Oral and Systemic Diseases: Critical Relationships Between Human Health, Tooth Decay, Periodontal Diseases and Multidisciplinary Care

Alison Prosper , Luna Desnot , Sylvie Lê , Matthieu Minty , Charlotte Thomas , Mathieu Marty , Vincent Blasco-Baque , Thibault Canceill

British Journal of Hospital Medicine ›› 2026, Vol. 87 ›› Issue (3) : 52082

PDF (8993KB)
British Journal of Hospital Medicine ›› 2026, Vol. 87 ›› Issue (3) :52082 DOI: 10.31083/BJHM52082
Review
review-article
Oral and Systemic Diseases: Critical Relationships Between Human Health, Tooth Decay, Periodontal Diseases and Multidisciplinary Care
Author information +
History +
PDF (8993KB)

Abstract

Oral health has long been considered to be on the bangs of systemic health. And yet, as recently as 2024, the World Health Organization stated once again that oral diseases rank first in the world in terms of prevalence. This review aims to highlight data from the literature demonstrating the relationships between oral and systemic diseases. The tissues of the oral cavity, teeth, their bony bases and supporting tissues can each suffer from pathologies, often infectious, whose consequences can be found at local, regional and systemic levels. These disorders affect children and adults of all ages. Their management is a public health issue that involves all medical practitioners.

Graphical abstract

Keywords

oral health / dentistry / cardiovascular diseases / diabetes mellitus / microbiota / infective endocarditis

Cite this article

Download citation ▾
Alison Prosper, Luna Desnot, Sylvie Lê, Matthieu Minty, Charlotte Thomas, Mathieu Marty, Vincent Blasco-Baque, Thibault Canceill. Oral and Systemic Diseases: Critical Relationships Between Human Health, Tooth Decay, Periodontal Diseases and Multidisciplinary Care. British Journal of Hospital Medicine, 2026, 87(3): 52082 DOI:10.31083/BJHM52082

登录浏览全文

4963

注册一个新账户 忘记密码

1. Introduction

In recent decades, the scientific community has witnessed a surge of interest in the complex relationships between oral health and systemic diseases [1]. This burgeoning field of research has revealed that the mouth is far more than just a gateway for nutrition; it’s a dynamic ecosystem with considerable implications for general health. The oral cavity hosts a diverse microbiome, home to hundreds of bacterial species that coexist in a delicate balance [2]. This microbial community is as unique as a fingerprint, shaped by factors ranging from diet and lifestyle to genetics and environmental exposures [3]. When in harmony, these microorganisms contribute to oral health and even support broader bodily functions. However, this equilibrium can be easily disrupted. Poor oral hygiene, dietary changes, or compromised immune function can tip the scales, leading to a state of dysbiosis. In this altered state, opportunistic pathogens can flourish, triggering a cascade of events that extend beyond the confines of the mouth. Dental caries and periodontal diseases, once considered isolated oral tissues, are now recognised as potential catalysts for systemic health problems. In the context of dental caries, bacterial species such as Streptococcus mutans (S.m.), Streptococcus sobrinus (S.s.), and various Lactobacillus strains are predominantly found [4]. Conversely, periodontal diseases are characterised by a concomitance of a local immunity dysfunction and the proliferation of different bacterial types [5]. When considering periodontitis, the microbial landscape shifts dramatically, with a predominance of strict anaerobic Gram-negative bacteria. Notable among these are genera from the Fusobacterium, Porphyromonas, and Prevotella families [6]. These anaerobic bacteria thrive in the oxygen-depleted environment of deep periodontal pockets, contributing to the inflammatory processes and tissue destruction associated with periodontal diseases. This distinct microbial profile in caries versus periodontitis underscores the specificity of bacterial involvement in different oral pathologies.

The oral-systemic connection is bidirectional because oral diseases can impact overall health, but systemic conditions can also have manifestations in the oral cavity. This review aims to shed light on the complex mechanisms of oral-systemic interactions, exploring how the health of the human mouth can influence—and be influenced by—the well-being of the entire body. From cardiovascular diseases to diabetes, from respiratory infections to adverse pregnancy outcomes, the implications of oral health are vast and varied. The critical role of oral health in the broader context of human health will be developed, thanks to cutting-edge research and clinical observations.

2. The Oral Cavity

The human dentition consists of 32 teeth in adults and 20 teeth in children, each specialised for different functions such as cutting, tearing, crushing, and grinding food [7]. The three main tissues of a tooth are the enamel, the hardest substance in the human body [8], the underlying dentin [9] and the soft tissue core, rich in blood vessels and nerves (Fig. 1).

The periodontium, crucial for tooth anchorage, is composed of four tissues [10]: the gingiva or gum (first line of defense against oral pathogens) [11], the cementum (located on the root surface and displays regenerative properties) [12, 13], the alveolar bone (surrounds dental roots and adapts to masticatory forces) [14] and the periodontal ligament (connects the alveolar bone to the tooth root and acts as a shock absorber) [15].

Understanding these structures and their functions is crucial not only for maintaining oral health but also for appreciating the potential impact of oral conditions on systemic health. The rich vascularisation and innervation of oral tissues, along with their constant exposure to environmental factors, make the oral cavity a potential gateway for systemic effects, highlighting the importance of oral health in overall well-being.

Furthermore, the oral cavity hosts a complex and dynamic microbial ecosystem known as the oral microbiome [16], which plays a significant role in both oral and systemic health and forms biofilms on tooth surfaces and oral mucosa.

Disruptions in the balance of the oral microbiome, known as dysbiosis, can lead to various oral diseases such as dental caries and periodontitis [16]. Moreover, the oral microbiome has been linked to numerous systemic conditions, including cardiovascular diseases, adverse pregnancy outcomes, and respiratory diseases. The potential for oral microbes to influence systemic health underscores the importance of maintaining a healthy oral ecosystem as part of overall health management.

Understanding the composition, dynamics, and interactions of the oral microbiome and biofilms is essential for developing effective preventive strategies and treatments for both oral and systemic diseases [17]. This knowledge reinforces the concept that oral health is an integral component of general health and well-being.

3. Dental and Periodontal Pathologies and the Risk of Remote Infection

3.1 Tooth Decay

A bacterial biofilm forms continuously in the oral cavity, adhering to the surfaces of teeth and mucous membranes within hours [18]. When oral hygiene is insufficient, the dynamics of oral biofilms lead to dysbiosis, resulting in pathologies in the oral cavity [19].

The silent epidemic of dental decay represents a global health challenge that goes far beyond the simple deterioration of teeth [20]. In November 2024, the World Health Organization published an alarming report in which oral diseases ranked first in diseases worldwide. The international organization also stated that more than 3.5 million people suffered from caries. This disease process results from frequent exposure to carbohydrates, poor oral hygiene, and host factors that promote the production of extracellular polymeric substances (EPS) and organic acids by biofilm bacteria. The environment acidification alters the microbial composition, favouring acidogenic and aciduric bacteria (Streptococcus mutans, Lactobacillus, Actinomyces, Bifidobacterium, Scardovia) while reducing beneficial bacterial diversity [21, 22, 23]. When the pH drops below 5.5, hydroxyapatite crystals found in the enamel begin to demineralise [24], leading to a progressive loss of calcium and phosphate, and a more porous and vulnerable enamel as a consequence.

Initially, patients may only experience some warning signs, but the more the infection penetrates into deeper dental layers and towards the pulp (Fig. 2), the more the body’s inflammatory response intensifies, transforming minor discomfort into significant pain. At this stage, called pulpitis, traditional treatments shift from conservative restoration to more invasive procedures like pulp excision and endodontic therapy [25].

If left untreated, the pulp may become necrotic due to bacterial invasion, potentially resulting in a periapical abscess (Fig. 3). At this point, antibiotic therapy, regularly discussed for misuse in medicine, is often essential alongside surgical interventions such as drainage of the abscess [26]. Once the immediate crisis is addressed, endodontic treatment is necessary to save the affected tooth.

The implications of periapical infections are not confined to the mouth; they can act as sources for distant infections, including sinusitis related to dental issues [27] (Fig. 4), infections in prosthetic joints [28], or in rare cases, brain abscesses [29]. According to Deppe et al. [30], oral bacteria may be implicated in approximately 10 to 35% of infective endocarditis cases, highlighting a potential link between oral health and cardiovascular conditions.

Overall, the potential for oral infections to affect systemic health underscores the importance of timely intervention and preventive care. Regular dental check-ups and prompt treatment of any dental issues are vital for maintaining not just oral but systemic health.

3.2 Periodontal Diseases

Dental health represents a critical aspect of overall well-being, with prevention strategies extending far beyond simple brushing techniques. The extended presence of certain bacterial species within dental plaque can result in gingival inflammation, commonly known as gingivitis, and superficial damage to the supporting tissues of the tooth. The persistence of dysbiosis in the oral (especially periodontal) microbiome is a significant factor in the onset of deeper periodontal diseases. These conditions arise from an imbalance between pathogenic bacteria and the host’s immune response. As bacteria infiltrate the subgingival area, they contribute to the formation of periodontal pockets and sustain a chronic inflammatory state.

Periodontal diseases as a whole actually include different grades and stages, reflective of a progressive deterioration of the supporting structures of the teeth. In advanced stages, these pathologies can lead to tooth loosening, mobility, and ultimately tooth loss [31, 32]. The classification of periodontal diseases has evolved significantly [33], with recent revisions taking into account the intricate relationships between oral health disturbances and associated systemic conditions [34]. This paradigm shift recognises the periodontal tissues as a mirror of overall patient health [35]. It has been known for nearly 30 years that certain aggressive periodontal conditions, such as necrotising ulcerative gingivitis or periodontitis (Fig. 5), may serve as indicators of underlying severe systemic disorders [36]. These conditions can be early manifestations of serious health issues like leukaemia or acquired immunodeficiency syndrome (AIDS), underscoring the importance of comprehensive health assessment in dental practice [37]. This evolving perspective on periodontal health emphasises the need for interdisciplinary approaches in healthcare. Dental professionals must be vigilant not only while treating local oral conditions but also in recognising potential systemic implications. Conversely, medical practitioners should be aware of the oral manifestations of systemic diseases. Thus, when patient care involves serious pathologies, it is beneficial to coordinate practitioners from all the involved specialities within the same structure, hospital for example [38].

4. Oral-Systemic Connections

The connection between oral dysbiosis and the onset or worsening of systemic diseases is largely attributed to the persistence of a low-grade inflammatory state throughout the body, which is exacerbated by active inflammation in the oral cavity. The impact of the oral microbiome on systemic health can extend beyond local effects [6]. Some researchers suggest that oral bacteria or their metabolic byproducts may enter the bloodstream and migrate to other organs, potentially leading to complications in distant sites [39]. Many systemic diseases can be, closely or remotely, linked to oral dysbiosis, highlighting the oral microbiome’s impact on general health. Pathologies such as rheumatoid arthritis [40], chronic obstructive pulmonary disease (COPD) [41], obstetric complications [42, 43], Alzheimer’s disease [44], inflammatory bowel diseases [45], and cardiovascular disorders are associated with imbalances in oral microbiome (Fig. 6). In the remainder of this manuscript, we propose a more specific focus on infective endocarditis, diabetes, nutritional deficiencies, Alzheimer’s disease, chronic pulmonary disease, pregnancy outcomes and paediatrics.

4.1 Infective Endocarditis

Infective endocarditis (IE) is a serious and often life-threatening infection of the heart’s inner lining, valves, or implanted cardiac devices, caused by bacteria entering the bloodstream and adhering to damaged heart tissues. Poor oral health is a significant risk factor for IE, as the oral cavity can serve as a reservoir for bacteria such as S.m., Streptococcus mitis (S.mi.), and other viridans group streptococci, which are involved in up to 50% of IE cases in the United States annually [46]. Once in the bloodstream, these bacteria can colonise heart valves or damaged endocardial surfaces, leading to infection [47]. People with predisposing conditions such as prosthetic heart valves, congenital heart defects or a history of IE are at particularly high risk [48]. While invasive dental procedures like tooth extractions have traditionally been associated with bacteremia and IE risk, experts explain that even the more basic daily procedures in the context of poor oral hygiene may represent an important threat [49]. The accumulation of plaque and calculus promotes periodontal disease, which not only exacerbates local inflammation but also increases systemic risks by facilitating bacterial dissemination [50]. Preventive measures such as maintaining good oral hygiene are essential to reduce bacterial load and prevent gingival bleeding. For high-risk patients undergoing invasive dental procedures, guidelines from organizations like the American Heart Association recommend antibiotic prophylaxis to minimise bacteremia risk [51]. However, there is growing consensus that improving overall oral health is a more effective strategy for reducing IE incidence than relying solely on prophylactic antibiotics. This underscores the need for integrated care between dental and medical professionals to safeguard cardiovascular health.

4.2 Diabetes

Diabetes, both type I and type II, significantly impact oral health, creating a bidirectional relationship that affects both glycemic control and dental well-being [52]. Moreover, periodontal diseases are recognised as the sixth complication of diabetes [53]. This reciprocal relationship suggests that treatment of any type of periodontal disease should improve glycemic control in diabetic patients. However, studies differ on this point. Conventional periodontal therapy, as it is available to the majority of patients, seems insufficient [54], whereas intensive therapy has positive effects on blood glycemia [55], thus creating limitations in equality of access to relevant treatments for the population [56]. What is proven is that people with diabetes are at a higher risk of developing various oral health issues due to elevated blood glucose levels [57]. High blood sugar increases glucose rates in saliva [58], providing a favourable environment for harmful bacteria to thrive and form plaque, leading to tooth decay and gum disease. Diabetes can also reduce saliva production, causing dry mouth (xerostomia), which further exacerbates dental problems by reducing the mouth’s natural protective mechanisms [59]. Periodontal disease, the most common oral health complication in diabetes, affects more than 60% of individuals with type I and type II diabetes [60]. Ultimately, the relationship between diabetes and oral health is reciprocal [61]. Chronic periodontal inflammation promotes systemic dissemination of pro-inflammatory mediators such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α), which contribute to insulin resistance and impaired glycemic control [62]. Additionally, subgingival pathogens and their lipopolysaccharides (LPS) can translocate into the bloodstream, stimulating hepatic C-reactive protein (CRP) production and systemic inflammation [63]. These mechanisms are now well documented in both human and experimental models. Notably, randomised clinical trials have demonstrated that non-surgical periodontal treatment can significantly reduce Haemoglobin A1c (HbA1c) levels in diabetic patients, underscoring the systemic impact of periodontal interventions [64].

4.3 Nutritional Deficiencies

Nutritional deficiencies in vitamins B, C and D can affect periodontal tissues, increasing the risk of periodontitis, tooth mobility, and tooth loss. Vitamin insufficiency is common among elderly individuals, those with eating disorders, or in the context of various systemic diseases such as gastrointestinal diseases, liver diseases, kidney diseases, cancers, heart failure and endocrine disorders [65]. As of 1983, Dummett [66] described that deficiencies in vitamins B1, B2, B3, B5, B6, and B8 could manifest as erosions, vesicles, and sometimes glossitis, accompanied by hypersensitivity of the mucous membranes. They can also cause skin and mucosal lesions, such as dermatitis, angular cheilitis, stomatitis, and gingival ulcers, as well as a pellagra syndrome, which can worsen oral symptoms like glossitis, stomatitis and gingivitis [67]. A deficiency in vitamin B12 can cause a burning sensation on the tongue, known as glossodynia [68]. These nutritional deficiencies reduce the regenerative capacity of mucous membranes and promote opportunistic infections, such as candidiasis [69]. Low levels of vitamins B9 and B12 are also associated with a higher prevalence of periodontitis [70, 71], that’s why supplementation with vitamin B9 may reduce gingival inflammation and improve the condition of periodontal pockets [72]. Numerous studies have also shown that low serum levels of vitamin C are linked to a higher prevalence of periodontitis and greater disease severity, potentially leading to the destruction of the tissues supporting the teeth and tooth loss due to bone resorption [73, 74, 75, 76]. Vitamin C deficiency is famous in history as it can lead to scurvy [77], one of the most widespread diseases on ships during the last centuries [78]. Regarding vitamin D, low serum levels are also associated with a higher risk of periodontitis [79] as it can lead to a decrease in bone mineral density, which increases the risk of alveolar bone loss and weakens the dental bone support, thus increasing the risk of periodontitis [80]. Thus, vitamin D supplementation can reduce gingival inflammation, probably due to its anti-inflammatory properties [81].

4.4 Alzheimer’s Disease

Alzheimer’s disease (AD) is a neurodegenerative disorder characterised by progressive memory loss, cognitive impairments, and executive dysfunction [82]. Two main pathological mechanisms can explain AD: the accumulation of amyloid plaques around neurons and neurofibrillary degeneration associated with tau protein [83]. Inflammation, particularly neuroinflammation, plays a crucial role in the progression of the disease [84]. So, it is not surprising that recent research has suggested that extrinsic factors, such as oral health issues, may contribute to the progression of AD [85]. A specific link has been established between periodontitis and AD [86]. Epidemiological studies have shown that individuals with periodontal problems, such as tooth loss or the presence of deep periodontal pockets, are more likely to develop cognitive impairments [87]. In a cohort study, Kamer et al. [44] revealed that significant tooth loss in elderly subjects was associated with faster cognitive decline. Furthermore, a link between periodontitis and the Apolipoprotein E epsilon 4 (APOE-ε4 allele), a major genetic risk factor for AD, has been observed, suggesting that individuals with this gene and poor dental health have an increased risk of cognitive decline [88]. The association between periodontitis and Alzheimer’s disease is now firmly established. Research has evolved from epidemiological observations to detailed mechanistic studies and therapeutic explorations.

First, pathogenic oral bacteria such as Porphyromonas gingivalis (P.g.) produce toxins (gingipains) that can induce systemic inflammation and, in particular, neuroinflammation [89]. Recent studies suggest a potential link between periodontal pathogens like Fusobacterium nucleatum (F.n.) and Alzheimer’s disease [90], because this bacterium and its virulence factors, like lipopolysaccharides (LPS), could cross the blood-brain barrier, particularly in older individuals or those genetically predisposed to AD [91]. In animal models, the introduction of P.g. promoted the accumulation of amyloid-β (Aβ) in the brain, a classic marker of AD [89]. The relationship between periodontitis and AD appears to be bidirectional: on one hand, periodontitis contributes to systemic inflammation that may accelerate neurodegeneration, while on the other hand, AD may impair the oral health of patients. Indeed, individuals with dementia often struggle to maintain proper oral hygiene, which exacerbates oral dysbiosis and periodontal infections. Finally, some studies have shown that periodontal treatment could have beneficial effects for AD patients [92, 93, 94]. For example, interventions to improve periodontal health might reduce brain atrophy, as observed in magnetic resonance imaging studies [95]. However, the direct causality between periodontitis and AD has not yet been fully confirmed, and further research is needed to better understand the complex interaction between these two conditions.

4.5 Chronic Obstructive Pulmonary Disease

The upper respiratory tract is an extension of the oral cavity, making the mouth a potential reservoir for respiratory pathogens. Chronic Obstructive Pulmonary Disease (COPD) is an inflammatory lung condition characterised by symptoms such as difficult breathing, chronic cough, excessive mucus production, and wheezing [96]. Although bronchodilators and anti-inflammatory drugs are first-line treatments for COPD, they are not always effective in controlling infectious exacerbations. In fact, the use of inhaled corticosteroids in patients with COPD and chronic bronchial infections can even increase bacterial load in the airways and raise the risk of pneumonia. In this context, long-term or intermittent antibiotic treatment has been shown to prevent COPD exacerbations and hospitalisations [97, 98]. Recent research has highlighted a connection between periodontitis and COPD [99]. Bacteria from periodontal tissues can easily contaminate the airways through the oral cavity, further worsening COPD symptoms. A study showed that bacterial diversity was higher in patients with COPD, with the Lachnospiraceae family often present in both periodontitis and COPD patients [100]. Conversely, treatments for COPD, particularly inhaled medications, can negatively affect oral health. These treatments are associated with dental issues such as periodontitis, dry mouth, oral mucosal ulcers, gingivitis, and taste alterations [101]. Inhaled corticosteroids also increase the risk of Candida infections [102] (Fig. 7). Co-infections involving bacteria like F.n. and Pseudomonas aeruginosa (P.a.) may also play a crucial role in respiratory inflammation [103]. Therefore, managing oral health in COPD patients is essential not only for preventing dental infections but also for reducing exacerbations of lung disease.

4.6 Pregnancy Outcomes

Oral health significantly impacts pregnancy outcomes and maternal well-being. Poor oral health during pregnancy has been linked to several adverse effects, including preterm delivery, low birth weight babies, and pre-eclampsia [104]. Several studies have demonstrated the possible translocation of oral bacteria into the placenta, which may play a role in complications during pregnancy [105, 106]. The hormonal changes during pregnancy, particularly increased levels of estrogen and progesterone, make women more susceptible to gum problems like gingivitis (Fig. 8) and periodontitis [107]. A study shows that pregnant women are more prone to oral diseases: they are 1.97 times more likely to develop dental caries [107] and nearly 47% suffer from periodontitis [42].

Certain medications used for oral health issues can also potentially affect the developing fetus if taken during pregnancy. Tetracycline antibiotics should be avoided as they can cause discolouration of the child’s developing teeth [108]. Nonsteroidal anti-inflammatory drugs (NSAIDs) are contraindicated, and benzodiazepines used for dental anxiety should be avoided due to potential risks to the fetus [109].

Recognising the importance of oral health during pregnancy, healthcare professionals recommend regular dental check-ups, proper oral hygiene habits, and preventive care to ensure the well-being of both mother and child [110]. Despite the reluctance of dentists, dental care can be performed during pregnancy, and has positive effects on both the future mother and the unborn child. In France, for example, a national program called “M’T Dents” (a wordplay that could be translated as “Love your teeth” in English), funded by the social security system, provides a free dental check-up for every pregnant woman. Timely treatment of oral health issues, while keeping in consideration the safety of medications, can help prevent complications and ensure better pregnancy outcomes.

5. A Focus on Paediatrics

The development of human dentition begins early in life, even before birth, then continues during childhood with the emergence of primary teeth. While primary teeth share anatomical features with their permanent counterparts, they possess distinct characteristics. They are smaller, lack tight contact points, and have a more globular appearance with a milky hue [111]. Surprisingly, some babies can be born with small, often highly mobile, natal teeth (Fig. 9), which can be extracted in the first few hours of life to avoid any risk of inhalation [112]. Maternity unit medical teams should be systematically prepared for this eventuality.

Children’s dental care requires particular attention, as primary teeth are surprisingly vulnerable to rapid decay processes. Infections in these early teeth are not merely isolated incidents but can have profound implications for future permanent dentition, such as enamel defect, shape alteration and delayed or ectopic eruption [113]. Modern preventive strategies emphasise a holistic perspective. Regular dental hygiene involves more than traditional brushing; it encompasses understanding dietary impacts, recognising early warning signs, and implementing proactive maintenance protocols. Fluoride-based products, balanced nutrition, and limiting sugar consumption emerge as fundamental protective measures. Parental education plays a crucial role in this preventive paradigm to transform passive care into an active, informed approach to maintaining children’s oral well-being.

Emerging researches continue to underscore the importance of early, comprehensive dental care, positioning prevention as the most effective strategy in managing oral health challenges [114, 115]. The impact of oral health on children’s overall well-being extends far beyond the confines of the oral cavity. Poor oral health in children can have significant systemic consequences, affecting various aspects of their physical and psychological development. Untreated dental caries and periodontal diseases can lead to chronic pain, difficulties in eating and speaking, and sleep disturbances, all of which can impair a child’s growth, cognitive development, and academic performance [116]. Moreover, oral infections can potentially spread to other parts of the body, leading to more serious conditions such as endocarditis or brain abscesses in rare cases [117]. Chronic oral inflammation has been associated with systemic diseases later in life, including cardiovascular diseases and diabetes. Psychosocially, visible dental problems can negatively impact a child’s self-esteem and social interactions [118], potentially leading to behavioural issues and reduced quality of life [119, 120]. Additionally, early childhood caries has been linked to increased risk of developing caries in permanent teeth, underscoring the long-term implications of maintaining good oral health from an early age [121]. These interconnections between oral and systemic health emphasise the critical importance of early prevention, regular dental check-ups, and proper oral hygiene habits for the promotion of overall health and well-being in children.

6. Hospital Dentistry and Multidisciplinary Care

Hospital dentistry plays a central role in ensuring comprehensive and coordinated healthcare by bridging the gap between oral health and systemic well-being [122]. Its integration within hospital settings is essential for delivering patient-centred care, particularly for individuals with complex medical conditions. By fostering interdisciplinary collaboration, hospital dentistry enhances the quality and safety of care across multiple medical specialities [123]. For instance, in oncology, pre-treatment dental screenings are critical for identifying and eliminating potential oral infection sources, thus preventing serious complications during chemotherapy or radiotherapy [124]. Similarly, in cardiology and cardiac surgery, the involvement of dental professionals in pre-operative assessments helps prevent oral-origin infections that could compromise surgical outcomes [125]. Hospital dentistry also contributes significantly to emergency care by providing specialised management of oral infections and trauma, ensuring timely and effective interventions.

A distinctive strength of hospital dentistry lies in its ability to provide treatment under general anesthesia for patients with special needs, such as those with severe intellectual or physical disabilities, extreme dental phobia, or complex comorbidities that preclude conventional dental treatment [126]. General anesthesia enables the delivery of comprehensive dental care in a single session, reducing patient stress and ensuring optimal treatment conditions. This approach is particularly beneficial for young children who are unable to cooperate due to age, anxiety, or developmental challenges [127].

Although general anesthesia involves inherent risks, its benefits often outweigh the potential complications, when accompanied by appropriate pre-operative evaluation, intra-operative monitoring, and post-operative care protocols [128]. Ultimately, by ensuring access to essential oral healthcare for vulnerable and medically complex populations, hospital dentistry not only promotes health equity but also underscores the importance of multidisciplinary collaboration in modern healthcare systems.

7. Conclusion

Recent research has clearly established that oral health is deeply interconnected with systemic health. Central to this relationship is the role of the oral microbiome and its influence on inflammation throughout the body. Oral dysbiosis can trigger local and systemic inflammatory responses, contributing to the development or aggravation of diseases such as diabetes and cardiovascular disorders.

This emerging understanding is reshaping medical practice: dental assessments are increasingly recognised as essential components of the prevention and management of systemic diseases. Integrating oral healthcare into multidisciplinary care pathways enhances treatment efficacy and reflects a more holistic vision of patient well-being.

As scientific evidence continues to grow, strengthening the systemic implications of oral health, interdisciplinary collaboration between dental and medical professionals will be crucial for advancing prevention, diagnosis, and patient care.

Key Points

Oral dysbiosis drives systemic inflammation, thereby exacerbating insulin resistance, atherogenesis, and neuroinflammation.

Dental biofilms constitute reservoirs for bacteremia and may be implicated in up to 35% of infective endocarditis cases.

Severe periodontitis can make it difficult to control HbA1c levels, while poor glycemic control worsens periodontal attachment loss.

Moderate–severe periodontitis in pregnancy is associated with an increased risk of preterm birth and low birth weight, supporting the inclusion of oral screening in prenatal care pathways.

Hospital dentistry and interdisciplinary collaboration improve patient care for high-risk cases.

Availability of Data and Materials

All data, figures and literature references included in this study are available from the corresponding author upon reasonable request.

References

[1]

Kapila YL. Oral health’s inextricable connection to systemic health: Special populations bring to bear multimodal relationships and factors connecting periodontal disease to systemic diseases and conditions. Periodontology 2000. 2021; 87: 11–16. https://doi.org/10.1111/prd.12398.

[2]

Fåk F, Tremaroli V, Bergström G, Bäckhed F. Oral microbiota in patients with atherosclerosis. Atherosclerosis. 2015; 243: 573–578. https://doi.org/10.1016/j.atherosclerosis.2015.10.097.

[3]

Feres M, Teles F, Teles R, Figueiredo LC, Faveri M. The subgingival periodontal microbiota of the aging mouth. Periodontology 2000. 2016; 72: 30–53. https://doi.org/10.1111/prd.12136.

[4]

Selwitz RH, Ismail AI, Pitts NB. Dental caries. Lancet. 2007; 369: 51–59. https://doi.org/10.1016/S0140-6736(07)60031-2.

[5]

Suárez LJ, Garzón H, Arboleda S, Rodríguez A. Oral Dysbiosis and Autoimmunity: From Local Periodontal Responses to an Imbalanced Systemic Immunity. A Review. Frontiers in Immunology. 2020; 11: 591255. https://doi.org/10.3389/fimmu.2020.591255.

[6]

Lamont RJ, Koo H, Hajishengallis G. The oral microbiota: dynamic communities and host interactions. Nature Reviews. Microbiology. 2018; 16: 745–759. https://doi.org/10.1038/s41579-018-0089-x.

[7]

Koussoulakou DS, Margaritis LH, Koussoulakos SL. A curriculum vitae of teeth: evolution, generation, regeneration. International Journal of Biological Sciences. 2009; 5: 226–243. https://doi.org/10.7150/ijbs.5.226.

[8]

Zhang YF, Zheng J, Yu JX, He HT. Impact of strain rate on the hardness and elastic modulus of human tooth enamel. Journal of the Mechanical Behavior of Biomedical Materials. 2018a; 78: 491–495. https://doi.org/10.1016/j.jmbbm.2017.12.011.

[9]

Goldberg M, Kulkarni AB, Young M, Boskey A. Dentin: structure, composition and mineralization. Frontiers in Bioscience-Elite. 2011; 3: 711–735. https://doi.org/10.2741/e281.

[10]

Nanci A, Bosshardt DD. Structure of periodontal tissues in health and disease. Periodontology 2000. 2006; 40: 11–28. https://doi.org/10.1111/j.1600-0757.2005.00141.x.

[11]

Preshaw PM. Antibiotics in the treatment of periodontitis. Dental Update. 2004; 31: 448–450, 453–454, 456. https://doi.org/10.12968/denu.2004.31.8.448.

[12]

Arzate H, Zeichner-David M, Mercado-Celis G. Cementum proteins: role in cementogenesis, biomineralization, periodontium formation and regeneration. Periodontology 2000. 2015; 67: 211–233. https://doi.org/10.1111/prd.12062.

[13]

Foster BL. On the discovery of cementum. Journal of Periodontal Research. 2017; 52: 666–685. https://doi.org/10.1111/jre.12444.

[14]

Lindhe J, Lang NP. Clinical Periodontology and Implant Dentistry, 2 Volume Set. 6th edn. Wiley-Blackwell: Chichester, West Sussex; Ames, ID, USA. 2015.

[15]

de Jong T, Bakker AD, Everts V, Smit TH. The intricate anatomy of the periodontal ligament and its development: Lessons for periodontal regeneration. Journal of Periodontal Research. 2017; 52: 965–974. https://doi.org/10.1111/jre.12477.

[16]

Rajasekaran JJ, Krishnamurthy HK, Bosco J, Jayaraman V, Krishna K, Wang T, et al. Oral Microbiome: A Review of Its Impact on Oral and Systemic Health. Microorganisms. 2024; 12: 1797. https://doi.org/10.3390/microorganisms12091797.

[17]

Ray RR. Biofilm architecture and dynamics of the oral ecosystem. Biotechnologia. 2024; 105: 395–402. https://doi.org/10.5114/bta.2024.145259.

[18]

Lebeaux D, Ghigo JM. Management of biofilm-associated infections: what can we expect from recent research on biofilm lifestyles? Medecine Sciences. 2012; 28: 727–739. https://doi.org/10.1051/medsci/2012288015. (In French)

[19]

Pitts NB, Zero DT, Marsh PD, Ekstrand K, Weintraub JA, Ramos-Gomez F, et al. Dental caries. Nature Reviews. Disease Primers. 2017; 3: 17030. https://doi.org/10.1038/nrdp.2017.30.

[20]

World Health Organization. International report on Oral health. 2025. Available at: https://www.who.int/news-room/fact-sheets/detail/oral-health (Accessed: 17 July 2025).

[21]

Bowen WH, Burne RA, Wu H, Koo H. Oral Biofilms: Pathogens, Matrix, and Polymicrobial Interactions in Microenvironments. Trends in Microbiology. 2018; 26: 229–242. https://doi.org/10.1016/j.tim.2017.09.008.

[22]

Marsh PD, Zaura E. Dental biofilm: ecological interactions in health and disease. Journal of Clinical Periodontology. 2017; 44: S12–S22. https://doi.org/10.1111/jcpe.12679.

[23]

Xiao J, Klein MI, Falsetta ML, Lu B, Delahunty CM, Yates JR, 3rd, et al. The exopolysaccharide matrix modulates the interaction between 3D architecture and virulence of a mixed-species oral biofilm. PLoS Pathogens. 2012; 8: e1002623. https://doi.org/10.1371/journal.ppat.1002623.

[24]

Chen X, Daliri EBM, Kim N, Kim JR, Yoo D, Oh DH. Microbial Etiology and Prevention of Dental Caries: Exploiting Natural Products to Inhibit Cariogenic Biofilms. Pathogens. 2020; 9: 569. https://doi.org/10.3390/pathogens9070569.

[25]

Yong D, Cathro P. Conservative pulp therapy in the management of reversible and irreversible pulpitis. Australian Dental Journal. 2021; 66: S4–S14. https://doi.org/10.1111/adj.12841.

[26]

Pulia M, Fox B. Antibiotics Should Not Be Routinely Prescribed After Incision and Drainage of Uncomplicated Abscesses. Annals of Emergency Medicine. 2019; 73: 377–378. https://doi.org/10.1016/j.annemergmed.2018.04.026.

[27]

Aukštakalnis R, Simonavičiūtė R, Simuntis R. Treatment options for odontogenic maxillary sinusitis: a review. Stomatologija. 2018; 20: 22–26.

[28]

Coll PP, Lindsay A, Meng J, Gopalakrishna A, Raghavendra S, Bysani P, et al. The Prevention of Infections in Older Adults: Oral Health. Journal of the American Geriatrics Society. 2020; 68: 411–416. https://doi.org/10.1111/jgs.16154.

[29]

Mylonas AI, Tzerbos FH, Mihalaki M, Rologis D, Boutsikakis I. Cerebral abscess of odontogenic origin. Journal of Cranio-Maxillo-Facial Surgery. 2007; 35: 63–67. https://doi.org/10.1016/j.jcms.2006.10.004.

[30]

Deppe H, Reitberger J, Behr AV, Vitanova K, Lange R, Wantia N, et al. Oral bacteria in infective endocarditis requiring surgery: a retrospective analysis of 134 patients. Clinical Oral Investigations. 2022; 26: 4977–4985. https://doi.org/10.1007/s00784-022-04465-2.

[31]

Chapple ILC. Time to take gum disease seriously. British Dental Journal. 2022; 232: 360–361. https://doi.org/10.1038/s41415-022-4113-1.

[32]

Usui M, Onizuka S, Sato T, Kokabu S, Ariyoshi W, Nakashima K. Mechanism of alveolar bone destruction in periodontitis - Periodontal bacteria and inflammation. The Japanese Dental Science Review. 2021; 57: 201–208. https://doi.org/10.1016/j.jdsr.2021.09.005.

[33]

Caton JG, Armitage G, Berglundh T, Chapple ILC, Jepsen S, Kornman KS, et al. A new classification scheme for periodontal and peri-implant diseases and conditions - Introduction and key changes from the 1999 classification. Journal of Clinical Periodontology. 2018; 45: S1–S8. https://doi.org/10.1111/jcpe.12935.

[34]

Holmstrup P, Plemons J, Meyle J. Non-plaque-induced gingival diseases. Journal of Clinical Periodontology. 2018; 45: S28–S43. https://doi.org/10.1111/jcpe.12938.

[35]

Albandar JM, Susin C, Hughes FJ. Manifestations of systemic diseases and conditions that affect the periodontal attachment apparatus: Case definitions and diagnostic considerations. Journal of Periodontology. 2018; 89: S183–S203. https://doi.org/10.1002/JPER.16-0480.

[36]

Rowland RW. Necrotizing ulcerative gingivitis. Annals of Periodontology. 1999; 4: 65–73. https://doi.org/10.1902/annals.1999.4.1.65.

[37]

Lomelí-Martínez SM, González-Hernández LA, Ruiz-Anaya ADJ, Lomelí-Martínez MA, Martínez-Salazar SY, Mercado González AE, et al. Oral Manifestations Associated with HIV/AIDS Patients. Medicina. 2022; 58: 1214. https://doi.org/10.3390/medicina58091214.

[38]

Ferreira-Vilaca C, Costa Mendes L, Campana SC, Bailleul-Forestier I, Audouin-Pajot C, Esclassan R, et al. Orofacial manifestations of SAPHO syndrome: a systematic review of case reports. Clinical Rheumatology. 2020; 39: 3277–3286. https://doi.org/10.1007/s10067-020-05084-6.

[39]

Hettne KM, Weeber M, Laine ML, ten Cate H, Boyer S, Kors JA, et al. Automatic mining of the literature to generate new hypotheses for the possible link between periodontitis and atherosclerosis: lipopolysaccharide as a case study. Journal of Clinical Periodontology. 2007; 34: 1016–1024. https://doi.org/10.1111/j.1600-051X.2007.01152.x.

[40]

de Pablo P, Dietrich T, McAlindon TE. Association of periodontal disease and tooth loss with rheumatoid arthritis in the US population. The Journal of Rheumatology. 2008; 35: 70–76.

[41]

Takeuchi K, Matsumoto K, Furuta M, Fukuyama S, Takeshita T, Ogata H, et al. Periodontitis Is Associated with Chronic Obstructive Pulmonary Disease. Journal of Dental Research. 2019; 98: 534–540. https://doi.org/10.1177/0022034519833630.

[42]

Thomas C, Timofeeva I, Bouchoucha E, Canceill T, Champion C, Groussolles M, et al. Oral and periodontal assessment at the first trimester of pregnancy: The PERISCOPE longitudinal study. Acta Obstetricia et Gynecologica Scandinavica. 2023; 102: 669–680. https://doi.org/10.1111/aogs.14529.

[43]

Vergnes JN, Sixou M. Preterm low birth weight and maternal periodontal status: a meta-analysis. American Journal of Obstetrics and Gynecology. 2007; 196: 135.e1–135.e7. https://doi.org/10.1016/j.ajog.2006.09.028.

[44]

Kamer AR, Craig RG, Niederman R, Fortea J, de Leon MJ. Periodontal disease as a possible cause for Alzheimer’s disease. Periodontology 2000. 2020; 83: 242–271. https://doi.org/10.1111/prd.12327.

[45]

Pereira MS, Munerato MC. Oral Manifestations of Inflammatory Bowel Diseases: Two Case Reports. Clinical Medicine & Research. 2016; 14: 46–52. https://doi.org/10.3121/cmr.2015.1307.

[46]

Lockhart PB, Brennan MT, Thornhill M, Michalowicz BS, Noll J, Bahrani-Mougeot FK, et al. Poor oral hygiene as a risk factor for infective endocarditis-related bacteremia. Journal of the American Dental Association (1939). 2009; 140: 1238–1244. https://doi.org/10.14219/jada.archive.2009.0046.

[47]

Bumm CV, Folwaczny M. Infective endocarditis and oral health-a Narrative Review. Cardiovascular Diagnosis and Therapy. 2021; 11: 1403–1415. https://doi.org/10.21037/cdt-20-908.

[48]

Yallowitz AW, Decker LC. Infectious Endocarditis. 2025. Available at: http://www.ncbi.nlm.nih.gov/books/NBK557641/ (Accessed: 17 July 2025).

[49]

Błochowiak KJ. Dental treatment and recommended management in patients at risk of infective endocarditis. Polish Journal of Cardio-Thoracic Surgery. 2019; 16: 37–41. https://doi.org/10.5114/kitp.2019.83944.

[50]

Falconer JL, Rajani R, Androshchuk V, Yogarajah A, Greenbury RA, Ismail A, et al. Exploring links between oral health and infective endocarditis. Frontiers in Oral Health. 2024; 5: 1426903. https://doi.org/10.3389/froh.2024.1426903.

[51]

Gupta K, Kumar S, Anand Kukkamalla M, Taneja V, Syed GA, Pullishery F, et al. Dental Management Considerations for Patients with Cardiovascular Disease-A Narrative Review. Reviews in Cardiovascular Medicine. 2022; 23: 261. https://doi.org/10.31083/j.rcm2308261.

[52]

Borgnakke WS. IDF Diabetes Atlas: Diabetes and oral health - A two-way relationship of clinical importance. Diabetes Research and Clinical Practice. 2019; 157: 107839. https://doi.org/10.1016/j.diabres.2019.107839.

[53]

Löe H. Periodontal disease. The sixth complication of diabetes mellitus. Diabetes Care. 1993; 16: 329–334.

[54]

Vergnes JN, Canceill T, Vinel A, Laurencin-Dalicieux S, Maupas-Schwalm F, Blasco-Baqué V, et al. The effects of periodontal treatment on diabetic patients: The DIAPERIO randomized controlled trial. Journal of Clinical Periodontology. 2018; 45: 1150–1163. https://doi.org/10.1111/jcpe.13003.

[55]

D’Aiuto F, Gkranias N, Bhowruth D, Khan T, Orlandi M, Suvan J, et al. Systemic effects of periodontitis treatment in patients with type 2 diabetes: a 12 month, single-centre, investigator-masked, randomised trial. The Lancet. Diabetes & Endocrinology. 2018; 6: 954–965. https://doi.org/10.1016/S2213-8587(18)30038-X.

[56]

Vergnes JN, Canceill T, Monsarrat P. Intensive periodontal therapy and type 2 diabetes. The Lancet. Diabetes & Endocrinology. 2019; 7: 174–175. https://doi.org/10.1016/S2213-8587(19)30029-4.

[57]

Grover A. From Glucose to Gums: Exploring the Oral Side of Diabetes. Journal of Dentistry and Oral Health. 2023; 10: 1–16. https://doi.org/10.17303/jdoh.2023.10.203.

[58]

Gupta S, Nayak MT, Sunitha JD, Dawar G, Sinha N, Rallan NS. Correlation of salivary glucose level with blood glucose level in diabetes mellitus. Journal of Oral and Maxillofacial Pathology. 2017; 21: 334–339. https://doi.org/10.4103/jomfp.JOMFP_222_15.

[59]

Borgnakke WS, Poudel P. Diabetes and Oral Health: Summary of Current Scientific Evidence for Why Transdisciplinary Collaboration Is Needed. Frontiers in Dental Medicine. 2021; 2: 709831. https://doi.org/10.3389/fdmed.2021.709831.

[60]

King R, Chasma F. Diabetes and periodontal disease. Faculty Dental Journal. 2022; 13: 78–81. https://doi.org/10.1308/rcsfdj.2022.18.

[61]

Stöhr J, Barbaresko J, Neuenschwander M, Schlesinger S. Bidirectional association between periodontal disease and diabetes mellitus: a systematic review and meta-analysis of cohort studies. Scientific Reports. 2021; 11: 13686. https://doi.org/10.1038/s41598-021-93062-6.

[62]

Hajishengallis G, Chavakis T. Local and systemic mechanisms linking periodontal disease and inflammatory comorbidities. Nature Reviews. Immunology. 2021; 21: 426–440. https://doi.org/10.1038/s41577-020-00488-6.

[63]

de Jongh CA, de Vries TJ, Bikker FJ, Gibbs S, Krom BP. Mechanisms of Porphyromonas gingivalis to translocate over the oral mucosa and other tissue barriers. Journal of Oral Microbiology. 2023; 15: 2205291. https://doi.org/10.1080/20002297.2023.2205291.

[64]

Chen YF, Zhan Q, Wu CZ, Yuan YH, Chen W, Yu FY, et al. Baseline HbA1c Level Influences the Effect of Periodontal Therapy on Glycemic Control in People with Type 2 Diabetes and Periodontitis: A Systematic Review on Randomized Controlled Trails. Diabetes Therapy. 2021; 12: 1249–1278. https://doi.org/10.1007/s13300-021-01000-6.

[65]

Ustianowski Ł Ustianowska K, Gurazda K, Rusiński M, Ostrowski P, Pawlik A. The Role of Vitamin C and Vitamin D in the Pathogenesis and Therapy of Periodontitis-Narrative Review. International Journal of Molecular Sciences. 2023; 24: 6774. https://doi.org/10.3390/ijms24076774.

[66]

Dummett CO. Effects of nutrition on dental health in Third World countries. Quintessence International, Dental Digest. 1983; 14: 247–251.

[67]

Moynihan PJ. The role of diet and nutrition in the etiology and prevention of oral diseases. Bulletin of the World Health Organization. 2005; 83: 694–699.

[68]

Hasan S, Ahmed S, Panigrahi R, Chaudhary P, Vyas V, Saeed S. Oral cavity and eating disorders: An insight to holistic health. Journal of Family Medicine and Primary Care. 2020; 9: 3890–3897. https://doi.org/10.4103/jfmpc.jfmpc_608_20.

[69]

Marder MZ. Oral Status in Eating Disorders. In Strumia R (ed.) Eating Disorders and the Skin (pp. 85–91). Springer: Berlin Heidelberg. 2013. https://doi.org/10.1007/978-3-642-29136-4_16.

[70]

Yu YH, Kuo HK, Lai YL. The Association Between Serum Folate Levels and Periodontal Disease in Older Adults: Data from the National Health and Nutrition Examination Survey 2001/02. Journal of the American Geriatrics Society. 2007; 55: 108–113. https://doi.org/10.1111/j.1532-5415.2006.01020.x.

[71]

Zong G, Holtfreter B, Scott AE, Völzke H, Petersmann A, Dietrich T, et al. Serum vitamin B12 is inversely associated with periodontal progression and risk of tooth loss: a prospective cohort study. Journal of Clinical Periodontology. 2016; 43: 2–9. https://doi.org/10.1111/jcpe.12483.

[72]

Perić M, Maiter D, Cavalier E, Lasserre JF, Toma S. The Effects of 6-Month Vitamin D Supplementation during the Non-Surgical Treatment of Periodontitis in Vitamin-D-Deficient Patients: A Randomized Double-Blind Placebo-Controlled Study. Nutrients. 2020; 12: 2940. https://doi.org/10.3390/nu12102940.

[73]

Lee JH, Shin MS, Kim EJ, Ahn YB, Kim HD. The association of dietary vitamin C intake with periodontitis among Korean adults: Results from KNHANES IV. PLoS ONE. 2017; 12: e0177074. https://doi.org/10.1371/journal.pone.0177074.

[74]

Nishida M, Grossi SG, Dunford RG, Ho AW, Trevisan M, Genco RJ. Dietary vitamin C and the risk for periodontal disease. Journal of Periodontology. 2000; 71: 1215–1223. https://doi.org/10.1902/jop.2000.71.8.1215.

[75]

Tada A, Miura H. The Relationship between Vitamin C and Periodontal Diseases: A Systematic Review. International Journal of Environmental Research and Public Health. 2019; 16: 2472. https://doi.org/10.3390/ijerph16142472.

[76]

Timmerman MF, Abbas F, Loos BG, Van der Weijden GA, Van Winkelhoff AJ, et al. Java project on periodontal diseases: the relationship between vitamin C and the severity of periodontitis. Journal of Clinical Periodontology. 2007; 34: 299–304. https://doi.org/10.1111/j.1600-051X.2007.01053.x.

[77]

Hujoel PP, Kato T, Hujoel IA, Hujoel MLA. Bleeding tendency and ascorbic acid requirements: systematic review and meta-analysis of clinical trials. Nutrition Reviews. 2021; 79: 964–975. https://doi.org/10.1093/nutrit/nuaa115.

[78]

Kinlin LM, Weinstein M. Scurvy: old disease, new lessons. Paediatrics and International Child Health. 2023; 43: 83–94. https://doi.org/10.1080/20469047.2023.2262787.

[79]

Costantini E, Sinjari B, Piscopo F, Porreca A, Reale M, Caputi S, et al. Evaluation of Salivary Cytokines and Vitamin D Levels in Periodontopathic Patients. International Journal of Molecular Sciences. 2020; 21: 2669. https://doi.org/10.3390/ijms21082669.

[80]

Yu B, Wang CY. Osteoporosis and periodontal diseases - An update on their association and mechanistic links. Periodontology 2000. 2022; 89: 99–113. https://doi.org/10.1111/prd.12422.

[81]

Gao W, Tang H, Wang D, Zhou X, Song Y, Wang Z. Effect of short-term vitamin D supplementation after nonsurgical periodontal treatment: A randomized, double-masked, placebo-controlled clinical trial. Journal of Periodontal Research. 2020; 55: 354–362. https://doi.org/10.1111/jre.12719.

[82]

Kumar A, Sidhu J, Lui F, Tsao JW. Alzheimer Disease. 2025. Available at: http://www.ncbi.nlm.nih.gov/books/NBK499922/ (Accessed: 17 July 2025).

[83]

Condello C, Stöehr J. Aβ propagation and strains: Implications for the phenotypic diversity in Alzheimer’s disease. Neurobiology of Disease. 2018; 109: 191–200. https://doi.org/10.1016/j.nbd.2017.03.014.

[84]

Rosenberg A, Ngandu T, Rusanen M, Antikainen R, Bäckman L, Havulinna S, et al. Multidomain lifestyle intervention benefits a large elderly population at risk for cognitive decline and dementia regardless of baseline characteristics: The FINGER trial. Alzheimer’s & Dementia. 2018; 14: 263–270. https://doi.org/10.1016/j.jalz.2017.09.006.

[85]

Harding A, Gonder U, Robinson SJ, Crean S, Singhrao SK. Exploring the Association between Alzheimer’s Disease, Oral Health, Microbial Endocrinology and Nutrition. Frontiers in Aging Neuroscience. 2017a; 9: 398. https://doi.org/10.3389/fnagi.2017.00398.

[86]

Beydoun MA, Beydoun HA, Hossain S, El-Hajj ZW, Weiss J, Zonderman AB. Clinical and Bacterial Markers of Periodontitis and Their Association with Incident All-Cause and Alzheimer’s Disease Dementia in a Large National Survey. Journal of Alzheimer’s Disease. 2020; 75: 157–172. https://doi.org/10.3233/JAD-200064.

[87]

Fang WL, Jiang MJ, Gu BB, Wei YM, Fan SN, Liao W, et al. Tooth loss as a risk factor for dementia: systematic review and meta-analysis of 21 observational studies. BMC Psychiatry. 2018; 18: 345. https://doi.org/10.1186/s12888-018-1927-0.

[88]

Lin L, Sun Y, Wang X, Su L, Wang X, Han Y. Resilience to Plasma and Cerebrospinal Fluid Amyloid-β in Cognitively Normal Individuals: Findings From Two Cohort Studies. Frontiers in Aging Neuroscience. 2021; 13: 610755. https://doi.org/10.3389/fnagi.2021.610755.

[89]

Dominy SS, Lynch C, Ermini F, Benedyk M, Marczyk A, Konradi A, et al. Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. Science Advances. 2019; 5: eaau3333. https://doi.org/10.1126/sciadv.aau3333.

[90]

Singhrao SK, Olsen I. Assessing the role of Porphyromonas gingivalis in periodontitis to determine a causative relationship with Alzheimer’s disease. Journal of Oral Microbiology. 2019; 11: 1563405. https://doi.org/10.1080/20002297.2018.1563405.

[91]

Poole S, Singhrao SK, Chukkapalli S, Rivera M, Velsko I, Kesavalu L, et al. Active invasion of Porphyromonas gingivalis and infection-induced complement activation in ApoE-/- mice brains. Journal of Alzheimer’s Disease. 2015; 43: 67–80. https://doi.org/10.3233/JAD-140315.

[92]

Borsa L, Dubois M, Sacco G, Lupi L. Analysis the Link between Periodontal Diseases and Alzheimer’s Disease: A Systematic Review. International Journal of Environmental Research and Public Health. 2021; 18: 9312. https://doi.org/10.3390/ijerph18179312.

[93]

Harding A, Robinson S, Crean S, Singhrao SK. Can Better Management of Periodontal Disease Delay the Onset and Progression of Alzheimer’s Disease? Journal of Alzheimer’s Disease. 2017b; 58: 337–348. https://doi.org/10.3233/JAD-170046.

[94]

Ryder MI, Xenoudi P. Alzheimer disease and the periodontal patient: New insights, connections, and therapies. Periodontology 2000. 2021; 87: 32–42. https://doi.org/10.1111/prd.12389.

[95]

Schwahn C, Frenzel S, Holtfreter B, Van der Auwera S, Pink C, Bülow R, et al. Effect of periodontal treatment on preclinical Alzheimer’s disease-Results of a trial emulation approach. Alzheimer’s & Dementia. 2022; 18: 127–141. https://doi.org/10.1002/alz.12378.

[96]

Vestbo J. COPD: definition and phenotypes. Clinics in Chest Medicine. 2014; 35: 1–6. https://doi.org/10.1016/j.ccm.2013.10.010.

[97]

Miravitlles M, Anzueto A. Antibiotic prophylaxis in COPD: Why, when, and for whom? Pulmonary Pharmacology & Therapeutics. 2015; 32: 119–123. https://doi.org/10.1016/j.pupt.2014.05.002.

[98]

Miravitlles M, Anzueto A. Antibiotics for acute and chronic respiratory infection in patients with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine. 2013; 188: 1052–1057. https://doi.org/10.1164/rccm.201302-0289PP.

[99]

Pathak JL, Yan Y, Zhang Q, Wang L, Ge L. The role of oral microbiome in respiratory health and diseases. Respiratory Medicine. 2021; 185: 106475. https://doi.org/10.1016/j.rmed.2021.106475.

[100]

Lin M, Li X, Wang J, Cheng C, Zhang T, Han X, et al. Saliva Microbiome Changes in Patients With Periodontitis With and Without Chronic Obstructive Pulmonary Disease. Frontiers in Cellular and Infection Microbiology. 2020; 10: 124. https://doi.org/10.3389/fcimb.2020.00124.

[101]

Godara N, Godara R, Khullar M. Impact of inhalation therapy on oral health. Lung India. 2011; 28: 272–275. https://doi.org/10.4103/0970-2113.85689.

[102]

Khijmatgar S, Belur G, Venkataram R, Karobari MI, Marya A, Shetty V, et al. Oral Candidal Load and Oral Health Status in Chronic Obstructive Pulmonary Disease (COPD) Patients: A Case-Cohort Study. BioMed Research International. 2021; 2021: 5548746. https://doi.org/10.1155/2021/5548746.

[103]

Li Q, Wang H, Tan L, Zhang S, Lin L, Tang X, et al. Oral Pathogen Fusobacterium nucleatum Coaggregates With Pseudomonas aeruginosa to Modulate the Inflammatory Cytotoxicity of Pulmonary Epithelial Cells. Frontiers in Cellular and Infection Microbiology. 2021; 11: 643913. https://doi.org/10.3389/fcimb.2021.643913.

[104]

Yenen Z, Ataçağ T. Oral care in pregnancy. Journal of the Turkish German Gynecological Association. 2019; 20: 264–268. https://doi.org/10.4274/jtgga.galenos.2018.2018.0139.

[105]

Fardini Y, Chung P, Dumm R, Joshi N, Han YW. Transmission of diverse oral bacteria to murine placenta: evidence for the oral microbiome as a potential source of intrauterine infection. Infection and Immunity. 2010; 78: 1789–1796. https://doi.org/10.1128/IAI.01395-09.

[106]

Vanterpool SF, Been JV, Houben ML, Nikkels PGJ, De Krijger RR, Zimmermann LJI, et al. Porphyromonas gingivalis within Placental Villous Mesenchyme and Umbilical Cord Stroma Is Associated with Adverse Pregnancy Outcome. PLoS ONE. 2016; 11: e0146157. https://doi.org/10.1371/journal.pone.0146157.

[107]

Jahan SS, Hoque Apu E, Sultana ZZ, Islam MI, Siddika N. Oral Healthcare during Pregnancy: Its Importance and Challenges in Lower-Middle-Income Countries (LMICs). International Journal of Environmental Research and Public Health. 2022; 19: 10681. https://doi.org/10.3390/ijerph191710681.

[108]

Muanda FT, Sheehy O, Bérard A. Use of antibiotics during pregnancy and the risk of major congenital malformations: a population based cohort study. British Journal of Clinical Pharmacology. 2017; 83: 2557–2571. https://doi.org/10.1111/bcp.13364.

[109]

Boggess KA, Edelstein BL. Oral health in women during preconception and pregnancy: implications for birth outcomes and infant oral health. Maternal and Child Health Journal. 2006; 10: S169–S174. https://doi.org/10.1007/s10995-006-0095-x.

[110]

Expert Opinion. Committee Opinion No. 569: oral health care during pregnancy and through the lifespan. Obstetrics and Gynecology. 2013; 122: 417–422. https://doi.org/10.1097/01.AOG.0000433007.16843.10.

[111]

Tafti A, Clark P. Anatomy, Head and Neck, Primary Dentition. 2025. Available at: http://www.ncbi.nlm.nih.gov/books/NBK573074/ (Accessed: 17 July 2025).

[112]

Brummund D, Chang A, Michienzi J. Pedunculated Natal Tooth: A Case Report. Cureus. 2022; 14: e25992. https://doi.org/10.7759/cureus.25992.

[113]

Cordeiro MMR, Rocha MJDC. The effects of periradicular inflamation and infection on a primary tooth and permanent successor. The Journal of Clinical Pediatric Dentistry. 2005; 29: 193–200. https://doi.org/10.17796/jcpd.29.3.5238p10v21r2j162.

[114]

Mohd Khairuddin AN, Bogale B, Kang J, Gallagher JE. Impact of dental visiting patterns on oral health: A systematic review of longitudinal studies. BDJ Open. 2024; 10: 18. https://doi.org/10.1038/s41405-024-00195-7.

[115]

Saccomanno S, De Luca M, Saran S, Petricca MT, Caramaschi E, Mastrapasqua RF, et al. The importance of promoting oral health in schools: a pilot study. European Journal of Translational Myology. 2023; 33: 11158. https://doi.org/10.4081/ejtm.2023.11158.

[116]

Borges TS, Vargas-Ferreira F, Kramer PF, Feldens CA. Impact of traumatic dental injuries on oral health-related quality of life of preschool children: A systematic review and meta-analysis. PLoS ONE. 2017; 12: e0172235. https://doi.org/10.1371/journal.pone.0172235.

[117]

Foster H, Fitzgerald J. Dental disease in children with chronic illness. Archives of Disease in Childhood. 2005; 90: 703–708. https://doi.org/10.1136/adc.2004.058065.

[118]

Broutin A, Blanchet I, Canceill T, Noirrit-Esclassan E. Association between Dentofacial Features and Bullying from Childhood to Adulthood: A Systematic Review. Children. 2023; 10: 934. https://doi.org/10.3390/children10060934.

[119]

Das P, Mishra L, Jena D, Govind S, Panda S, Lapinska B. Oral Health-Related Quality of Life in Children and Adolescents with a Traumatic Injury of Permanent Teeth and the Impact on Their Families: A Systematic Review. International Journal of Environmental Research and Public Health. 2022; 19: 3087. https://doi.org/10.3390/ijerph19053087.

[120]

Quadri MFA, Jaafari FRM, Mathmi NAA, Huraysi NHF, Nayeem M, Jessani A, et al. Impact of the Poor Oral Health Status of Children on Their Families: An Analytical Cross-Sectional Study. Children. 2021; 8: 586. https://doi.org/10.3390/children8070586.

[121]

Jordan AR, Becker N, Jöhren HP, Zimmer S. Early Childhood Caries and Caries Experience in Permanent Dentition: A 15-year Cohort Study. Swiss Dental Journal. 2016; 126: 114–119. https://doi.org/10.61872/sdj-2016-02-141.

[122]

Nazir MA, Izhar F, Akhtar K, Almas K. Dentists’ awareness about the link between oral and systemic health. Journal of Family & Community Medicine. 2019; 26: 206–212. https://doi.org/10.4103/jfcm.JFCM_55_19.

[123]

Pagliusi MEM, Toledo DM, Kassis EN. Relevance of dental care in hospitals: A brief systematic review. MedNEXT Journal of Medical and Health Sciences. 2022; 3. https://doi.org/10.54448/mdnt22S406.

[124]

Schuurhuis JM, Stokman MA, Witjes MJH, Dijkstra PU, Vissink A, Spijkervet FKL. Evidence supporting pre-radiation elimination of oral foci of infection in head and neck cancer patients to prevent oral sequelae. A systematic review. Oral Oncology. 2015; 51: 212–220. https://doi.org/10.1016/j.oraloncology.2014.11.017.

[125]

Souza AF, Rocha AL, Castro WH, Gelape CL, Nunes MCP, Oliveira SR, et al. Dental management for patients undergoing heart valve surgery. Journal of Cardiac Surgery. 2017; 32: 627–632. https://doi.org/10.1111/jocs.13211.

[126]

Lim MAWT, Borromeo GL. The use of general anesthesia to facilitate dental treatment in adult patients with special needs. Journal of Dental Anesthesia and Pain Medicine. 2017; 17: 91–103. https://doi.org/10.17245/jdapm.2017.17.2.91.

[127]

Puri S, Kapur A, Mathew PJ. General Anesthesia for Dental Procedures in Children: A Comprehensive Review. Journal of Postgraduate Medicine, Education and Research. 2022; 56: 29–33. https://doi.org/10.5005/jp-journals-10028-1555.

[128]

Silva CC, Lavado C, Areias C, Mourão J, Andrade DD. Conscious sedation vs general anesthesia in pediatric dentistry–a review. MedicalExpress. 2015; 2: M150104. https://doi.org/10.5935/MedicalExpress.2015.01.04.

PDF (8993KB)

0

Accesses

0

Citation

Detail

Sections
Recommended

/