| Abstract|| |
While contemporary periodontics has witnessed the continued emergence of sophisticated techniques to resolve esthetic concerns through various periodontal procedures, frequently the early stages of periodontal diseases are best treated with non-surgical periodontal therapy. This short communication presents a case of reactive positioning of pathologically migrated anterior tooth following non-surgical periodontal therapy.
Keywords: Non-surgical periodontal therapy, pathological tooth migration, reactive positioning, spontaneous correction
|How to cite this article:|
Agrawal N, Siddani PS. Reactive positioning of pathologically migrated tooth following non-surgical periodontal therapy. Indian J Dent Res 2011;22:591-3
Pathological tooth migration (PTM) is defined as a "Change in tooth position that occurs when there is disruption of forces that maintain teeth in a normal relationship."  It is a common manifestation of periodontal disease with prevalence studies reporting a range of 30%-55%. , Based on clinical observation, several etiological factors have been implicated in PTM, including periodontal bone loss, pressure from granulation tissue, many occlusal factors (eg, posterior bite collapse, arch integrity, class I malocclusion, occlusion interferences, anterior component of forces, protrusive pattern of occlusion, proximal and shortened dental arches), and soft tissue pressure of the tongue, cheek and lips. , However, evidence-based information suggests that destruction of periodontal tissues plays a significant role in the etiology of PTM. , Early stages of PTM can be managed either by nonsurgical periodontal therapy alone or occasionally with the combination of surgical periodontal therapy, but longstanding cases might require adjunctive or conventional orthodontic therapy. Several case reports have been published on reactive positioning or spontaneous correction following periodontal therapy, , but the predictability of this phenomenon is not well documented yet. The following case, lends further support to the "Reactive positioning of migrated tooth following nonsurgical periodontal therapy."
|How to cite this URL:|
Agrawal N, Siddani PS. Reactive positioning of pathologically migrated tooth following non-surgical periodontal therapy. Indian J Dent Res [serial online] 2011 [cited 2017 Jan 23];22:591-3. Available from: http://www.ijdr.in/text.asp?2011/22/4/591/90306
| Case Report|| |
A 35-year-old female reported to Department of Periodontics, with a chief complaint of increasing gap between her upper front teeth since last 2 years. She had no history of smoking or destructive habits and had no contraindication to periodontal therapy. Intraoral examination revealed a 3 mm diastema [Figure 1] between the maxillary central incisors. Her generalized plaque control record was 58%. Bleeding on probing was present and average generalized probing pocket depth was approximately 3-4 mm with clinical attachment loss of approximately 1-2 mm. Supra- and subgingival calculus were detected, which were concomitant with the attachment loss. The maxillary left central incisor had pocket depths ranging from 5 to 8 mm, with greater probing depth mesially and palatally. The tooth had migrated to facial, distal, and occlusal direction with grade II mobility. Both mandibular first and second molars were absent bilaterally [Figure 2]. A deep overbite and fremitus was associated with maxillary and mandibular central incisors. Radiographic evaluation showed widening of periodontal ligament space and bone loss around upper central incisors with no sign of periapical infection [Figure 3].
|Figure 1: Pretreatment photograph showing diastema between maxillary central incisors|
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|Figure 2: Pretreatment occlusal photograph, absence of mandibular molars|
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|Figure 3: Pretreatment intraoral periapical X-ray showing periodontal space widening, bone loss, and extrusion of the central incisor nr21|
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Full mouth scaling and root planning was performed. This was followed by meticulous plaque control instructions, which include demonstration of proper brushing technique as well as interdental brushing and flossing; 0.2% chlorhexidine rinsing (10 mL per rinse) was prescribed on a 12 h frequency for 2 weeks. Reconstruction of the occlusion was accomplished with a removable partial denture [Figure 4]. Three weeks after initial therapy the patient was re-evaluated. At this time the maxillary diastema was reduced to 1 mm and signs and symptoms of periodontal disease were significantly controlled [Figure 5]. The mobility of the migrated incisor was also reduced to one degree. Oral hygiene maintenance instructions were reinforced. The patient was placed on a 3-month maintenance program, and after 6 months of follow-up, the periodontal condition was stable [Table 1]. The patient was referred to the orthodontist for further adjunctive orthodontic therapy for full closure of the diastema.
|Figure 5: Posttreatment photograph showing marked reduction in diastema as well as gingival inflammation and probing depth|
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|Table 1: Comparison of pretreatment and posttreatment probing depth and clinical attachment level in tooth #21|
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| Discussion|| |
Periodontal bone loss appears to be a major factor in the etiology of the pathological tooth migration and many aspects of occlusion can also contribute to abnormal migration of teeth and more than one of these factors may be present in an individual patient.  Although the physiological mechanism leading to reactive repositioning of migrated teeth after periodontal therapy has not been documented, there are many possible explanations.
First, following periodontal therapy there is a reduction in edema and inflammatory cell infiltration of the soft tissues, resulting in the reduction in erythema and shrinkage of soft tissues. With this, healthy collagen fibers replace the inflammatory cell infiltrate and may contribute in the re-establishment of a normal equilibrium of forces, leading to reactive movement of migrated tooth to its original position.  During the healing process, wound contraction can also contribute to the repositioning of the tooth. It occurs during healing, as fibroblasts populate the newly formed granulation tissue.  Gaumet et al.  also supported the role of wound contraction in spontaneous repositioning. Second, abnormal occlusal forces can also cause pathological tooth migration.  In this case both mandibular first and second molars were absent and there was a posterior bite collapse (PBC). Shifman et al. comprehensively reviewed the various definitions of PBC and reported three cases that illustrate the complexity of the etiology of PTM. 
In the present case, after restoration of occlusion by removable partial denture, PBC as well as abnormal forces on anterior teeth were eliminated and also, after periodontal therapy, the tissue remodeling that takes place during healing might be able to regenerate normal biomechanical environment at the tooth periodontium interface. Thus, this newly re-established equilibrium of forces could be responsible for reactive movement of the tooth back into the previous alignment in the dental arch.
The predictability of this phenomenon is not well documented. In the study by Gaumet et al.,  16 patients with 33 diastema sites of anterior teeth that had developed in the last 5 years were monitored and treated. Out of 33, 17 sites of diastema closed completely (51.5%), whereas various degrees of repositioning occurred in 23 of the sites (69.7%). They concluded that, if a recently formed diastema of anterior teeth associated with periodontal disease is ≤1 mm in dimension, complete closure is predictable after periodontal therapy. In the current case, since the diastema was more than 1 mm (3 mm), it was partially persisted even after the periodontal therapy, although it was reduced by 2 mm.
Hence, a complete repositioning of migrated teeth is possible in early stages of its displacement. However, once spaces are >1 mm, this occurrence is unpredictable. The current case supports the concept of reactive positioning of the migrated tooth at various degrees following initial periodontal therapy.
| Acknowledgment|| |
Authors thank Dr. Amit Vanka for his constant support and editing of the manuscript.
| References|| |
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Department of Periodontics, People's Dental Academy, Bhopal
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]