INTRODUCTION

The concept of the envelope of discrepancy has been used to indicate the limits of orthodontic tooth movement based on the alveolar bone housing.¹ The cortical plate, which determines the alveolar boundary, has long been considered an anatomical limit for tooth movement.² The maxillary sinus floor, the distal end of the maxillary tuberosity, and the palatal or lingual cortex of the incisors are well-known anatomical structures that restrict tooth movement.^3–5 Regarding mandibular posterior space available, previous studies using two-dimensional radiographs mentioned that the anterior border of the ascending ramus was the posterior limit for distal molar movement.^6,7 However, after cone-beam computed tomography (CBCT) became widespread for three-dimensional (3D) analysis, recent studies ascertained that the mandibular lingual cortical plate can limit molar distalization.^8–10 In addition, as mandibular molars can now be distalized effectively and extensively with the aid of microimplants, potential root exposure outside the alveolar bone housing has increased.^8,11 Such considerable tooth movement may raise clinician concerns about bone dehiscence and associated clinical complications. Interestingly, previous CBCT studies on long-term retention checkups after radiographic bone dehiscence caused by extensive incisor retraction revealed noticeable palatal bone recovery.^12,13 Similarly, a case report using CBCT images observed favorable recovery of mandibular lingual bone dehiscence with protruding molar roots after substantial molar distalization using microimplants, with a newly formed cortical layer.¹⁴ This case suggested the potential for bone regeneration over the lingual bone dehiscence. However, no research has specifically investigated mandibular lingual bone changes during retention after molar distalization-induced bone dehiscence.

Therefore, this study aimed to assess the mandibular lingual bone changes after molar distalization with microimplants and during the retention period. The study compared tooth movement, posterior space available, and alveolar bone thickness at pretreatment (T0), posttreatment (T1), and retention (T2) using CBCT images. The null hypothesis was that there would be no significant difference in mandibular posterior lingual bone thickness between T0, T1, and T2.

MATERIALS AND METHODS

CBCT Measurements

CBCT scans (HDX WILL, Seoul, Korea; 85 kVp, 8 mA, voxel size of 0.300 mm) were acquired at T0, T1, and T2. Measurements were performed using 3D imaging software (Invivo 6; Anatomage Inc., San Jose, CA, USA).

The mandibular occlusal plane was established as a horizontal reference plane using the T1 CBCT image (Figure 1). Each T0 or T2 CBCT image was then superimposed onto the T1 image using voxel-based mandibular superimposition.^16,17 Once superimposed, axial planes were set at 0-, 2-, 4-, and 6-mm levels apical to the second molar root furcation, parallel to the mandibular occlusal plane. Next, the posterior space available for the mandibular second molar distalization, lingual bone thickness, and root movement were measured on each axial plane (Figure 2A–C). Linear variables were measured parallel to the posterior occlusal line connecting the contact points of the posterior teeth. Using the sagittal section of the mandibular second molar, crown movement and root length change were measured between T0 and T1, or T1 and T2 (Figure 2D). In addition, a distolingual point on the outer lingual cortex or distal root protruding outside the outer cortex was established at the 6-mm root level to investigate the direction of lingual bone remodeling during the treatment and retention periods (Figure 2E). This point was defined as the intersection of the distally extended line from the posterior space measurement and the outer lingual cortex. For samples showing lingual bone dehiscence after distalization, the distolingual point of the exposed distal root was used. The mesiodistal change of distolingual points, parallel to the posterior occlusal line, was only measured in adult patients to exclude mandibular growth effects in growing patients.

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RESULTS

The method error, calculated using Dahlberg’s formula, ranged from 0.05 to 0.27 mm. The intraclass correlation coefficients were greater than .90, indicating excellent reliability of the measurements.

The mean treatment duration was 32.3 ± 12.1 months, and the mean retention duration was 41.4 ± 20.7 months (range: 18.0–87.0 months).

During treatment, the mandibular second molar moved distally by 3.0 mm at the crown level and 1.2–1.8 mm at each root level (Table 1). Subsequently, during the retention period, the molar moved mesially by 0.7mm at the crown and 0.07–0.26 mm at each root level. The root length of the second molar decreased slightly by 0.36–0.46 mm after treatment.

Table 1.Tooth Movement and Change in Root Length of the Mandibular Second Molar^a,*

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Regarding the posterior space available for mandibular second molar distalization, the measurement significantly decreased at all root levels after treatment. At the 6-mm root level, all samples exhibited contact between the molar distal root and the lingual cortical plate (Table 2). During the retention period, the posterior space available increased but with no statistical significance except at the root furcation level. The lingual bone thickness distal to the mandibular second molar distal root significantly decreased after treatment, suggesting that the distal root moved into the cortical plate. Conversely, after retention, a significant increase in cortical bone thickness was observed, indicating new bone apposition at the previously thinned or penetrated cortical plate. However, the bone thickness at T2 was significantly less than at T0, except at the root furcation level.

Table 2.Posterior Space Available, Lingual Bone Thickness, and Distolingual Point Change Distal to the Mandibular Second Molar at Each Root Level^a,*^,**

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Concerning the positional changes of the distolingual point at the 6-mm root level (Table 2), all points were moved distally by 0.54 mm during treatment. During the retention period, the points moved mesially by 0.25 mm on average, which may indicate new bone apposition following mesial relapse of the molar root. However, when examined individually, distolingual points were observed to have moved distally in five molars from four patients, suggesting bone deposition on the outer surface over the roots protruding outside the cortex (Figure 3).

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When evaluating the factors correlated with lingual bone thickness changes at the 6-mm root level (Table 3), the bone thickness decrease was positively correlated with crown and root distal movement after treatment. In contrast, an increase in lingual bone thickness during the retention period was not significantly related to crown and root movement, age at T1, or retention duration.

Table 3.Pearson’s Correlation Coefficient of the Relationship Between Mandibular Lingual Bone Thickness Changes at 6 mm Root Level, and Mandibular Second Molar Movements and Clinical Variables^a

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DISCUSSION

All samples demonstrated that the distal movement of the mandibular second molar root achieved after treatment was significantly greater than the posterior space at T0 at the 6-mm root level, leading to root-cortex contact and a significant decrease in lingual bone thickness (Figure 4). In addition, 11 samples exhibited radiographic bone dehiscence with the root protruding outside the outer cortex. This finding was consistent with previous research, which reported a critical decrease in lingual cortex thickness following considerable mandibular molar distalization with microimplants.¹¹ Extensive distalization of the entire dentition can result in a counterclockwise rotation of the mandibular occlusal plane, accompanied by molar intrusion.^8,15 Therefore, this simultaneous molar intrusion likely contributed to earlier root-cortex contact and a greater decrease in lingual bone thickness than expected, based on the T0 posterior space available.

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At T2, the thinned lingual bone recovered critically with newly formed cortical bone (Figure 4). Intriguingly, the recovered lingual cortex, nevertheless, remained significantly thinner than the T0 cortex. This finding was in agreement with an earlier study on palatal bone changes after incisor retraction which demonstrated that the thickness of the palatal cortex that recovered during retention remained smaller than at pretreatment.¹² Once the cortex is damaged by tooth movement, it is likely that bone tissue tends to maintain its integrity for alveolar bone homeostasis by forming a new cortical layer that reaches an adequate thickness to support the tooth against occlusal forces. This was also consistent with previous research suggesting that occlusal or mechanical forces are key triggers of alveolar bone remodeling.¹⁸ Generally, higher forces are expected to increase cortical bone thickness and density.¹⁹ In addition, the current finding that bone apposition was not correlated with retention duration suggests that lingual bone deposition continues until the bone reaches a minimal thickness sufficient for homeostasis, rather than returning to its original thickness.

During the retention period, the distalized mandibular molars moved forward slightly. This tooth movement back into the alveolar bone housing may have contributed to the thickening of the lingual cortex, as reported in a previous animal study, which showed that complete bone repair occurred once the root moved back into the cortical bone boundary.²⁰ However, in this study, compared with the amount of relapse tooth movement (ΔT2–T1, 0.07 ± 0.50 mm; Table 1) at the 6-mm root level, the corresponding increase in lingual bone thickness (ΔT2–T1, 0.69 ± 0.48 mm) was greater. In other words, the relapse of tooth movement back into the alveolar boundary may not fully explain the extent of new bone formation over the bone dehiscence. Additionally, five molars from four patients exhibited distal movement of the distolingual point during retention (Figure 3). This indicated that there was outer surface bone apposition at the distolingual point of the root that previously had protruded outside the lingual cortex (Figure 5). Accordingly, bone recovery formation might not merely be a repair process returning the bone to its initial state, but rather a homeostatic response to the altered root position, aimed at maintaining tooth position through supporting the bone structure.

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None of the samples in this study exhibited any adverse clinical signs, such as gingival recession, root exposure, or severe tooth mobility. An intact periodontal ligament and periosteum can play a crucial role in promoting favorable bone regeneration over a bone dehiscence.^21,22 The posterior lingual gingiva tissue in the mandible is widely keratinized,^23,24 resistant to inflammation and traumatic damage.²⁵ However, detrimental changes in the lingual gingiva should be monitored, particularly since the molar distalization rate slows down due to root-cortex contact.¹⁴ Although no critical root resorption was observed, possibly because of the mild-to-moderate extent of molar distalization in this study, clinicians should be aware that root-cortex contact during distalization can increase root resorption.^26,27

This study may enhance the understanding of long-term bone recovery over radiographic dehiscence of the mandibular lingual cortex caused by considerable molar distalization. However, because of limitations of a small sample size and inclusion of growing patients, the current findings need to be interpreted carefully. Future research with larger sample sizes comparing bone recovery formation in adults and growing patients would be worthwhile to generalize these findings.

CONCLUSIONS

• The null hypothesis was rejected since lingual bone thickness changed during molar distalization and after retention.

• A significant decrease in lingual bone thickness was observed after mandibular molar distalization with microimplants.

• Thinned lingual cortical plate or radiographic bone dehiscence recovered with newly formed cortical bone during retention.

• The extent of recovery bone apposition was not correlated with the amount of tooth movement, retention duration, or patient age posttreatment.