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Year : 2014  |  Volume : 5  |  Issue : 1  |  Page : 7-10

A possible etiology for the dilaceration and flexion of permanent tooth roots relative to bone remodeling gradients in alveolar bone

Department of Orthodontics, University of British Columbia, Faculty of Dentistry, Vancouver, British Columbia, Canada; Private Practice, Langley, British Columbia, Canada

Date of Web Publication3-Mar-2014

Correspondence Address:
Richard G Standerwick
20159 88th Ave, Suite E207, Langley, BC
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2155-8213.128105

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Introduction: Trauma, altered tooth germ position and delayed tooth eruption have been hypothesized as possible causes of tooth root dilacerations and flexion, however these anatomical variations appear more commonly associated with posterior teeth and absence of traumatic history. The Hypothesis: Postulated is that tooth root dilaceration or flexion may be a result of tooth root sheath displacement due to gradients of bone remodeling present within alveolar bone. Evaluation of the Hypothesis: Alveolar bone displays bone remodeling gradients between coronal, apical and basal sections which affect bone plasticity. As a tooth is erupting or experiences delayed eruption, there are other relative dento-skeletal alterations occurring, such as the mesial drift of the dentition and transverse growth of the maxilla. It is plausible that during the physiologic and growth related alteration of the alveolar and basal bones, portions of developing tooth could be found within one or more of the plasticity zones, contributing to alteration of the root sheath and tooth root dilaceration.

Keywords: Alveolar bone, dilaceration, remodeling, tooth

How to cite this article:
Standerwick RG. A possible etiology for the dilaceration and flexion of permanent tooth roots relative to bone remodeling gradients in alveolar bone. Dent Hypotheses 2014;5:7-10

How to cite this URL:
Standerwick RG. A possible etiology for the dilaceration and flexion of permanent tooth roots relative to bone remodeling gradients in alveolar bone. Dent Hypotheses [serial online] 2014 [cited 2023 Mar 22];5:7-10. Available from:

  Introduction Top

Tooth root dilaceration and flexion can: increase the treatment difficulty by impeding dental implant placement, root apex access through the root canal system, tooth extraction, affect crown root ratios/periodontal support, orthodontic anchorage and root positioning within the bone. A clear definition of tooth root dilaceration is lacking, with some authors describing dilaceration as a 90° or greater root deflection, 20° or greater deflection or as a distorted root form. [1],[2],[3],[4] Teeth with a lesser bending of roots, which is observed in the absence of trauma may be better defined by the term flexion [5] [Figure 1]. The etiology of tooth root dilaceration and flexion may differ but the process seems developmentally similar, resulting from an altered position of the tooth crown relative to the developing root and root sheath. [6] Tooth root dilaceration has been attributed to trauma in cases involving trauma to anterior teeth, [5],[6],[7] and the direction of traumatic tooth displacement seems to dictate the direction of the dilaceration due to rotation around the tooth's center of resistance. [8] The result is that permanent central incisor crowns subluxated apically will often display a root apex that is positioned facially when the incisor is eventually aligned in the dental arch. [5],[6],[9] More commonly, tooth root dilaceration is observed on posterior teeth in the absence of trauma [3],[7],[10],[11] [Figure 2] and is better explained by alternative hypotheses that describe dilaceration resulting from genetic alteration of the tooth germ position, in the absence of trauma, [6],[7],[11] or effects of delayed eruption of teeth. [4]
Figure 1: Displays an impacted maxillary right central incisor that erupted spontaneously after space creation but displays dilaceration possibly due to delayed eruption or previous trauma. The mandibular canines display a degree of flexion which may have resulted from delayed eruption due to altered eruption patterns; mandibular canine teeth usually erupt prior to the mandibular 1st premolars.[35] The mandibular 1st premolars display dilaceration in a direction opposite to that anticipated with normal growth and may reflect early bracketing of teeth for space creation prior to 2/3 root formation

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Figure 2: Displays an impacted right mandibular canine tooth. Tooth root flexion of the apical 1/3 is evident on the mandibular canines and premolars

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  The Hypothesis Top

Tooth root dilaceration associated with trauma is less prevalent than atraumatic dilaceration observe on posterior teeth and therefore primary causation of tooth root dilaceration hypothesized as a result of trauma is limited. The altered tooth germ hypothesis is inadequate to explain instances of tooth root dilaceration that seem to initiate at the midroot level or further apical, and a delayed eruption hypothesis is inadequate to explain why tooth root dilaceration formation occurs in situations of normal eruption especially when observed of mandibular molars.

The proposed hypothesis describes tooth root dilaceration and flexion resulting from tooth root sheath displacement due to gradients of plasticity present within the alveolar bone.

  Evaluation of the Hypothesis Top

The traditional understanding of root dilaceration and flexion has been postulated from observation of dental trauma and the hypothesis of atraumatic altered tooth germ position. The proposed hypothesis supplements traditional theories of tooth root dilaceration etiology by considering the dynamic physiology of the orofacial skeleton. Tooth development and eruption occur in stages and individual tooth stages can occur at different ages. Succedaneous and non succedaneous permanent teeth development begins from an ectomesenchymal primordium, which for succedaneous teeth develops in association with the primary tooth bud. Damage or dislodgment of the primary tooth might alter the position of the permanent tooth; however, this is inadequate to explain the occurrence of dilaceration at the midroot or apical level instead at the cervical 1/3 of the tooth. Teeth develop from this primordial ectomensenchyme through a bud stage, cap stage and then bell stage, in which the ectomesenchyme initiates differentiation of the ameloblasts that are responsible for the development of tooth enamel and [12] odontoblasts, which are responsible for the development of the dentin. [13] Following differentiation to ameloblast and odontoblasts, progressive mineralization of tooth crown occurs until the cervical region is reached and there is a progression to root formation through Hertwig's root sheath. [14],[15] Eruption of the tooth seems to result from a combination bone resorption preceding the crown, along with a periodontal ligament/root mediated eruption process. [4],[16],[17],[18],[19] Root sheath stretching occurs as the tooth root grows from a stationary origin in the bone, rather than the root sheath growing into the jaws, [15] and the relative amount of eruption displayed by primary and permanent teeth may affect the amount of alveolar bone that an adjacent unerupted permanent tooth may need to pass through prior to emergence into the mouth.

The alveolar bone height and the relative position of the erupting tooth in the jaw bones are important due to variable remodeling rates observed at the coronal alveolus, apical alveolus and basal maxillary and mandibular bones. [20],[21],[22],[23] Greater amounts of localized remodeling correlate with decreased bone mineralization and stiffness which translates into increased bone plasticity and possibly increased rates of tooth movement. [20],[21],[22],[23],[24],[25],[26] As a tooth is erupting or experiences delayed eruption, there are other relative dento-skeletal alterations occurring, such as the mesial drift of the dentition [27] and transverse growth of the maxilla. [27],[28],[29] It is plausible that during the physiologic and growth related alteration of the alveolar and basal bones, portions of developing tooth could be found within one or more of the plasticity zones. Root dilaceration may result from a decreased rate of tooth movement for a developing tooth root within a less plastic zone if the more coronal portions of the tooth are within a more plastic zone displaying a greater rate of tooth movement [Figure 3]. Maxillary molars tend to migrate mesially approximately 5mm between the ages of 10 and 20 years of age, while mandibular molar migration is similar or slightly less if tooth interdigitation is to be maintained relative to the rotations of the maxilla and the mandible (mandible rotation with growth is greater than the maxilla, therefore less tooth movement may be required in the mandible to match maxillary dental migration). [28],[30],[31]
Figure 3: The formation of a tooth root may be affected by the fluctuation of tooth positions relative to the alveolar and basal bone with normal growth and modeling of the maxilla and mandible. A decreased bone remodeling rate equates to decreased bone plasticity which is hypothesized to increase the resistance to movement of the root growth site relative to the mineralized root, resulting in stretching of the root sheath and dilaceration or flexion

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Questions still arise, such as why teeth do not display tipping due to physiologic mesial drift and plasticity gradients after root apexification has occurred? In some cases teeth do display mesial tipping, [27] but often they do not for a number of reasons such as occlusal forces, craniofacial growth type, or genetics. [32],[33],[34]

Plasticity zones are more easily visualized but it is likely that gradients of plasticity occur rather than distinct zones. Compounding local or systemic factors affecting development of tooth root dilaceration relative to bone plasticity gradients could include the rate of eruption, jaw rotation, length of the root, length of eruption path, [35] delayed eruption, [36] transverse uprighting of molar teeth during eruption [28],[37],[38] and root resorption.

  References Top

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9.Wei YJ, Lin YC, Kaung SS, Yang SF, Lee SY, Lai YL. Esthetic periodontal surgery for impacted dilacerated maxillary central incisors. Am J Orthod Dentofacial Orthop 2012;142:546-51.  Back to cited text no. 9
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11.Malcic A, Jukiæ S, Brzoviæ V, Miletiæ I, Pelivan I, Aniæ I. Prevalence of root dilaceration in adult dental patients in Croatia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102:104-9.  Back to cited text no. 11
12.Zeichner-David M, Vo H, Tan H, Diekwisch T, Berman B, Thiemann F, et al. Timing of the expression of enamel gene products during mouse tooth development. Int J Dev Biol 1997;41:27-38.  Back to cited text no. 12
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26.Roberts WE, Roberts JA, Epker BN, Burr DB, Hartsfield JK Jr. Remodeling of Mineralized Tissues, Part I: The Frost Legacy. Seminars in orthodontics 2006;12:216-37.  Back to cited text no. 26
27.Thilander B, Rygh P, Reitan K. Tissue reactions in orthodontics, in Orthodontics: Current Principles and Techniques. In: Graber TM, Vanarsdall RL, Vig KW, editors, 4 th ed. Elsevier Mosby: St. Louis; 2005. p. 152-7.  Back to cited text no. 27
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29.Johnston LE. Growing jaws for fun and profit: A modest proposal, in What Works, What Doesn't, and Why. Craniofacial Growth Series 35. In: McNamara AJ, editor. Needham Press: Ann Arbor; 1998. p. 63-83.  Back to cited text no. 29
30.Bjork A, Skieller V. Facial development and tooth eruption. An implant study at the age of puberty. Am J Orthod 1972;62:339-83.  Back to cited text no. 30
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32.Iwasaki LR, Chandler JR, Marx DB, Pandey JP, Nickel JC. IL-1 gene polymorphisms, secretion in gingival crevicular fluid, and speed of human orthodontic tooth movement. Orthod Craniofac Res 2009;12:129-40.  Back to cited text no. 32
33.Iwasaki LR, Gibson CS, Crouch LD, Marx DB, Pandey JP, Nickel JC. Speed of tooth movement is related to stress and IL-1 gene polymorphisms. Am J Orthod Dentofacial Orthop 2006;130:698 e1-9.  Back to cited text no. 33
34.You ZH, Fishman LS, Rosenblum RE, Subtelny JD. Dentoalveolar changes related to mandibular forward growth in untreated Class II persons. Am J Orthod Dentofacial Orthop 2001;120:598-607.  Back to cited text no. 34
35.Lo RT, Moyers RE. Studies in the etiology and prevention of malocclusion: I. The sequence of eruption of the permanent dentition. Am J Orthod 1953;39:460-7.  Back to cited text no. 35
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37.Marshall S, Dawson D, Southard KA, Lee AN, Casko JS, Southard TE. Transverse molar movements during growth. Am J Orthod Dentofacial Orthop 2003;124:615-24.  Back to cited text no. 37
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  [Figure 1], [Figure 2], [Figure 3]

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