Sie können Operatoren mit Ihrer Suchanfrage kombinieren, um diese noch präziser einzugrenzen. Klicken Sie auf den Suchoperator, um eine Erklärung seiner Funktionsweise anzuzeigen.
Findet Dokumente, in denen beide Begriffe in beliebiger Reihenfolge innerhalb von maximal n Worten zueinander stehen. Empfehlung: Wählen Sie zwischen 15 und 30 als maximale Wortanzahl (z.B. NEAR(hybrid, antrieb, 20)).
Findet Dokumente, in denen der Begriff in Wortvarianten vorkommt, wobei diese VOR, HINTER oder VOR und HINTER dem Suchbegriff anschließen können (z.B., leichtbau*, *leichtbau, *leichtbau*).
The interplay among diabetes, obesity, and periodontal disease is well-established. In addition to diabetes and obesity, numerous factors contribute to the risk of tooth loss, including age, smoking status, and oral care practices. However, most previous studies included fewer than 10,000 participants, limiting the ability to conduct comprehensive quantitative analyses of remaining teeth. This review examines the impacts of diabetes and obesity on the number of remaining teeth using large-scale data, such as national databases, to provide real-world evidence.
Recent Findings
Recent studies have identified linear relationships between the number of remaining teeth and factors such as fasting plasma glucose, glycated hemoglobin, and body mass index across different age groups. Periodontal disease exacerbation has emerged as an important mechanism of tooth loss. Hyperglycemia-associated chronic inflammation and endothelial dysfunction are suspected to worsen periodontal disease, which would constitute a causal link between systemic and periodontal conditions. Furthermore, several clinical trials have demonstrated that resolution of periodontal disease can improve glycemic control in patients with type 2 diabetes or delay the onset of type 2 diabetes in individuals with insulin resistance. This evidence suggests a bidirectional relationship between periodontal and systemic diseases.
Summary
Large-scale data analyses have provided clearer insights into the cyclical relationship among diabetes, obesity, and periodontal disease, emphasizing its potential role in preventing tooth loss.
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Introduction
Periodontal disease is an inflammatory condition caused by periodontal pathogens and constitutes a leading cause of tooth loss in adults [1]. This disease leads to tooth loss through prolonged inflammation in periodontal tissues, which activates osteoclasts and results in resorption of the alveolar bone that supports the teeth. According to the Global Burden of Disease study, oral diseases affect 3.5 billion people worldwide [2], and the majority of cases can be attributed to untreated dental caries and periodontitis [3]. It is estimated that over 50% of U.S. adults have periodontal disease, depending on the disease definition, which substantially impacts their quality of life [4]. A survey of dental diseases in Japan revealed that more than 40% of individuals aged 45 or older had periodontal pockets measuring 4 mm or greater [5]. Severe periodontal disease is considered the sixth-most prevalent health condition worldwide, affecting 743 million people [6]. The global prevalence of untreated dental caries is 34.1%; increasing rates are observed in low- to middle-income countries [2]. Although the combined burden of oral conditions has declined in more economically developed nations, it has risen in less economically developed countries, indicating disparities in oral health outcomes among regions [3].
Previous studies have partially elucidated the relationship among diabetes, obesity, and periodontal disease [7‐9]. Adipocytes play a key role in energy storage and produce various adipocytokines. Visceral fat accumulation disrupts adipocytokine balance, inducing chronic inflammation and insulin resistance (Fig. 1). Although insulin resistance is a primary factor in diabetes, periodontal disease reportedly also contributes to systemic insulin resistance, as measured by the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), through prolonged inflammation in periodontal tissues [10, 11]. However, the numbers of remaining teeth and retention rates among tooth sites in individuals with diabetes or obesity remain poorly understood. One challenge in clarifying these relationships is that analyses using the number of remaining teeth as an outcome are strongly influenced by factors such as age and sex, hindering effective stratification of risk factors in studies with limited sample sizes. This review summarizes the studies of the impacts of diabetes and obesity on oral health, with a focus on the number of remaining teeth, by using a large database created by linking dental visit records from insurance claims with health check-up results.
Fig. 1
Relationships among obesity, diabetes, and periodontal disease
A meta-analysis of 15 cohort studies revealed that individuals with periodontal disease had a significantly increased risk of developing diabetes, with a summary relative risk of 1.26 among 427,620 participants. Conversely, in a cohort of 295,804 individuals, participants with diabetes exhibited a 1.24-fold higher summary relative risk for developing periodontal disease relative to participants without diabetes [12]. This evidence implies a bidirectional relationship between periodontitis and diabetes [12]. Patients with diabetes are considered more susceptible to periodontal disease, likely due to hyperglycemia-induced impairments in immunity and resistance to periodontal pathogens. Periodontal disease is more prevalent among individuals with diabetes [7, 8, 12, 13], and poor glycemic control is associated with greater periodontal disease severity [8, 14, 15]. Both type 1 and type 2 diabetes are associated with higher risks of tooth loss; poorly controlled diabetes further amplifies the risks of periodontal disease and tooth loss [9, 16]. Treatment for diabetes has been shown to improve periodontal inflammation and related parameters [17, 18]. Periodontal inflammation can aggravate systemic conditions by releasing pro-inflammatory cytokines, contributing to insulin resistance and worsening glycemic control. Individuals with periodontitis exhibit a higher risk of developing diabetes [12, 19]. Furthermore, meta-analyses and reviews have demonstrated that periodontal treatment effectively improves glycemic control in patients with diabetes [20‐23]. Studies have shown that periodontal therapy can enhance insulin sensitivity, as indicated by improved HOMA-IR values, and reduce levels of high-sensitivity C-reactive protein and inflammatory cytokines [17, 24, 25].
We analyzed the relationships between the number of remaining teeth and glycemic control indices using a dataset of 230,000 individuals. This dataset was generated by matching dental visit records from employment-based health insurance claims with health check-up results. The analysis revealed inverse relationships of glycated hemoglobin (HbA1c) and fasting blood glucose levels with the number of remaining teeth [26]. This trend was evident even in individuals without a diabetes diagnosis (HbA1c levels of 5.5%–6.5% and fasting glucose levels of 110–126 mg/dL) and could be observed as early as the third decade of life [26].
A site-specific analysis of natural tooth retention showed that individuals in their 30 s with HbA1c levels < 7% were significantly more likely to lose posterior teeth than similarly aged individuals with HbA1c levels ≥ 7%. As individuals aged into their 40 s and 50 s, this pattern extended to the loss of teeth adjacent to posterior teeth and anterior teeth [27]. These findings suggest that poor glycemic control increases the likelihood of posterior tooth loss at a relatively young age, and that progression to more extensive tooth loss occurs with increasing age (Fig. 2) [27].
Fig. 2
Percentage of subjects with natural teeth at each position in groups with HbA1c < 7% and ≥ 7.0% by age groups (30s–60s)
Obesity exacerbates various chronic diseases, such as diabetes and atherosclerotic diseases. Obesity-induced chronic inflammation causes insulin resistance, which contributes to diabetes development while increasing the risks of periodontal disease onset and progression [28]. Additionally, multiple studies have demonstrated a relationship between periodontal disease and metabolic syndrome, a condition characterized by visceral obesity combined with hyperglycemia and dyslipidemia [29‐31]. Among the components of metabolic syndrome, hyperglycemia and obesity appear to have the strongest associations with periodontal disease risk [29]. Furthermore, the likelihood of developing periodontal disease increases according to the number of metabolic syndrome components present [29, 32]. Factors shared between periodontal disease and metabolic syndrome include elevated oxidative stress, which promotes insulin resistance, and a persistent state of chronic inflammation [33]. Another proposed mechanism underlying the increased risk of periodontal disease in obesity involves alterations in the gut microbiota and its metabolic activity [34].
Anzeige
The relationship between obesity and periodontal disease has been demonstrated in a health check-up study, which showed that the relative risk of periodontal disease increased according to body mass index (BMI) [35]. Similar results were obtained in the Third National Health and Nutrition Examination Survey, which analyzed data from approximately 13,000 individuals in the United States [36]. Systematic review findings reinforce the notion that obesity and increased waist circumference are significant risk factors for the development and progression of periodontal disease [37]. A recent study involving 57,496 individuals identified obesity and nonalcoholic fatty liver disease (NAFLD) comorbidity as the most influential systemic conditions in a feature importance analysis using the eXtreme Gradient Boosting machine learning algorithm, with periodontitis as the target variable [30].
Conversely, epidemiological study results suggest that periodontal disease increases the risk of obesity by reducing masticatory function. Tooth loss impairs chewing ability, leading to a preference for processed foods high in carbohydrates that require minimal chewing, thereby raising the risk of obesity [38, 39].
Our study also revealed an association between increased BMI and a decline in the number of remaining teeth beginning at age 40 [40]. Compared with non-obese individuals (BMI < 25 kg/m2), those with obesity (BMI ≥ 25 kg/m2) had significantly fewer remaining teeth at 10 sites (six maxillary, four mandibular) in their 30 s, 19 sites (11 maxillary, eight mandibular) in their 40 s, 24 sites (14 maxillary, 10 mandibular) in their 50 s, and 21 sites (13 maxillary, eight mandibular) in their 60 s. These findings are consistent with previous studies [41, 42] but add novel insights based on examinations of specific age groups and tooth sites.
Combined Effect of Smoking on Periodontal Disease in Diabetes and Obesity
Smoking is a significant risk factor for periodontitis, associated with both increased prevalence and severity of the disease [43‐45]. Multiple studies have established a causal link between smoking and tooth loss [46‐48]. A recent large-scale study investigating chronic diseases and tooth loss among 471,107 participants confirmed a strong association between smoking and tooth loss. It also identified significant associations with diabetes and chronic obstructive pulmonary disease (COPD)—both conditions linked to smoking—and tooth loss [49]. Intriguingly, the study showed a stronger association with COPD than with diabetes, emphasizing the effects of smoking on these outcomes.
The risk of tooth loss further increases when smoking is combined with diabetes. Smoking adversely alters the oral environment; the toxic substances in tobacco affect the oral cavity and respiratory tract while contributing to systemic chronic inflammation, including intestinal infections. Our analysis of 233,567 individuals revealed that nonsmokers with HbA1c ≥ 6.5% had a 1.83-fold increased risk of possessing fewer than 24 remaining teeth relative to nonsmokers with HbA1c < 6.5%. Among smokers with HbA1c ≥ 6.5%, the risk increased 3.55-fold compared with the same reference group [26].
A recent machine learning study identified smoking and obesity as two of the top five factors most strongly associated with periodontitis [30]. In our analysis of natural tooth retention according to site, the addition of smoking as a variable revealed an additional impact on tooth loss in locations unaffected by obesity alone. Further examination of the risk of possessing fewer than 24 remaining teeth showed a 1.47-fold increase in individuals with BMI ≥ 25 kg/m2 relative to those with BMI < 25 kg/m2. The risk increased by 1.35-fold when smoking status and diabetes were included as explanatory variables in the model [26].
The maintenance of good oral hygiene is a critical component of glycemic control in diabetic patients; effective glycemic control can help to prevent periodontal disease and tooth loss. This bidirectional relationship is also present among individuals with obesity and those with metabolic syndrome. Recommendations of regular dental visits for patients with diabetes and obesity, as well as screening for diabetes and metabolic syndrome in patients with periodontal disease, may prove beneficial. Smoking, a well-established risk factor for tooth loss, can decrease this risk upon cessation; former smokers have no greater risk compared with nonsmokers [49].
The combination of large-scale medical data, such as receipt information and health check-up results, used in this study has yielded important insights into oral health conditions and healthcare costs [50]. This approach holds promise for broader applications in medical and dental clinical research.
Anzeige
Conclusion
In conclusion, this study utilized a large database integrating receipt data and health check-up results to examine the effects of diabetes and obesity on dental health, focusing on the number of remaining teeth. The findings, supported by previous reports, emphasize the importance of addressing the interconnected cycle of diabetes, obesity, and periodontal disease as a key strategy to prevent tooth loss.
Key References
Harada K, Morino K, Ishikawa M, Miyazawa I, Yasuda T, Hayashi M, et al. Glycemic control and number of natural teeth: analysis of cross-sectional Japanese employment-based dental insurance claims and medical check-up data. Diabetol Int. 2022;13:244–52.
A study of 230,000 individuals examined the correlation between tooth loss and blood glucose levels. The utilisation of big data facilitated an investigation which demonstrated an inverse correlation between HbA1c and fasting blood glucose levels and the number of remaining teeth.
Wilensky A, Frank N, Mizraji G, Tzur D, Goldstein C, Almoznino G. Periodontitis and Metabolic Syndrome: Statistical and Machine Learning Analytics of a Nationwide Study. Bioengineering (Basel). 2023;10.
Using machine learning algorithm, this study identified multiple factors related to metabolic syndrome are associated with periodontitis in 57,496 records of patients.
Acknowledgements
We thank Ryan Chastain-Gross, Ph.D., from Edanz (https://jp.edanz.com/ac) for editing a draft of this manuscript.
Declarations
Ethics Approval
Research using anonymized data does not require ethical review. The paper presented in this review is also a study using anonymized data, and it was determined that ethical review was not required.
Anzeige
Human and Animal Rights and Informed Consent
All studies with human subjects are published and followed ethical standards.
Conflicts of Interest
IM received research support unrelated to this study from Sunstar Inc. KH and AI are employees of Sunstar Inc. The authors were solely responsible for the analysis and writing of the paper on which this review is based. KM received research support unrelated to this study from Sunstar Inc. SK received research support unrelated to this study from Boehringer Ingelheim, Eli Lilly, Sumitomo Pharma, and Mitsubishi Tanabe Pharma Corporation. No other potentially relevant conflicts of interest are declared.
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Bahrami G, Vaeth M, Kirkevang LL, Wenzel A, Isidor F. Risk factors for tooth loss in an adult population: a radiographic study. J Clin Periodontol. 2008;35:1059–65.PubMedCrossRef
2.
Peres MA, Macpherson LMD, Weyant RJ, Daly B, Venturelli R, Mathur MR, et al. Oral diseases: a global public health challenge. Lancet. 2019;394:249–60.PubMedCrossRef
3.
Collaborators GBDOD, Bernabe E, Marcenes W, Hernandez CR, Bailey J, Abreu LG, et al. Global, Regional, and National Levels and Trends in Burden of Oral Conditions from 1990 to 2017: A Systematic Analysis for the Global Burden of Disease 2017 Study. J Dent Res. 2020;99:362–73.CrossRef
4.
Tonetti MS, Eickholz P, Loos BG, Papapanou P, van der Velden U, Armitage G, et al. Principles in prevention of periodontal diseases: Consensus report of group 1 of the 11th European Workshop on Periodontology on effective prevention of periodontal and peri-implant diseases. J Clin Periodontol. 2015;42(Suppl 16):S5-11.PubMed
Kassebaum NJ, Bernabe E, Dahiya M, Bhandari B, Murray CJ, Marcenes W. Global burden of severe periodontitis in 1990–2010: a systematic review and meta-regression. J Dent Res. 2014;93:1045–53.PubMedPubMedCentralCrossRef
7.
Nelson RG, Shlossman M, Budding LM, Pettitt DJ, Saad MF, Genco RJ, et al. Periodontal disease and NIDDM in Pima Indians. Diabetes Care. 1990;13:836–40.PubMedCrossRef
8.
Tsai C, Hayes C, Taylor GW. Glycemic control of type 2 diabetes and severe periodontal disease in the US adult population. Community Dent Oral Epidemiol. 2002;30:182–92.PubMedCrossRef
9.
Demmer RT, Holtfreter B, Desvarieux M, Jacobs DR Jr, Kerner W, Nauck M, et al. The influence of type 1 and type 2 diabetes on periodontal disease progression: prospective results from the Study of Health in Pomerania (SHIP). Diabetes Care. 2012;35:2036–42.PubMedPubMedCentralCrossRef
10.
Song IS, Han K, Park YM, Ji S, Jun SH, Ryu JJ, et al. Severe Periodontitis Is Associated with Insulin Resistance in Non-abdominal Obese Adults. J Clin Endocrinol Metab. 2016;101:4251–9.PubMedCrossRef
11.
Andriankaja OM, Munoz-Torres FJ, Vivaldi-Oliver J, Leroux BG, Campos M, Joshipura K, et al. Insulin resistance predicts the risk of gingival/periodontal inflammation. J Periodontol. 2018;89:549–57.PubMedPubMedCentralCrossRef
12.
Stohr J, Barbaresko J, Neuenschwander M, Schlesinger S. Bidirectional association between periodontal disease and diabetes mellitus: a systematic review and meta-analysis of cohort studies. Sci Rep. 2021;11:13686.PubMedPubMedCentralCrossRef
13.
Mealey BL, Oates TW, American Academy of P. Diabetes mellitus and periodontal diseases. J Periodontol. 2006;77:1289–303.PubMedCrossRef
14.
Ervasti T, Knuuttila M, Pohjamo L, Haukipuro K. Relation between control of diabetes and gingival bleeding. J Periodontol. 1985;56:154–7.PubMedCrossRef
15.
Romano F, Perotto S, Mohamed SEO, Bernardi S, Giraudi M, Caropreso P, et al. Bidirectional Association between Metabolic Control in Type-2 Diabetes Mellitus and Periodontitis Inflammatory Burden: A Cross-Sectional Study in an Italian Population. J Clin Med. 2021;10:1787. https://doi.org/10.3390/jcm10081787.CrossRefPubMedPubMedCentral
16.
Inagaki K, Kikuchi T, Noguchi T, Mitani A, Naruse K, Matsubara T, et al. A large-scale observational study to investigate the current status of diabetic complications and their prevention in Japan (JDCP study 6): baseline dental and oral findings. Diabetol Int. 2021;12:52–61.PubMedCrossRef
17.
Katagiri S, Nitta H, Nagasawa T, Izumi Y, Kanazawa M, Matsuo A, et al. Effect of glycemic control on periodontitis in type 2 diabetic patients with periodontal disease. J Diabetes Investig. 2013;4:320–5.PubMedPubMedCentralCrossRef
18.
Mizutani K, Minami I, Mikami R, Kido D, Takeda K, Nakagawa K, et al. Improvement of periodontal parameters following intensive diabetes care and supragingival dental prophylaxis in patients with type 2 diabetes: A prospective cohort study. J Clin Periodontol. 2024;51:733–41.PubMedCrossRef
19.
Graziani F, Gennai S, Solini A, Petrini M. A systematic review and meta-analysis of epidemiologic observational evidence on the effect of periodontitis on diabetes An update of the EFP-AAP review. J Clin Periodontol. 2018;45:167–87.PubMedCrossRef
20.
Di Domenico GL, Minoli M, Discepoli N, Ambrosi A, de Sanctis M. Effectiveness of periodontal treatment to improve glycemic control: an umbrella review. Acta Diabetol. 2023;60:101–13.PubMedCrossRef
21.
Simpson TC, Weldon JC, Worthington HV, Needleman I, Wild SH, Moles DR, et al. Treatment of periodontal disease for glycaemic control in people with diabetes mellitus. Cochrane Database Syst Rev. 2015;2015:CD004714.PubMedPubMedCentral
22.
Engebretson S, Kocher T. Evidence that periodontal treatment improves diabetes outcomes: a systematic review and meta-analysis. J Periodontol. 2013;84:S153–69.PubMedPubMedCentralCrossRef
23.
Li Q, Hao S, Fang J, Xie J, Kong XH, Yang JX. Effect of non-surgical periodontal treatment on glycemic control of patients with diabetes: a meta-analysis of randomized controlled trials. Trials. 2015;16:291.PubMedPubMedCentralCrossRef
24.
Munenaga Y, Yamashina T, Tanaka J, Nishimura F, Hiroshima Study Group. Improvement of glycated hemoglobin in Japanese subjects with type 2 diabetes by resolution of periodontal inflammation using adjunct topical antibiotics: results from the Hiroshima Study. Diabetes Res Clin Pract. 2013;100:53–60.PubMedCrossRef
25.
Sun WL, Chen LL, Zhang SZ, Wu YM, Ren YZ, Qin GM. Inflammatory cytokines, adiponectin, insulin resistance and metabolic control after periodontal intervention in patients with type 2 diabetes and chronic periodontitis. Intern Med. 2011;50:1569–74.PubMedCrossRef
26.
Harada K, Morino K, Ishikawa M, Miyazawa I, Yasuda T, Hayashi M, et al. Glycemic control and number of natural teeth: analysis of cross-sectional Japanese employment-based dental insurance claims and medical check-up data. Diabetol Int. 2022;13:244–52.PubMedCrossRef
27.
Morino K, Miyazawa I, Maegawa H. Diabetes and periodontal disease based on a large database. Gekkan Tonyobyo. 2022;147:6–10.
28.
Saito T, Shimazaki Y, Koga T, Tsuzuki M, Ohshima A. Relationship between upper body obesity and periodontitis. J Dent Res. 2001;80:1631–6.PubMedCrossRef
29.
Lamster IB, Pagan M. Periodontal disease and the metabolic syndrome. Int Dent J. 2017;67:67–77.PubMedCrossRef
Campos JR, Martins CC, Faria SFS, Carvalho AP, Pereira AG, Costa FO, et al. Association between components of metabolic syndrome and periodontitis: a systematic review and meta-analysis. Clin Oral Investig. 2022;26:5557–74.PubMedCrossRef
33.
Bullon P, Morillo JM, Ramirez-Tortosa MC, Quiles JL, Newman HN, Battino M. Metabolic syndrome and periodontitis: is oxidative stress a common link? J Dent Res. 2009;88:503–18.PubMedCrossRef
34.
Sato K, Yamazaki K, Kato T, Nakanishi Y, Tsuzuno T, Yokoji-Takeuchi M, et al. Obesity-Related Gut Microbiota Aggravates Alveolar Bone Destruction in Experimental Periodontitis through Elevation of Uric Acid. mBio. 2021;12:e0077121.PubMedCrossRef
35.
Saito T, Shimazaki Y, Sakamoto M. Obesity and periodontitis. N Engl J Med. 1998;339:482–3.PubMedCrossRef
36.
Wood N, Johnson RB, Streckfus CF. Comparison of body composition and periodontal disease using nutritional assessment techniques: Third National Health and Nutrition Examination Survey (NHANES III). J Clin Periodontol. 2003;30:321–7.PubMedCrossRef
37.
Keller A, Rohde JF, Raymond K, Heitmann BL. Association between periodontal disease and overweight and obesity: a systematic review. J Periodontol. 2015;86:766–76.PubMedCrossRef
38.
Wakai K, Naito M, Naito T, Kojima M, Nakagaki H, Umemura O, et al. Tooth loss and intakes of nutrients and foods: a nationwide survey of Japanese dentists. Community Dent Oral Epidemiol. 2010;38:43–9.PubMedCrossRef
39.
Iwasaki T, Fukuda H, Kitamura M, Kawashita Y, Hayashida H, Furugen R, et al. Association between number of pairs of opposing posterior teeth, metabolic syndrome, and obesity. Odontology. 2019;107:111–7.PubMedCrossRef
40.
Hayashi M, Morino K, Harada K, Miyazawa I, Ishikawa M, Yasuda T, et al. Real-world evidence of the impact of obesity on residual teeth in the Japanese population: A cross-sectional study. PLoS ONE. 2022;17:e0274465.PubMedPubMedCentralCrossRef
41.
Forslund HB, Lindroos AK, Blomkvist K, Hakeberg M, Berggren U, Jontell M, et al. Number of teeth, body mass index, and dental anxiety in middle-aged Swedish women. Acta Odontol Scand. 2002;60:346–52.PubMedCrossRef
42.
Ostberg AL, Nyholm M, Gullberg B, Rastam L, Lindblad U. Tooth loss and obesity in a defined Swedish population. Scand J Public Health. 2009;37:427–33.PubMedCrossRef
43.
Haber J, Wattles J, Crowley M, Mandell R, Joshipura K, Kent RL. Evidence for cigarette smoking as a major risk factor for periodontitis. J Periodontol. 1993;64:16–23.PubMedCrossRef
44.
Torrungruang K, Nisapakultorn K, Sutdhibhisal S, Tamsailom S, Rojanasomsith K, Vanichjakvong O, et al. The effect of cigarette smoking on the severity of periodontal disease among older Thai adults. J Periodontol. 2005;76:566–72.PubMedCrossRef
45.
Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: findings from NHANES III. National Health and Nutrition Examination Survey. J Periodontol. 2000;71:743–51.PubMedCrossRef
46.
Albandar JM, Streckfus CF, Adesanya MR, Winn DM. Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss. J Periodontol. 2000;71:1874–81.PubMedCrossRef
47.
Ravida A, Troiano G, Qazi M, Saleh MHA, Saleh I, Borgnakke WS, et al. Dose-dependent effect of smoking and smoking cessation on periodontitis-related tooth loss during 10–47 years periodontal maintenance-A retrospective study in compliant cohort. J Clin Periodontol. 2020;47:1132–43.PubMedCrossRef
48.
Hanioka T, Ojima M, Tanaka K, Matsuo K, Sato F, Tanaka H. Causal assessment of smoking and tooth loss: a systematic review of observational studies. BMC Public Health. 2011;11:221.PubMedPubMedCentralCrossRef
49.
Souto MLS, Rovai ES, Villar CC, Braga MM, Pannuti CM. Effect of smoking cessation on tooth loss: a systematic review with meta-analysis. BMC Oral Health. 2019;19:245.PubMedPubMedCentralCrossRef
50.
Ishikawa M, Yasuda T, Takase N. Relationship between Oral Health Conditions and Medical Care Expenditure Based on Receipt Information. Jpn J Dent Pract Adm. 2021;56:32–41.
Immer mehr Ärztinnen und Ärzte arbeiten angestellt in Praxen bzw. MVZ. Was im Arbeitsvertrag geklärt werden kann und sollte und wo Risiken liegen, erklärt Medizin- und Arbeitsrechtlerin Gabriele Leucht.
Medizinischen Rat von Chatbots auf der Basis sogenannter künstlicher Intelligenz haben laut Umfragen bereits knapp die Hälfte aller Erwachsenen schon einmal eingeholt. Welche Chancen und Risiken birgt das?
Folgen Patienten einem Arzt in eine andere Praxis, braucht er Zugriff auf deren Akten. Wie das korrekt funktionieren kann, zeigt Hessens Datenschützer. Und er warnt vor unbefugtem Streaming aus Praxen.
Das Institut der Deutschen Zahnärzte (IDZ), die Bundeszahnärztekammer (BZÄK) und die Kassenzahnärztliche Bundesvereinigung (KZBV) stellen Längsschnittergebnisse der Sechsten Deutschen Mundgesundheitsstudie (DMS 6) vor.