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Article

Impact of Aging on Periodontitis Progression: A Murine Model Study of Porphyromonas gingivalis-Induced Alveolar Bone Loss

by
Mitsutaka Nishimura
1,
Motohiro Komaki
2,
Shuntaro Sugihara
2,* and
Toshiro Kodama
3
1
Department of Oral and Maxillofacial Implantology, Kanagawa Dental University, 3-31-6 Tsuruya, Kanagawa, Yokohama 221-0835, Kanagawa, Japan
2
Department of Periodontology, Kanagawa Dental University, 82 Inaoka, Yokosuka 238-8580, Kanagawa, Japan
3
Kanagawa Dental University Yokohama Clinic, 3-31-6 Tsuruya, Kanagawa, Yokohama 221-0835, Kanagawa, Japan
*
Author to whom correspondence should be addressed.
Oral 2025, 5(3), 51; https://doi.org/10.3390/oral5030051
Submission received: 11 April 2025 / Revised: 25 June 2025 / Accepted: 1 July 2025 / Published: 10 July 2025
(This article belongs to the Collection Oral and Systemic Health: Border Dentistry and the Borders of Dental Practice)
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Abstract

Background: Periodontitis is a chronic inflammatory disease influenced by host aging, yet the specific effects of aging on disease susceptibility remain unclear. Objective: This study aimed to evaluate whether aging increases susceptibility to Porphyromonas gingivalis (P. gingivalis)-induced periodontitis in a murine model. We formulated the null hypothesis that age does not affect susceptibility to periodontal bone loss. Methods: Young (8 weeks) and aged (78 weeks) male C57BL/6 mice were randomly assigned into four groups: young control, young infected, old control, and old infected (n = 8 per group, except for old control, where n = 7). Experimental periodontitis was induced by oral application of P. gingivalis suspended in 5% carboxymethylcellulose (CMC), administered every other day, for a total of three applications. Alveolar bone loss was assessed 39 days after the last inoculation using histomorphometric measurement of buccal distance from the cemento-enamel junction to the alveolar bone crest (CEJ–ABC distance) and micro-computed tomography (μCT) at mesial and distal interdental sites. Bonferroni’s correction was applied to the Mann–Whitney U Test to determine statistical significance. A p-value of less than 0.05 was considered statistically significant. Results: Morphometric analysis showed significantly greater buccal bone loss in infected mice versus controls in both age groups (young: 0.193 mm vs. 0.100 mm, p < 0.01; old: 0.262 mm vs. 0.181 mm, p < 0.01). μCT analysis revealed that interdental bone loss was significant only in aged infected mice (mesial: 0.155 mm vs. 0.120 mm, p < 0.05; distal: 0.185 mm vs. 0.100 mm, p < 0.01), and not significant in young infected mice. Conclusions: Aging significantly exacerbates P. gingivalis-induced alveolar bone loss, particularly in interdental regions. These results allowed us to reject the null hypothesis. This study validates a clinically relevant murine model for analyzing age-related periodontitis and provides a foundation for investigating underlying molecular mechanisms and potential therapeutic interventions.
Keywords:
periodontitis; aging; mouse; μCT

Graphical Abstract

1. Introduction

Periodontitis is an inflammatory disease caused by pathogenic bacteria, which leads to the destruction of periodontal tissues and resorption of alveolar bone. It is also known to be associated with systemic diseases [1]. In addition to bacterial factors, which are the main factors in the development and progression of periodontitis, environmental factors such as stress and dietary habits, and host factors such as diabetes are also involved in the pathogenesis and progression of periodontitis [2]. The prevalence and severity of the disease have been shown to increase with age [3,4,5,6]. In particular, the number of teeth with periodontal pockets and clinical attachment loss increases in elderly people [7,8,9,10].
Although periodontitis is caused by oral bacteria such as P. gingivalis, the extent and outcome of the disease are controlled by the host immune response. Several studies have shown that aging is associated with changes in immune function, leading to altered responses to microbial challenge [7]. The senescence-associated secretory phenotype (SASP) has also been suggested to be involved in the development and progression of age-related diseases, including periodontitis [11,12]. Previously, we performed oral examinations of three different age groups of monkeys (young, middle-aged, and elderly) raised in the same environment and found that the relationship between aging and periodontitis was significantly different among the monkey age groups [13].
However, although there are reports linking age-related immune changes with the progression of periodontal tissue destruction [14,15,16], the detailed mechanism remains unclear. In this situation, it is important to understand how aging in vivo affects the host response to periodontal pathogens. Although bone loss has been reported in elderly animals even without infection [17], it remains unclear whether aging increases susceptibility to periodontal bone loss when infected with P. gingivalis, especially under natural oral exposure conditions. Because human epidemiological studies are limited by uncontrollable factors such as disease activity, severity, and duration [18], animal models are essential to elucidate the mechanism.
To address this issue, we used a mouse model of oral infection with P. gingivalis that closely mimics human chronic periodontitis. Mice are used in many periodontal disease studies because of their short life cycle, ability to reproduce pathology in a short time, ease of genetic manipulation, and small cost and space required to collect large amounts of samples. In addition, mouse models have ethical and cost-effective advantages compared to large animal models. This model allows us to analyze alveolar bone changes in the context of natural infection and host response.
Importantly, various animal models (e.g., ligation and LPS (lipopolysaccharide) injection) have been used to study periodontitis, but there have been no direct comparisons of the effects of aging in oral infection models, which represents a novel aspect of this study.
We formulated the null hypothesis that age does not significantly affect susceptibility to periodontal bone loss. We analyzed alveolar bone changes using micro-CT and histological analysis in young and aged mice orally inoculated with P. gingivalis.
This study provides insight into how age-related immune dysregulation affects periodontal bone loss and may aid in understanding the increased severity of periodontitis in elderly people.

2. Materials and Methods

Animals: Young (8 weeks old) and old (78 weeks old) C57BL/6 male mice were purchased from Jackson Laboratory Japan and stratified by age (young, old), and each age group was randomly assigned into control and P. gingivalis-infected groups (n = 8 per group, except old control: n = 7 due to one dropout).Random assignment was performed using a computer-generated randomization list to allocate animals evenly across the groups while minimizing selection bias. Previous reports have shown that 6 mice/group is sufficient to detect statistically significant differences (Cohen’s d ≈ 4.8) [19]. However, because this experiment was conducted using elderly individuals (78 weeks old) as a long-term infection model, we assumed that approximately 20% of the mice would drop out, and therefore used 8 mice/group. All mice were allowed to drink water and eat freely except for approximately 2 h after infection with P. gingivalis, and were kept at a temperature of 22 °C, a humidity of 50%, and a 12 h light/dark cycle. This experiment was approved by the Committee on Experimental Animals and Recombinant DNA of Kanagawa Dental University (Approval No. 19-033).
Creation of experimental periodontitis: The animals were then fed drinking water mixed with 1 mg/mL sulfamethoxazole and 200 μg/mL trimethoprim in ion-exchanged water for 4 days, followed by ion-exchanged water without the above agents, in order to decrease the number of oral commensal bacteria prior to the development of periodontitis. P. gingivalis ATCC 33277 was cultured in Brain Heart Infusion medium supplemented with 5 mg/mL yeast extract, 5 μg/mL hemin, and 0.2 μg/mL vitamin K1. Cultures were grown under anaerobic conditions of 85% N2, 10% H2, 5% CO2 at 37 °C for 24 h. P. gingivalis-infected groups were prepared with P. gingivalis bacterial suspension (ATCC 33277 109 CFU/mL) prepared with 5% carboxymethylcellulose solution (CMC solution) to induce experimental periodontitis. A 0.1 mL suspension was applied every other day for a total of three applications directly to the molar gingival margin using a syringe. The control group was treated with 5% CMC solution alone. After application, the animals were kept without food and water for approximately 2 h to allow the bacteria to remain in the oral cavity. Thirty-nine days after the last application, cervical dislocation was performed under isoflurane inhalation anesthesia, and samples were collected (Figure 1).
Bone specimen measurement: Mice were sacrificed by cervical dislocation under isoflurane inhalation anesthesia, and the head was dissected with scissors. The soft tissues of the head were removed, the mandible was separated, and the maxilla was split into right and left sides. The left-side maxilla was heated under 2 atm for 15 min, immersed in 3% sodium hypochlorite solution to dissolve the soft tissues, and then rinsed and dried, and then stained with 1% methylene blue solution. The degree of alveolar bone loss was measured with a stereomicroscope (VH-7000 Digital HD Microscope, Keyence, Osaka, Japan) at a magnification of 40×, according to a previous report [19]. The occlusal plane of the molars was leveled and the CEJ–ABC distance of the buccal side of the maxillary left first, second, and third molars was measured at 7 points and the average value of those individuals was calculated (Figure 2).
μCT image measurements: µCT imaging of the right maxilla was performed at 0.1 pixel size, 70 kV tube voltage, and the obtained imaging data were used to measure the CEJ–ABC distance of the two first molar mesial and distal points (ScanXmate-L080, Comscan Techno Corporation, Kanagawa, Japan). The horizontal plane was set parallel to the occlusal plane, and the sagittal plane was defined as the line connecting the centers of the pulp cavities of the mesial roots of the first molars on the horizontal plane. The coronal image was rotated, and the sagittal plane was defined so that the four roots of the first and second molars were visible up to their apexes. To maintain comparability between groups, anatomical landmarks were identified before each image generation (RadiAnt DICOM VIEWER, Medixant) (Figure 3). All measurements were taken by a single person in a blinded manner. Values are in millimeters.
Statistical analysis: The Shapiro–Wilk Test was used to check for normality, the F-test was used to check for equal variance, and the test for normality showed p = 0.02 for the µCT measurement data of the mesial first molar in the young P. gingivalis-infected group. The Kruskal–Wallis Test was used to check for statistical significance, and the Bonferroni-corrected Mann–Whitney U Test was used to check for statistical significance. If the significance level was less than 0.05, it was considered statistically significant. The statistical analysis software used was EZR, a customized package of R developed by Kanda at Saitama Medical Center affiliated with Jichi Medical University [20].

3. Results

P. gingivalis was orally challenged to mice to induce experimental periodontitis and the degree of alveolar bone loss was compared in young (8 weeks old) and old (78 weeks old) mice. One mouse from the old control group dropped out during the experiment.

3.1. Buccal CEJ–ABC Distance Measurement Points in Maxillary Left First, Second, and Third Molar in Bone Specimens

The young controls had a median of 0.100 mm (25%: 0.092 mm—75%: 0.113 mm), and the young P. gingivalis-infected group had a median of 0.193 mm (25%: 0.181 mm—75%: 0.206 mm). The median value of the old controls was 0.181 mm (25%: 0.168 mm—75%: 0.188 mm), and that of the P. gingivalis-infected group was 0.262 mm (25%: 0.257 mm—75%: 0.267 mm). In the control and P. gingivalis-infected groups, there was a trend toward significantly greater CEJ–ABC distance in the old than in the young. In addition, a significantly larger bone loss was observed in the P. gingivalis-infected group than in the control group in both the young and old groups (Figure 4 and Figure 5).

3.2. Measurement Results in µCT Images of the Mesial and Distal Maxillary Right First Molar

In representative images of each group, both the control and P. gingivalis-infected groups, there was a trend toward greater CEJ–ABC distance in old compared to young (Figure 6).

3.2.1. First Molar Mesial

The CEJ–ABC distance of the mesial first molars in the young group was median 0.080 mm (25%: 0.062 mm—75%: 0.086 mm) in the control group, and median 0.085 mm (25%: 0.077 mm—75%: 0.102 mm) in the P. gingivalis-infected group. In the old group, the median value was 0.120 mm (25%: 0.101 mm—75%: 0.135 mm) in the control group and median 0.155 mm (25%: 0.140 mm—75%: 0.190 mm) in the P. gingivalis-infected group, respectively. Significantly greater CEJ–ABC distances were observed in the control and P. gingivalis-infected groups, respectively, and in the old compared to the young. There was no significant difference between the control group and the P. gingivalis-infected group in the young age group, but in the old age group, significant bone loss was observed in the P. gingivalis-infected group compared to the control group (Figure 7).

3.2.2. First Molar Distal

The CEJ–ABC distance of the first molar distal in the young age was median 0.087 mm in the control group (25%: 0.084 mm—75%: 0.090 mm), and median 0.115 mm in the P. gingivalis-infected group (25%: 0.090 mm—75%: 0.132 mm). The median value in the old group was 0.100 mm (25%: 0.092 mm—75%: 0.130 mm) in the control and median 0.185 mm (25%: 0.168 mm—75%: 0.215 mm) in the P. gingivalis-infected group. Comparing young and old in the control groups, there was a trend toward greater CEJ–ABC distance in the old, but the difference was not statistically significant. There was no significant difference between the control group and the P. gingivalis-infected group in the young age group. In the old age group, significant bone loss was observed in the P. gingivalis-infected group compared to the control group (Figure 8).

4. Discussion

In this study, we compared the effects of oral infection with P. gingivalis on alveolar bone loss in young and aged mice. Although bone loss was observed in both age groups, the extent was significantly higher in the aged group. These results allowed us to reject the null hypothesis that aging does not significantly affect the susceptibility to periodontal bone loss. This finding is consistent with previous reports that aging is associated with bone loss.
Most previous reports on experimental periodontitis used young mice, and few reports compared disease progression in young and aged mice. A recent report induced periodontitis in both young and aged mice using a ligature model [21]. However, there are limited studies using oral bacterial exposure across age groups.
Experimental periodontitis can be induced in a variety of ways, including injection of inactivated bacteria or bacterial components (e.g., LPS) [22], ligation [23], oral bacterial exposure [19], and combinations of these [24]. Each method has its own advantages and limitations. Ligation can cause rapid and significant bone loss in as little as 7 days [17]. On the other hand, the acute periodontitis process, which involves the trauma of ligature insertion, tends to heal after the thread is removed, and bone loss decreases over time. Ligation can cause trauma and acute inflammation that do not accurately mimic the characteristics of chronic periodontitis in humans [25]. The ligated and heat-sterilized P. gingivalis injection model was used as a short-term experimental model to understand the pathogenesis of the disease and the complex host response to the microbe [17]. Oral exposure to P. gingivalis may be the closest approach to human periodontitis, as oral exposure results in a longer induction period, significant bone loss, and the development of chronic periodontitis over time. In addition, this method alters the gut microbiota and increases the levels of inflammatory markers [26]. This allows for a more extensive investigation of the systemic effects [27]. Recent studies support this systemic interaction. Giri et al. demonstrated that oral administration of P. gingivalis disrupted the intestinal microbiota and impaired epithelial barrier function more severely in aged mice compared with young mice, suggesting that aging enhances the oral–gut axis in periodontitis [28].
Similarly, Chen et al. reported that hepatocyte growth factor (HGF) plays an important role in aggravating intestinal barrier dysfunction in periodontitis by acting on junctional proteins and promoting intestinal microbiota dysbiosis [29]. These findings highlight the importance of considering both microbial and host factors in studying age-related periodontitis susceptibility and its systemic effects.
The results of μCT supported these findings and demonstrated that this imaging method is useful for evaluating bone changes. Alveolar bone loss in animal experiments is measured by histology, morphometry, and linear measurements by X-ray and CT. A study comparing histology, morphometry, and μCT measurements [30] showed that all three techniques can accurately quantify alveolar bone loss. Morphometric methods cannot capture intrabony defects as effectively as μCT. However, consistent age-related differences were observed with both techniques in this study.
The significance of this study is also the validation of an oral infection model that mimics the natural history of periodontitis and reveals age-related susceptibility. This model provides a valuable platform to study the complex host–microbe interactions and age-related immune responses involved in the progression of periodontitis. Furthermore, it is adaptable to the evaluation of therapeutic interventions and genetic factors in a controlled and highly reproducible environment.
Several limitations of this study need to be acknowledged. First, although inflammatory responses play a central role in the progression of periodontitis, we did not measure cytokine levels such as IL-1β and TNF-α in this study. Therefore, we cannot discuss the underlying immunological mechanisms. Second, we did not perform histological analysis of osteoclast activity and immune cell infiltration. Third, although the mouse model provides valuable insights, age-related changes in immunity and bone metabolism may differ between mice and humans.
The results of this study suggest that age-related periodontal bone destruction is exacerbated not only by baseline bone loss but also by changes in the host response to bacterial infection. This suggests that aging may increase susceptibility to periodontitis by reducing the host’s ability to control inflammation, leading to more severe tissue damage. Indeed, aging is known to be associated with immunosenescence, a decline in immune function, and the development of chronic low-level inflammation, often referred to as “inflammaging” [31], all of which may affect the course of periodontal disease. In addition, our mouse oral infection model mimics the chronic nature of human periodontitis, making it a valuable and clinically relevant tool for future research. In humans, bone defects occur most frequently on adjacent mesial and distal surfaces [32,33]. Furthermore, the level of clinical attachment in the interdental area is an important factor in the definition of periodontitis in the new staging and grading of periodontitis [34]. Although the present study primarily focused on alveolar bone, future studies will require cytokine profiling (e.g., IL-1β, TNF-α, IL-6), immune cell infiltration, bone remodeling markers (e.g., RANKL, OPG, CTX, TRAP, MMP-8), histopathological evaluation, microbiome composition, and long-term follow-up to fully understand the mechanisms involved.

5. Conclusions

In this study, we demonstrated that aging significantly increased the susceptibility of mice to P. gingivalis-induced alveolar bone loss. Morphological and μCT analyses revealed that older mice exhibited more pronounced buccal and interdental bone loss in response to infection compared with younger mice. Notably, interdental bone loss was not significant in younger mice, highlighting the impact of aging as a risk factor for periodontal disease progression. These findings support the usefulness of this oral infection mouse model as a physiologically relevant translational tool to study age-related periodontitis and its underlying mechanisms.

Author Contributions

Conceptualization, M.K. and T.K.; methodology, M.K. and T.K.; software, M.N. and M.K.; validation, M.N. and M.K.; formal analysis, M.N. and M.K.; investigation, M.N. and M.K.; resources, M.N. and M.K.; data curation, M.N. and M.K.; writing—original draft preparation, M.N. and T.K.; writing—review and editing, M.N., M.K. and S.S.; visualization, M.N., M.K. and S.S.; supervision, M.K., T.K., and S.S.; project administration, M.K. and T.K.; funding acquisition, M.K. All authors have read and agreed to the published version of the manuscript.

Funding

This work was supported by a Grant-in-Aid for Scientific Research (C) (General) (Grant Number 18K09586) from the Japan Society for the Promotion of Science (JSPS).

Institutional Review Board Statement

The animal study protocol was approved by the Ethics Committee on Experimental Animals and Recombinant DNA of Kanagawa Dental University (Approval code 19-033, date 3 January 2021).

Informed Consent Statement

Not applicable.

Data Availability Statement

The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author.

Conflicts of Interest

The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

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Oral 05 00051 g001
Figure 1. Experimental schedule. The animals were fed drinking water mixed with 1 mg/mL sulfamethoxazole and 200 μg/mL trimethoprim in ion-exchanged water for 4 days, followed by ion-exchanged water without the above agents. P. gingivalis-infected groups were prepared with P. gingivalis bacterial suspension in 5% CMC solution to induce experimental periodontitis. Three times every 2 days, 0.1 mL was applied directly to the molar gingival margin. Thirty-nine days after the last application, cervical dislocation was performed under isoflurane inhalation anesthesia, and samples were collected.
Figure 1. Experimental schedule. The animals were fed drinking water mixed with 1 mg/mL sulfamethoxazole and 200 μg/mL trimethoprim in ion-exchanged water for 4 days, followed by ion-exchanged water without the above agents. P. gingivalis-infected groups were prepared with P. gingivalis bacterial suspension in 5% CMC solution to induce experimental periodontitis. Three times every 2 days, 0.1 mL was applied directly to the molar gingival margin. Thirty-nine days after the last application, cervical dislocation was performed under isoflurane inhalation anesthesia, and samples were collected.
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Figure 2. Buccal CEJ–ABC distance measurement points in maxillary left first, second, and third molar in bone specimens are shown by two-headed arrows.
Figure 2. Buccal CEJ–ABC distance measurement points in maxillary left first, second, and third molar in bone specimens are shown by two-headed arrows.
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Figure 3. Method of defining µCT images. µCT imaging data of the right maxilla were used to measure the CEJ–ABC distance (shown by two-headed arrows) of the two first molar mesial and distal points. The horizontal plane was set parallel to the occlusal plane, and the sagittal plane was defined as the line connecting the centers of the pulp cavities of the mesial roots of the first molars on the horizontal plane. The coronal image was rotated, and the sagittal plane was defined so that the four roots of the first and second molars were visible up to their apexes.
Figure 3. Method of defining µCT images. µCT imaging data of the right maxilla were used to measure the CEJ–ABC distance (shown by two-headed arrows) of the two first molar mesial and distal points. The horizontal plane was set parallel to the occlusal plane, and the sagittal plane was defined as the line connecting the centers of the pulp cavities of the mesial roots of the first molars on the horizontal plane. The coronal image was rotated, and the sagittal plane was defined so that the four roots of the first and second molars were visible up to their apexes.
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Figure 4. Representative photographs of bone specimens from each of the groups. Old mice show significant tooth wear and alveolar bone loss compared to young mice. Significant bone loss was observed in the P. gingivalis-infected group compared to the control group.
Figure 4. Representative photographs of bone specimens from each of the groups. Old mice show significant tooth wear and alveolar bone loss compared to young mice. Significant bone loss was observed in the P. gingivalis-infected group compared to the control group.
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Figure 5. Buccal CEJ–ABC distance measurements on maxillary left first, second, and third molar in bone specimens. In the control and P. gingivalis-infected groups, there was a trend toward significantly greater CEJ–ABC distance in the old than in the young. In addition, a significantly larger bone loss was observed in the P. gingivalis-infected group than in the control group in both the young and old groups. Data are shown by box and whisker plots with median values.
Figure 5. Buccal CEJ–ABC distance measurements on maxillary left first, second, and third molar in bone specimens. In the control and P. gingivalis-infected groups, there was a trend toward significantly greater CEJ–ABC distance in the old than in the young. In addition, a significantly larger bone loss was observed in the P. gingivalis-infected group than in the control group in both the young and old groups. Data are shown by box and whisker plots with median values.
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Figure 6. µCT images for each group. In both the control and P. gingivalis-infected groups, there was a trend toward greater CEJ–ABC distance in old compared to young. The sagittal sections set parallel to the occlusal plane are shown by blue lines. The pink line was used as a guide axis to rotate the coronal section so that the root apex of the first and second molar would be visible in the sagittal section image.
Figure 6. µCT images for each group. In both the control and P. gingivalis-infected groups, there was a trend toward greater CEJ–ABC distance in old compared to young. The sagittal sections set parallel to the occlusal plane are shown by blue lines. The pink line was used as a guide axis to rotate the coronal section so that the root apex of the first and second molar would be visible in the sagittal section image.
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Figure 7. Measurement results in µCT images of the mesial maxillary right first molar. Significantly greater CEJ–ABC distances were observed in the control and P. gingivalis-infected groups, respectively, in the old mice compared to the young. There was no significant difference between the control group and the P. gingivalis-infected group in the young mice, but in the old mice, significant bone loss was observed in the P. gingivalis-infected group compared to the control group. Data are shown by box and whisker plots with median values.
Figure 7. Measurement results in µCT images of the mesial maxillary right first molar. Significantly greater CEJ–ABC distances were observed in the control and P. gingivalis-infected groups, respectively, in the old mice compared to the young. There was no significant difference between the control group and the P. gingivalis-infected group in the young mice, but in the old mice, significant bone loss was observed in the P. gingivalis-infected group compared to the control group. Data are shown by box and whisker plots with median values.
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Figure 8. Measurement results in µCT images of distal maxillary right first molar. Comparing young and old in the control group, there was a trend toward greater CEJ–ABC distance in the old, but the difference was not statistically significant. There was no significant difference between the control group and the P. gingivalis-infected group in the young age group. In the old age group, significant bone loss was observed in the P. gingivalis-infected group compared to the control group. Data are shown by box and whisker plots with median values.
Figure 8. Measurement results in µCT images of distal maxillary right first molar. Comparing young and old in the control group, there was a trend toward greater CEJ–ABC distance in the old, but the difference was not statistically significant. There was no significant difference between the control group and the P. gingivalis-infected group in the young age group. In the old age group, significant bone loss was observed in the P. gingivalis-infected group compared to the control group. Data are shown by box and whisker plots with median values.
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MDPI and ACS Style

Nishimura, M.; Komaki, M.; Sugihara, S.; Kodama, T. Impact of Aging on Periodontitis Progression: A Murine Model Study of Porphyromonas gingivalis-Induced Alveolar Bone Loss. Oral 2025, 5, 51. https://doi.org/10.3390/oral5030051

AMA Style

Nishimura M, Komaki M, Sugihara S, Kodama T. Impact of Aging on Periodontitis Progression: A Murine Model Study of Porphyromonas gingivalis-Induced Alveolar Bone Loss. Oral. 2025; 5(3):51. https://doi.org/10.3390/oral5030051

Chicago/Turabian Style

Nishimura, Mitsutaka, Motohiro Komaki, Shuntaro Sugihara, and Toshiro Kodama. 2025. "Impact of Aging on Periodontitis Progression: A Murine Model Study of Porphyromonas gingivalis-Induced Alveolar Bone Loss" Oral 5, no. 3: 51. https://doi.org/10.3390/oral5030051

APA Style

Nishimura, M., Komaki, M., Sugihara, S., & Kodama, T. (2025). Impact of Aging on Periodontitis Progression: A Murine Model Study of Porphyromonas gingivalis-Induced Alveolar Bone Loss. Oral, 5(3), 51. https://doi.org/10.3390/oral5030051

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