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Effects of Occlusal Stimuli on Alveolar/Jaw Bone FormationOrthodontic Science, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8549, Japan; Correspondence: * corresponding author, yasuorts{at}tmd.ac.jp
Occlusion is known to influence the growth and development of the craniofacial complex. However, the consequences of occlusal hypofunction, or its recovery, on the amount of formation and development of alveolar bone and the jaw are not fully understood. Therefore, the present study was designed to elucidate the relationship between the occlusal stimuli and alveolar and jaw bone growth by the use of a hypofunction/recovered occlusal function model in growing rats. Bone histomorphometric analyses, including bone apposition rate and mineral apposition rate, were evaluated in double-labeled frontal sections of mandibular second molars. Results showed that occlusal hypofunction significantly suppressed alveolar and jaw bone formation compared with that in animals growing normally (p < 0.05). However, recovered occlusal function induced an enhancement in jaw bone formation. These results indicate the influence of occlusal function on alveolar and jaw bone formation during the growth period.
Key Words: occlusal stimuli • alveolar and jaw bone • growth • bone formation • double labeling
Mechanical stimuli are known to affect formation, maintenance, and remodeling of the bone (Bourrin et al., 1995). They can act upon the skeleton, playing an important role in the regulation of bone mass and architecture. Alveolar bone is considered an appropriate region for study of the relationship between bone modeling and mechanical stimuli, because of its high turnover rate in response to stimuli, such as occlusion (Vignery and Baron, 1980). Upon occlusion, mechanical stimulation is distributed to the teeth, periodontal ligament, and throughout the alveolar bone. The loss of normal occlusal function, i.e., occlusal hypofunction due to the loss of tooth or malocclusion, leads to atrophic changes in the periodontal ligament, such as narrowing of the periodontal space, vascular constriction, and deformation of the mechanoreceptor structure (Tanaka et al., 1998; Muramoto et al., 2000; Iwasaki-Hayashi et al., 2001). Occlusal hypofunction is also known to decrease alveolar bone mass (Johnson, 1990; Enokida et al., 2005), and to accelerate bone resorption (Nomura, 1982; Toyooka et al., 2001). Alveolar and jaw bone formation is suppressed in certain areas in growing rats in response to occlusal hypofunction (Shimomoto et al., 2005). Clinically, local factors that induce loss of occlusal function or occlusal contact—such as open-bite malocclusion, early loss of teeth, congenitally missing teeth, and/or delayed restorations—are known to result in the loss of regional alveolar bone and its support (von Wowern et al., 1979; Beckmann et al., 1998; Usami et al., 2003). In particular, occlusal hypofunction during the growth period may also influence the vertical growth of the alveolar bone (Hsieh et al., 1994). However, the effect of occlusal hypofunction and its recovery on alveolar and jaw bone formation, especially during the growth period, is still not fully understood. Therefore, the aim of this study was to investigate the direct influence of occlusal function on the changes of spatial and temporal alveolar and jaw bone formation, by means of a hypofunction/recovered occlusal function model (Watarai et al., 2004).
Animals and Experimental Model Five-week-old male growing Wistar rats (Sankyo Lab Service Corporation, Inc., Tokyo, Japan) were randomly divided into 2 groups: a control group (n = 5) and a hypofunction/recovered occlusal function group (n = 5). The hypofunction/recovered occlusal function model was based on previous reports (Suhr et al., 2002; Watarai et al., 2004). Briefly, we induced occlusal hypofunction in the molar region by attaching, in each of the 5 rats, a removable anterior bite plate and a metal cap constructed from band material (0.180 x 0.005 inch; Rocky Mountain Morita, Tokyo, Japan) to the maxillary and mandibular incisors, respectively, by means of light-curing composite resin (Clearfil Liner Bond II Kuraray Co. Ltd., Okayama, Japan) for 2 wks. The devices prevented molar contact during the experimental period, which induced occlusal hypofunction (Fig. 1a  ). After 2 wks of occlusal hypofunction, the devices were removed by means of orthodontic pliers. After the removal of the devices, occlusal contact of the molar area was recovered in 2 wks. Untreated normally growing rats served as controls (Fig. 1b). Rats in both the control and experimental groups were fed water and a powdered diet (CE-2, Clea Japan Inc., Shizuoka, Japan), and their body weight was monitored during the experimental period (Fig. 1c).
All experimental procedures were approved by the Animal Ethics Committee of Tokyo Medical and Dental University.
Xylenol Orange/Calcein Administration and Section Preparation
Quantitative Analysis
Based on the reference line along the long axis of the buccal root, the area superior to the root apex was considered alveolar bone, while the area inferior to the root apex was considered the jaw bone. The lingual side of the bone was excluded, because the existence of the incisor root may influence bone formation. The periosteal surfaces of the mandible were divided into 4 regions for analysis (Fig. 1d
Statistical Analysis
Weight Changes of the Animals The body weights in the normal and hypofunction/recovered occlusal function groups increased during the experimental period. There was no significant difference in the mean body weight between the 2 groups, similar to results reported previously (Watarai et al., 2004; Enokida et al., 2005) (Fig. 1c  ).
Continuous Apposition of Alveolar and Jaw Bone during the Experiment Period
In the hypofunction/recovered occlusal function group, quintuple fluorescent labeling was also detected around the alveolar bone, jaw bone, and the incisor root. The inter-label width during the hypofunction period, which indicates the speed of mineral apposition, was narrow compared with that in the control (Fig. 2b ).
Changes in Alveolar Bone Formation Due to Hypofunction and Recovered Occlusal Function
In the alveolar crest (region 1), the mineral apposition rates were similar regardless of occlusal hypofunction. However, recovered occlusal function induced significant enhancements in the mineral apposition rate compared with that in the control (Fig. 3a
The alveolar bone (region 2) indicated a gradual decrease in mineral apposition rate and bone formation rate in the control. Hypofunction induced significant suppression of mineral apposition rate and bone formation rate compared with those in the control group (P < 0.05). However, during occlusal recovery, both indices reached similar or even enhanced levels compared with those in the control group (Figs. 3b, 3d ).
Changes in Jaw Bone Formation Due to Occlusal Hypofunction and Recovered Occlusal Function
We investigated the spatial and temporal changes in alveolar and jaw bone formation in response to occlusion. Occlusal hypofunction induced by the anterior bite plate appliance suppressed alveolar and jaw bone formation during the growth period, while recovered occlusal function enhanced bone formation. These results indicated the important regulatory role of occlusion during alveolar and jaw bone growth. In growing animals, bone modeling is reported to occur principally in the cortical bone (Li and Jee, 1991). Bone apposition of the outer cortex increases the diameter and cortical cross-sectional area, and thus the stiffness and strength of the cortex can be increased (Frost, 1988). The alveolar region of the mandible is also reported to indicate active bone remodeling, similar to that in other general areas (Takagi et al., 2001). In particular, the lower molar shows remarkable eruption, with continuous root elongation along with growth, which has been reported to induce dramatic changes in these regions in five-week-old rats (Kinoshita et al., 1982). Thus, for our study, we selected five-week-old growing rats for evaluation for a four-week period, to detect the dynamics changes in growth and bone formation in response to occlusal function. Bone formation has been reported to be very active but to decline gradually with age in general (Burr and Marin, 1989; Kabasawa et al., 1996). Accordingly, we noticed maximum bone formation at the periosteal surface of the alveolar and jaw bone during the initial stage, with a gradual decline as the animals aged (normal controls). Occlusal hypofunction significantly suppressed bone formation during this maximum growth period, as previously reported (Enokida et al., 2005; Shimomoto et al., 2005). However, our results clearly showed that the suppression of bone formation due to occlusal hypofunction can be reversed by a recovery of occlusal function. An increase in bone formation after recovered occlusal function was consistently noticed in most of the regions evaluated. Interestingly, region 4, the inferior border of the jaw bone, showed remarkable instantaneous changes after occlusal recovery, despite its considerable distance from the occlusal stimuli. Since occlusion mainly delivers vertical force to the jaw, which coincides with the direction of growth in the case of the inferior border, recovered occlusal function may have induced instantaneous response compared with that in other regions. In addition, the masseter is anatomically attached near the inferior border of the jaw in the lower molar area (Nakata, 1981). A decrease in functional forces of the masseter, with the use of an anterior biteplate appliance, has been reported to cause a decrease in mandibular bone growth (Mavropoulos et al., 2004). Thus, bone formation of the inferior border could have been stimulated by the combined effects of the increase in masseter muscle functions along with the direction of force application in response to recovered occlusal function. In regions 1, 2, and 3 (alveolar crest, alveolar bone, buccal surface of the jaw bone), mineral apposition rate and bone formation rate showed some statistical discrepancies, despite their similar tendencies after occlusal recovery. Increased mineral apposition rate after recovered occlusal function indicates the increase in osteoblastic activity at the cellular level. The bone formation rate indicates the changes in numbers of bone-producing osteoblasts, and thus, bone formation at the tissue level (Miller et al., 1997). Our study showed that bone formation at the cellular level (mineral apposition rate) can be enhanced in response to recovered occlusal function after hypofunction, although it was not sufficient to enhance the total amount of bone formation per se (bone formation rate) during the experimental period. Previously, it was reported that active bone remodeling occurs during the growth spurt, with a decrease in the number of osteogenic cells, such as osteoblasts, at the end of the growth spurt (Takagi et al., 2001). Based on that report, we postulated that, although cellular activity was enhanced in the pre-existing osteoblasts following occlusal recovery (enhancement in MAR [mineral apposition rate]), occlusal recovery at the end stage of the growth spurt (the latter half of our experiment) may not be sufficient to enhance the total numbers of osteoblasts required for bone formation (bone formation rate, BFR). These results suggest that occlusion and timing at the proper age are important regulatory factors for bone formation and growth, especially in regions 1, 2, and 3. In summary, our study demonstrated that alveolar and jaw bone formation is suppressed in occlusal hypofunction, while it can be enhanced following occlusal recovery during the growth period. This indicates that the recovery of the proper occlusal function during the early growing stage may induce positive changes in the pattern of bone growth.
This study was financially supported by Grants-in-Aid for Scientific Research (15592158, 15791202, 1604250) from the Ministry of Education, Culture, Sports, Science and Technology of Japan. Part of this study was presented at the 64th Annual Meeting of the Japanese Orthodontic Society, Yokohama City, October 12–14, 2005 (Shimomoto et al., 2005). Received for publication January 6, 2006. Revision received September 15, 2006. Accepted for publication September 29, 2006.
Journal of Dental Research, Vol. 86, No. 1,
47-51 (2007)
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