely necrotic pulp, ligand) [5]. It has also been suggested that dentin contains coronal to the site of resorption, thereby allowing a constant a noncollagenous component which may function as a entry of microorganisms and its antigens into the root canal. resorption inhibitor [5]. Microbial stimulus is an essential factor for the persistence of Internal inflammatory resorption commence following a resorption [5]. The extent of progression is also determined stimulus (inflammation) with the elimination of inhibitory bytheintensityofthestimuliandinflammatoryprocess.The mechanism, that is, the loss or alteration of the protective origin of clastic cells is related to the viable blood supply and (predentin/odontoblastic) layer and pulpal invasion by mult- the necrotic tissue acts a stimulus for the formation of these inuclear giant cells/odontoclasts/dentinoclasts [10, 11]. These cells. This probably explains as to why IR is stated as a rare giant cells are morphologically similar to osteoclasts, with occurrence compared to external root resorption [21]. The related enzymatic properties and resorption patterns. They vascular changes in the pulp produce hyperaemia, causing are probably derived from tartrate resistant acid phosphatase an increased oxygen tension resulting in low pH levels, thus (TRAP) positive circulating monocytes [12]. However, odon- attracting numerous macrophages to the site, thereby piloting toclasts are smaller in dimension, with fewer numbers of the onset of resorptive process [22]. The connective tissue, nuclei, and are present within smaller resorption lacunae following the resorptive activity, may undergo metaplasia to [1, 13]. They do not show the well-developed clear zones of form granulation tissue [22]. Predominance of a progressing active osteoclasts. This has been attributed to the difference infection causes necrosis of the entire pulp tissue and limits in composition of the dental tissues and bone [14]. theresorptiveprocessandthisactsasaprotectivemechanism preventing its progression [5]. The presence of a collateral bloodsupplythroughanaccessorycanalfromtheperiodon- 3.1. Etiology. It has been documented that the process is tal ligament to the resorption site can add to maintaining the initiated by a variety of stimuli such as trauma, pulpotomy, resorptive process. Internal inflammatory root resorption in extreme heat produced during cutting of dentin [15], chronic its most classical form spreads symmetrically in all directions inflammation of the pulp following caries
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