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Tooth loss

Tooth loss refers to the absence of one or more teeth from the dental arch, occurring either physiologically during the natural exfoliation of primary (deciduous) teeth in childhood or pathologically in permanent dentition due to untreated dental caries, periodontitis, trauma, or iatrogenic extractions.^[1]^[2] In adults, pathological tooth loss predominates as a preventable outcome of chronic oral infections, with periodontitis—the inflammatory destruction of supporting periodontal tissues—and caries-induced pulp necrosis as the primary causal mechanisms, exacerbated by risk factors including tobacco use, poor oral hygiene, and systemic conditions like diabetes.^[1]^[3] Globally, severe tooth loss affects nutritional intake and masticatory function, contributing to broader health burdens such as malnutrition and increased chronic disease risk.^[4]^[5] Epidemiological data indicate a high prevalence, with an estimated 7% of individuals aged 20 years or older experiencing complete edentulism worldwide, though rates vary by region, socioeconomic status, and access to dental care.^[4] In the United States, approximately 11% of adults aged 65–74 years have lost all teeth, rising to 20% among those 75 and older, with average missing teeth due to disease reaching 6.4 per person in older cohorts.^[1]^[6] Tooth loss correlates strongly with age, low income, smoking, and comorbidities like cardiovascular disease and arthritis, reflecting cumulative exposure to modifiable risk factors rather than inevitable senescence.^[7]^[8] Prevention through fluoride application, regular professional cleanings, and cessation of tobacco mitigates incidence, underscoring tooth loss as a largely avoidable sequela of neglected oral microbial dysbiosis.^[1]^[9]

Physiological Tooth Loss

Deciduous Tooth Exfoliation in Humans

Deciduous tooth exfoliation in humans represents a genetically programmed physiological process essential for the transition to permanent dentition, characterized by selective root resorption that facilitates shedding without underlying pathology. This resorption primarily affects the roots of primary teeth, initiated by the activity of odontoclasts—multinucleated cells akin to osteoclasts—that degrade dentin and cementum in a controlled manner. The process is triggered by mechanical forces from the erupting succedaneous permanent teeth, which exert pressure on the primary tooth roots, promoting odontoclast recruitment and activation along the root surfaces.^[10]^[11] The timeline of exfoliation typically commences around age 6 years with the mandibular central incisors, followed sequentially by the maxillary central incisors, lateral incisors, and canines, with second primary molars shed last, often by age 11 to 12 years. This order mirrors the reverse of primary tooth eruption and aligns with the developmental timing of permanent tooth crown completion and root formation beneath. Variations in shedding timing occur, influenced by genetic factors, with twin studies indicating heritability estimates exceeding 80% for primary tooth eruption and analogous loss patterns.^[12]^[13] Hormonal regulation plays a role, particularly parathyroid hormone-related protein (PTHrP), which modulates extracellular matrix remodeling and inhibits premature resorption; deficiencies lead to accelerated root breakdown in animal models, underscoring its protective and timing influence. Exfoliation proceeds with minimal discomfort under normal conditions, as the gradual resorption avoids acute inflammation, though rare instances of primary tooth ankylosis—fusion to alveolar bone—can delay shedding and necessitate clinical monitoring to prevent interference with permanent tooth eruption.^[14]

Evolutionary and Comparative Perspectives

In vertebrates, tooth replacement patterns vary significantly across taxa, reflecting evolutionary trade-offs between durability, energy allocation, and dietary demands. Non-mammalian vertebrates, such as reptiles and most fish, exhibit polyphyodonty, characterized by continuous, lifelong tooth replacement facilitated by persistent dental lamina stem cells that generate multiple successive generations of teeth.^[15]^[16] This system supports high wear rates from abrasive diets but incurs ongoing metabolic costs for regeneration. In contrast, mammals evolved diphyodonty, limited to two dentition sets—deciduous and permanent—as an energy-efficient adaptation that prioritizes robust, long-lasting permanent teeth over frequent replacement, coinciding with the Mesozoic emergence of mammalian traits like endothermy and rapid juvenile growth.^[17]^[18] Fossil records indicate diphyodonty originated in late Triassic cynodonts, non-mammalian synapsids ancestral to mammals, as evidenced by specimens like Brasilodon displaying sequential deciduous-permanent replacement patterns distinct from reptilian polyphyodonty.^[17] Among primates, this diphyodont condition persists with species-specific variations in deciduous tooth shedding and permanent eruption ages; for instance, chimpanzees shed deciduous teeth between 2-4 years, aligning closely with human timelines but varying by up to 20% across great apes due to ecological factors like weaning age and diet hardness.^[19]^[20] Hominin fossils further reveal conserved replacement mechanics, with early ancestors like Australopithecus maintaining similar two-set dentitions despite progressive tooth size reduction over 2-5 million years.^[21] This limited replacement in mammals may contribute to an evolutionary mismatch in modern humans, where ancestral selective pressures for abrasion-resistant teeth—driven by tough, unprocessed foods—have diminished with cooking, agriculture, and softer diets, potentially elevating susceptibility to pathological loss without corresponding adaptations in tooth durability or jaw robustness.^[22] Paleontological evidence links post-Pleistocene dietary shifts to smaller, less wear-tolerant teeth under relaxed selection, contrasting with polyphyodont species that retain regenerative capacity amid variable diets.^[21]^[22]

Epidemiology of Pathological Tooth Loss

Global Prevalence and Trends

Globally, complete tooth loss, or edentulism, affects approximately 350 million people, with severe periodontal disease—a primary precursor—impacting over 1 billion individuals worldwide.^[4]^[23] For adults aged 60 years and older, the estimated global prevalence of edentulism reaches 23%, though rates vary substantially by region and socioeconomic status, remaining markedly higher in low- and middle-income countries where access to dental care is limited.^[4] These figures underscore the scale of pathological tooth loss, predominantly driven by untreated infections, with edentulism cases numbering around 353 million as of recent Global Burden of Disease assessments.^[24] Trends indicate a decline in age-standardized incidence rates of edentulism in many regions over the past three decades, reflecting improvements in oral health practices and access in higher-income settings, yet absolute numbers have doubled due to population growth and aging demographics.^[25] In the United States, for instance, edentulism prevalence among adults aged 20-64 years has fallen to approximately 5.9% in the 50-64 subgroup, with overall rates for this age band remaining low amid broader reductions from historical highs.^[26]^[27] Projections suggest continued slowdowns in decline rates, potentially stabilizing around 2-3% in developed nations by mid-century, while global edentulism incidence has risen sharply, with cases increasing by over 93% to 26.5 million new instances in recent years.^[28]^[27] The COVID-19 pandemic disrupted dental services worldwide, leading to deferred treatments and potential exacerbations of untreated conditions, with some studies observing increases in missing teeth post-restrictions due to reduced preventive care.^[29] This interruption, coupled with rising burdens in aging populations—where two-thirds of those over 60 will reside in low- and middle-income countries by 2050—signals risks of stalled progress, particularly in resource-constrained areas.^[30] Despite these challenges, empirical data affirm that pathological tooth loss remains largely preventable through consistent interventions, as evidenced by persistent disparities tied to hygiene access rather than inevitability.^[4]

Demographic and Risk Factor Associations

Tooth loss prevalence escalates with advancing age, reflecting cumulative exposure to risk factors over time. In the United States, complete edentulism affects 17.8% of adults aged 75 years and older, rising from 8.9% among those aged 65–69 years and 10.6% for ages 70–74, based on National Health and Nutrition Examination Survey data from 2011–2017.^[6] This age gradient persists across populations, with older adults retaining fewer teeth due to longstanding untreated caries and periodontal disease, though overall tooth retention has improved in recent decades compared to prior generations.^[31] Socioeconomic disparities exhibit steep gradients in tooth loss rates, with lower income and education levels correlating to substantially elevated risks—often tripled—primarily through modifiable behavioral pathways such as inconsistent oral hygiene, poorer dietary habits, and elevated smoking prevalence rather than inherent destiny.^[32] For instance, edentulism prevalence among seniors is three times higher in low-income groups (34%) versus higher-income counterparts (11%), as derived from geospatial analyses of U.S. census data.^[33] Similarly, individuals with low educational attainment retain fewer natural teeth than those with higher education, a pattern mediated by adult socioeconomic status in longitudinal cohort studies.^[34] Gender differences show males experiencing higher tooth loss rates than females, linked to behavioral neglect patterns including lower utilization of preventive dental care and higher engagement in risks like tobacco use.^[35] In population surveys, males accounted for 64.3% of tooth loss cases compared to 37.2% for females, consistent with men's greater periodontitis burden from lifestyle factors.^[36] Among behavioral risks, current smoking triples the likelihood of tooth loss, with heavy smokers (≥15 cigarettes daily) facing over 3.6 times the odds compared to non-smokers in prospective studies.^[37] Complete edentulism is more than twice as prevalent among older smokers (29%) versus non-smokers, underscoring smoking's dose-dependent role independent of other demographics.^[7] These correlations, while robust, do not imply direct causation from immutable traits; for example, low socioeconomic status elevates risk predominantly via indirect channels like increased smoking and suboptimal diet, amenable to intervention.^[38]^[39]

Etiology of Pathological Tooth Loss

Primary Infectious Mechanisms

The primary infectious mechanisms underlying pathological tooth loss involve microbial biofilms that colonize tooth surfaces, leading to dental caries and periodontitis through localized acid production, tissue invasion, and dysregulated host immune responses. Dental plaque, a polymicrobial biofilm, adheres to enamel and subgingival areas; inadequate mechanical disruption allows maturation into pathogenic communities dominated by acidogenic and proteolytic bacteria. This biofilm architecture shields microbes from host defenses and antimicrobials, enabling persistent inflammation and structural damage that culminates in tooth extraction when restorative interventions fail.^[40]^[41] Periodontitis, a leading cause of tooth loss, arises from subgingival biofilms enriched in anaerobes such as Porphyromonas gingivalis, which invades gingival epithelium and triggers hyperinflammatory cascades via lipopolysaccharide and gingipains. These virulence factors degrade connective tissue, form periodontal pockets, and induce alveolar bone resorption through osteoclast activation and impaired immune resolution, resulting in tooth mobility and eventual loss. P. gingivalis dysregulates host responses by mimicking self-antigens and evading phagocytosis, establishing causality beyond mere association; experimental models confirm its necessity for disease progression in susceptible hosts. Globally, severe periodontitis affected approximately 1.07 billion cases in 2021, with incidence rising 76% since 1990 due to population aging and growth.^[42]^[43]^[24] Dental caries progresses via supragingival biofilms where Streptococcus mutans predominates, fermenting dietary sugars into lactic acid that demineralizes enamel hydroxyapatite, creating subsurface lesions. Untreated caries advances to dentinal invasion, pulpal necrosis, and periapical abscesses, often requiring extraction to halt infection spread. S. mutans enhances biofilm cohesion through glucans and tolerates low pH, perpetuating the cariogenic cycle; while not the sole etiological agent, its levels correlate strongly with lesion severity in longitudinal studies. Among adults aged 20-64, untreated caries prevalence reached 21% in the United States by 2020, with global estimates indicating up to 60% in older cohorts where access to care is limited, frequently leading to extractions in low-resource settings.^[44]^[45]^[26] Causal primacy lies in biofilm accumulation from suboptimal plaque control, as evidenced by long-term cohorts showing tooth loss rates below 2% over 30 years with rigorous mechanical hygiene, versus rapid progression without it; genetic or systemic modifiers amplify but do not independently initiate these infectious processes absent unchecked microbial overgrowth.^[46]^[47]

Traumatic and Iatrogenic Causes

Traumatic tooth loss most commonly results from avulsion, the complete displacement of a tooth from its alveolar socket due to high-impact forces. Prevalent mechanisms include falls (26%), traffic accidents (20.5%), sports-related incidents (19.2%), and violence (16.4%), particularly affecting permanent incisors in children and adolescents.^[48] In youth aged 7-12 years, such injuries peak among boys, often from falls, collisions with objects, or bicycle accidents, with avulsion identified as a leading cause of permanent tooth loss in this demographic (median age 13.8 years).^[49]^[50] Overall, traumatic dental injuries occur in 1-3% of the population annually, with avulsions representing approximately 5-6% of such cases, though untreated avulsions invariably lead to loss.01078-3/fulltext)^[51] Successful management of avulsed teeth hinges on minimizing extra-oral time to preserve periodontal ligament (PDL) viability; dry storage beyond 20-30 minutes initiates PDL cell necrosis, sharply reducing replantation success and increasing risks of ankylosis or resorption.^[52] Guidelines emphasize immediate replantation within 5 minutes ideally, or storage in media like milk or saline if delayed, as prognosis deteriorates markedly after 60 minutes, with long-term survival rates dropping below 50% in delayed cases.^[53]^[54] Iatrogenic tooth loss stems from unintended consequences of dental procedures, such as endodontic treatments causing root perforations, overfilling, or instrumentation errors that induce gingival necrosis or periodontitis, often necessitating extraction.^[55] Orthodontic interventions, including premolar extractions to facilitate alignment, can contribute via associated attachment and bone loss in adjacent teeth.^[56] Implant placements elevate adjacent tooth loss risk by up to 2.5-fold, with root fractures accounting for 45% of cases, followed by caries (29%) and periodontitis (24%).^[57] In restored endodontically treated teeth, iatrogenic failures like inadequate post placement or procedural mishaps occur in 10-33% of complications, frequently leading to extraction.^[58] Prior to widespread antibiotic use (pre-1940s), extraction rates were elevated due to aggressive interventions for pulpal infections, though contemporary iatrogenesis arises primarily from technical errors rather than therapeutic overreach.^[59]

Systemic, Genetic, and Lifestyle Contributors

Systemic conditions such as diabetes mellitus contribute to pathological tooth loss primarily through mechanisms impairing immune response and wound healing, exacerbating periodontitis progression. A meta-analysis of observational studies indicated that type 2 diabetes significantly elevates the odds of tooth loss, with unadjusted odds ratios demonstrating a clear association independent of other confounders in adjusted models.^[60] Hyperglycemia in diabetes compromises neutrophil function and collagen synthesis, fostering unchecked bacterial proliferation in gingival tissues and accelerating alveolar bone resorption.^[61] Similarly, osteoporosis correlates with diminished jawbone mineral density, synergizing with periodontal inflammation to heighten attachment loss and tooth mobility; cohort data link baseline osteoporosis to greater numbers of teeth exhibiting periodontitis progression over time, particularly in postmenopausal women.^[62] Genetic predispositions influence tooth loss susceptibility, though effects are often amplified by environmental factors. Periodontitis, the leading infectious precursor to edentulism, exhibits moderate heritability estimated at around 50%, with genome-wide association studies identifying loci such as those in the CXCL gene family that modulate inflammatory responses to plaque biofilms.^[63]^[64] Common polygenic variants confer modest risk elevations for aggressive periodontitis forms, but monozygotic twin studies underscore that lifestyle modulators like oral hygiene override genetic baselines in determining actual tooth retention. Rare Mendelian disorders, including amelogenesis imperfecta variants disrupting enamel matrix proteins, directly precipitate hypoplastic enamel prone to rapid carious breakdown and premature exfoliation, though these account for fewer than 1% of cases. Lifestyle factors exert modifiable causal influences on tooth loss via direct biochemical and vascular pathways. Tobacco smoking substantially heightens risk through nicotine-induced vasoconstriction and delayed epithelial repair, with epidemiological data attributing a disproportionate share of periodontitis-mediated edentulism to smokers over non-smokers.^[65] Chronic exposure impairs fibroblast proliferation and collagen turnover in periodontal ligaments, compounding bacterial virulence. Dietary patterns rich in fermentable carbohydrates sustain low pH environments favoring Streptococcus mutans acidogenesis, eroding enamel and dentin integrity; this aligns with evolutionary evidence where Neolithic adoption of starchy staples shifted oral microbiomes toward cariogenic dominance, markedly raising caries incidence compared to Paleolithic hunter-gatherer dentitions adapted to fibrous, low-glycemic foods.^[66]^[67] Such mismatches persist in modern high-sugar intakes, where frequent carbohydrate fermentation outpaces salivary buffering, initiating cascades from demineralization to pulp necrosis and eventual extraction.^[68]

Prevention Strategies

Individual Oral Hygiene and Behavioral Measures

Regular toothbrushing and interdental cleaning, such as flossing, constitute the cornerstone of individual oral hygiene for preventing plaque accumulation, which initiates caries and periodontitis—the predominant infectious causes of tooth loss.^[69] Mechanical disruption of plaque through these methods reduces gingival inflammation and bleeding indices more effectively than brushing alone, with interdental aids like floss achieving superior interproximal cleaning.^[70]^[71] Supervised or consistent brushing regimens demonstrably lower caries incidence compared to irregular practices, underscoring technique and frequency as causal determinants over adjuncts like fluoride, which primarily enhance remineralization on a plaque-reduced surface.^[72]^[73] Twice-daily brushing with a soft-bristled toothbrush and fluoride toothpaste, combined with daily flossing, mitigates the risk of periodontitis by twofold to fivefold relative to poor hygiene compliance, as plaque biofilm persistence directly correlates with disease progression.^[74] Non-adherence to these routines remains the primary modifiable failure mode in pathology development, even among those with access to professional care, emphasizing personal agency in causal prevention.^[74]^[1] For instance, smokers exhibit elevated tooth loss rates attributable to impaired immune response and vascular effects, persisting despite equivalent oral hygiene efforts to non-smokers.^[75]^[76] Optimal technique—such as the Bass method for subgingival plaque removal—prioritizes thorough coverage over duration or tool novelty, with evidence showing no superior caries prevention from powered versus manual brushes when manual technique is proficient.^[77]^[78] Interproximal caries risk, a key pathway to premature loss, is particularly responsive to adjunct flossing in low-fluoride environments, though overall efficacy hinges on consistent mechanical removal rather than chemical reliance alone.^[79] Thus, sustained behavioral adherence, not sporadic intensification, drives long-term retention of dentition.^[74]

Dietary Modifications and Nutritional Factors

Frequent consumption of fermentable carbohydrates, particularly sucrose, provides substrate for Streptococcus mutans and other plaque bacteria to produce acids, lowering oral pH and promoting enamel demineralization, which initiates caries that can progress to pulp involvement and eventual tooth loss.^[80]^[81] This process is exacerbated by the frequency of intake rather than total quantity, as repeated acid challenges overwhelm salivary buffering and remineralization capacity.^[82] Epidemiological data link higher sugar-sweetened beverage consumption—even at less than daily levels—to increased permanent tooth loss in young adults, independent of other factors.^[83] Archaeological evidence indicates that tooth decay rates were low in pre-agricultural hunter-gatherer populations, with cavities affecting at most 14% of teeth, rising sharply with the adoption of starch-rich agricultural diets that increased fermentable carbohydrate availability.^[84]^[85] Reducing dietary carbohydrates can mitigate this risk; studies show low-carbohydrate regimens improve periodontal parameters, reduce inflammation, and decrease caries incidence by limiting bacterial acid production, often diminishing the reliance on fluoride interventions.^[86]^[87] Nutritional deficiencies contribute causally to tooth loss vulnerability. Vitamin D deficiency impairs enamel formation, leading to hypoplasia—a thinned or defective enamel layer that heightens caries susceptibility and resorption akin to rickets effects on bone.^[88]^[89] Prenatal or early childhood deficits specifically correlate with developmental enamel defects and elevated decay risk.^[90] Similarly, vitamin C deficiency disrupts collagen synthesis in periodontal tissues, manifesting as scurvy with gingival hemorrhage, attachment loss, and rapid tooth mobility or exfoliation.^[91]^[92] Diets emphasizing nutrient-dense foods rich in these vitamins, calcium, and phosphorus—while minimizing free sugars—support enamel integrity and gingival health, as evidenced by lower caries in populations adhering to such patterns.^[93]

Public Health Interventions and Policy Considerations

Community water fluoridation adjusts fluoride levels in public water supplies to approximately 0.7 mg/L, reducing tooth decay by about 25% in both children and adults through frequent low-dose exposure that strengthens enamel and inhibits bacterial acid production.^[94] This intervention has contributed to substantial declines in caries prevalence since its widespread adoption in the mid-20th century, with meta-analyses confirming sustained benefits when maintained at optimal concentrations.^[95] However, excessive fluoride intake from multiple sources can lead to dental fluorosis, characterized by enamel mottling, particularly in children under 8 years whose teeth are developing, necessitating monitoring of total exposure beyond water alone.^[96] School-based dental sealant programs apply resin coatings to occlusal surfaces of permanent molars in children, preventing up to 80% of caries in sealed teeth over two years and reducing overall cavity incidence by a median of 50% compared to unsealed teeth.^[97]^[98] These programs, often targeting schools in low-income areas, are deemed cost-effective by public health analyses, averting fillings and associated disability-adjusted life years at a ratio exceeding benefits from routine care alone.^[99] Integrated screenings in such initiatives identify high-risk students for targeted sealants, enhancing reach without relying on parental consent barriers.^[100] Despite these benefits, public health interventions exhibit limitations in addressing tooth loss drivers, as they do not fully compensate for inadequate personal oral hygiene or dietary habits, with empirical data showing persistent caries burdens in populations with poor compliance.^[101] Uptake remains uneven among high-risk groups, such as low-socioeconomic or minority communities, where barriers like access and cultural factors limit program participation and equitable outcomes.^[7] Policy considerations thus emphasize evidence-based scaling, such as prioritizing high-prevalence areas while weighing fluorosis risks against caries reductions, without supplanting individual responsibility; cost-benefit models indicate net savings but underscore the need for surveillance to avoid overexposure.^[102]

Consequences of Tooth Loss

Immediate and Long-Term Oral Health Effects

Following tooth extraction, immediate biomechanical disruptions occur in the oral cavity, primarily due to the sudden absence of occlusal support, which alters force distribution across the dental arch and can lead to uneven masticatory loading on remaining teeth.^[103] Adjacent teeth may experience initial tipping or extrusion as they migrate into the edentulous space, compromising arch stability and potentially causing temporary occlusal interferences that exacerbate chewing inefficiencies.^[104] In the long term, alveolar bone resorption represents a primary sequela, driven by disuse atrophy and lack of periodontal ligament stimulation; quantitative assessments indicate reductions of up to 50% in ridge width within the first year post-extraction, with vertical height losses of approximately 1-2 mm occurring predominantly in the initial 6 months.^[105] ^[106] This progressive bone loss diminishes the foundational support for prostheses and heightens vulnerability to further structural compromise. Concurrently, unchecked tooth drift—characterized by mesial tilting of posterior teeth and overeruption of unopposed dentition—fosters malocclusion, creating plaque-retentive areas that elevate risks of caries and gingival inflammation on adjacent surfaces.^[103] Biomechanical overload on surviving teeth, resulting from redistributed occlusal forces, accelerates wear facets, mobility, and fracture susceptibility, often culminating in accelerated loss of neighboring dentition; clinical observations link such shifts to heightened periodontal attachment loss in partially edentulous patients.^[107] Studies of maintenance cohorts demonstrate that residual teeth in advanced periodontitis cases face compounded progression risks, with probing depths ≥5 mm post-treatment correlating to sustained disease advancement and up to twofold higher tooth loss rates compared to fully intact arches.^[108] These effects underscore the cascade of local adaptations that perpetuate oral deterioration without intervention.^[109]

Systemic Health Implications

Tooth loss, often resulting from chronic periodontitis, facilitates systemic dissemination of oral pathogens through transient bacteremia, particularly during mastication, toothbrushing, or invasive procedures, elevating the risk of infective endocarditis. Meta-analyses indicate that periodontal disease, a primary precursor to tooth loss, is associated with a 19% to 34% increased relative risk of cardiovascular events, including myocardial infarction, with odds ratios ranging from 1.49 to 2.13 in cohort studies adjusting for confounders like smoking and diabetes.^[110]^[111]^[112] However, Mendelian randomization analyses provide no evidence of direct causality between periodontitis and endocarditis, suggesting shared risk factors or residual confounding may contribute to observed associations rather than unidirectionally causal pathways from oral bacteria.^[113] Impaired masticatory function following tooth loss reduces chewing efficiency, leading to avoidance of fibrous and protein-rich foods, which compromises nutritional intake and exacerbates sarcopenia in older adults. Cross-sectional and longitudinal studies demonstrate that fewer occlusal pairs correlate with poorer nutritional status, mediating up to partial associations between tooth loss and sarcopenia prevalence, independent of age and comorbidities.^[114]^[115] In elderly cohorts, this pathway manifests as decreased protein consumption and altered dietary patterns, heightening frailty risks through muscle mass decline.^[116] Tooth loss trajectories independently predict elevated all-cause mortality, with faster progression linked to higher death rates in prospective Chinese cohorts of adults aged 65 and older, potentially mediated by chronic systemic inflammation markers like high-sensitivity C-reactive protein (hs-CRP).^[117]^[118] Edentulism or severe tooth loss raises mortality hazard by 15% to 30%, persisting after adjustment for socioeconomic and health factors, with inflammation from residual periodontal pathogens or unmet masticatory needs as plausible causal intermediaries.^[119]^[120]

Psychological and Socioeconomic Outcomes

Tooth loss, particularly edentulism, is associated with elevated risks of depression and psychological distress among adults. Longitudinal studies indicate that individuals with fewer than 20 remaining teeth face higher odds of developing incident depression over 2- to 4-year follow-ups, with effect sizes varying by gender and age.^[121] Rapid declines in tooth count further exacerbate this risk, correlating with increased psychological symptoms independent of baseline oral health.^[122] These associations persist after adjusting for confounders like age and comorbidities, suggesting that impaired masticatory function, chronic pain, and diminished facial aesthetics contribute causally to reduced self-esteem and social withdrawal.^[123] Aesthetic and functional deficits from tooth loss often lead to avoidance of social and professional interactions, reinforcing isolation. In population-based surveys, edentulous individuals report lower subjective wellbeing and self-rated health, with tooth loss mediating links between oral function and mental health outcomes.^[124] This pattern underscores behavioral factors: edentulism prevalence is markedly higher among smokers, who exhibit accelerated periodontal destruction and bone loss, and those with lower educational attainment, reflecting cumulative effects of poor hygiene and delayed care rather than isolated misfortune.^[125]^[32] Socioeconomically, tooth loss perpetuates disadvantage through diminished employability and heightened financial strain from lost productivity. Edentulism correlates with lower income levels and occupational limitations, as visible dental gaps impair confidence in interviews and client-facing roles, creating self-reinforcing cycles where initial behavioral risks (e.g., smoking, inadequate education-linked care) compound into sustained economic marginalization.^[126] Cross-national data from low- and middle-income settings show edentulous adults experiencing reduced workforce participation, with inequalities decomposing into contributions from education (favoring higher attainment) and health behaviors over structural barriers alone.^[127] These outcomes highlight causal pathways from modifiable habits to long-term socioeconomic erosion, without evidence of reversal absent intervention in root behaviors.^[128]

Management and Replacement Options

Conventional Prosthetic and Restorative Techniques

Removable partial dentures (RPDs) and complete dentures represent foundational options for replacing multiple missing teeth, with RPDs supported by abutment teeth and mucosal tissues, and complete dentures relying on edentulous ridges for retention via adhesion and border seal. Fixed partial dentures, or bridges, provide tooth-supported replacements for edentulous spans by cementing pontics to prepared abutments. These techniques, dating to the early 20th century refinements, prioritize mechanical retention and biocompatibility over biological integration.^[129] Denture bases are typically fabricated from heat-cured acrylic resin for its processability and mucosal tolerance, while prosthetic teeth employ either acrylic or porcelain. Acrylic teeth offer advantages in weight reduction (approximately 20-30% lighter than porcelain equivalents) and reduced risk of catastrophic fracture under occlusal load, though they exhibit higher wear rates (up to 0.1 mm/year in vitro) leading to diminished occlusal vertical dimension over 5-10 years. Porcelain teeth provide enhanced hardness (Vickers 700-800 vs. acrylic's 20-25) and color stability but increase opposing tooth abrasion by 2-3 times and pose fracture risks from brittleness (flexural strength ~60-90 MPa vs. acrylic's 70-100 MPa).^[130]^[131] Clinical longevity varies by prosthesis type and criteria such as replacement or functional failure. RPDs demonstrate 5-year survival rates of 75%, dropping to 50% at 10 years when accounting for non-wear or remake. Complete dentures average 10.1 years before replacement, with maxillary variants outlasting mandibular by ~1.7 years due to greater ridge stability. Fixed bridges achieve 93-94% 5-year survival, superior to removable options owing to rigid anchorage, though debonding affects 10-20% within this period.^[129]^[132]^[133] Functional outcomes reveal masticatory efficiency limitations: complete dentures yield 20-50% of natural dentition's particle size reduction capacity during comminution tests (e.g., optosil sieving method), correlating with reduced bite force (50-150 N vs. 500-700 N natural) and selective food avoidance in 60-70% of wearers. Fixed bridges mitigate this to 60-80% efficiency but require sufficient abutment vitality. Ill-fitting appliances exacerbate issues, with trauma inducing denture stomatitis in 20-70% of cases, facilitating Candida-associated infections via epithelial disruption and biofilm accumulation if hygiene lapses.^[134]^[135] Alveolar bone resorption persists unabated (1-3 mm/year initially, stabilizing to 0.1-0.2 mm/year), driven by disuse atrophy absent occlusal stimuli from roots, necessitating periodic relines (every 2-5 years) and favoring fixed prosthetics empirically for their biomechanical mimicry of natural load distribution over removable alternatives' mucosal reliance.^[136]^[137]

Surgical and Implant-Based Solutions

Surgical dental implants represent a primary invasive approach to tooth replacement, relying on the principle of osseointegration, wherein titanium fixtures achieve direct structural and functional connection with living bone through cellular attachment and remodeling processes without intervening soft tissue.^[138]^[139] These endosseous implants, typically cylindrical screws, are surgically inserted into the jawbone following extraction site healing or immediate placement protocols, with prosthetic restoration occurring after a 3-6 month integration period to allow osteoblast-mediated bone apposition.^[140] Long-term survival rates for dental implants exceed 95% at 10 years, based on systematic reviews aggregating data from prospective studies, with implant-level estimates reaching 96.4% (95% CI: 95.2%-97.5%).^[141] This durability stems from titanium's biocompatibility, enabling stable anchorage superior to conventional removable prosthetics in terms of retention and load distribution, as evidenced by comparative analyses showing reduced tissue resorption and improved masticatory efficiency with implant-supported options.^[142]^[143] In cases of alveolar bone atrophy, which compromises implant stability due to insufficient height or volume, preparatory bone grafting procedures are employed to regenerate supportive osseous structure using autologous, allogeneic, or synthetic materials.^[144] For the posterior maxilla, where pneumatization exacerbates resorption, maxillary sinus augmentation—via lateral window or crestal approaches—elevates the sinus floor to gain 4-10 mm of bone height, achieving implant survival rates of 97.4% in sites with residual bone ≥4 mm.^[145] These interventions, performed prior to or simultaneously with implant placement, demonstrate predictable outcomes in systematic evaluations, with graft incorporation rates supporting subsequent osseointegration.^[146] Implant failures, occurring in approximately 2-5% of cases over a decade, are predominantly linked to modifiable risk factors such as smoking, which elevates odds ratios to 2.4 (95% CI: 2.176-2.652) by impairing vascularization and osseointegration, and suboptimal oral hygiene, fostering peri-implantitis through biofilm accumulation.^[147]^[148] Patient selection excluding heavy smokers and emphasizing rigorous post-operative maintenance thus optimizes outcomes, underscoring the causal role of biological and behavioral determinants in procedural efficacy.^[149]

Emerging Regenerative Therapies

Emerging regenerative therapies for tooth loss aim to restore functional dental tissues through biological mechanisms rather than prosthetic replacement, leveraging stem cells, bioactive scaffolds, and molecular interventions to induce de novo tooth formation or pulp vitality. These approaches draw from preclinical models demonstrating tooth bud reactivation and tissue engineering, with human trials initiating in 2024 to assess safety and feasibility.^[150]^[151] While promising in animal studies, clinical translation remains limited by challenges in scalability, vascularization, and long-term integration, with efficacy data pending from ongoing Phase I evaluations as of 2025.^[152] Stem cell-based scaffolds have advanced dental pulp regeneration by combining mesenchymal stem cells from dental pulp (DPSCs) with biocompatible hydrogels or extracellular matrix mimics to recapitulate the pulp-dentin complex. In vitro and ex vivo models using DPSCs seeded on collagen or hydrogel scaffolds have shown odontoblastic differentiation and mineralized matrix deposition, restoring pulp vitality in immature teeth with necrotic pulp.^[153]^[154] Recent protocols incorporate growth factors like VEGF and BMP-2 within these scaffolds to enhance angiogenesis and dentinogenesis, with preclinical success in canine models yielding histologically viable pulp tissue up to 12 months post-implantation.^[155] Human applications remain experimental, primarily in regenerative endodontics for vital pulp therapy, but face hurdles in sourcing autologous cells and ensuring sterile, scalable production.^[156] Tooth organoids represent a step toward whole-tooth bioengineering, utilizing pluripotent or multipotent stem cells to form self-organizing structures mimicking enamel, dentin, and periodontal ligaments. Protocols involving human DPSCs and epithelial cells cultured in bioorthogonally cross-linked hydrogels have generated organoids exhibiting tooth germ-like morphology, including cusp formation and innervation precursors, as reported in 2024 studies.^[157] These models, often derived from induced pluripotent stem cells (iPSCs), enable high-throughput screening of developmental cues but have not yet progressed to in vivo implantation for full tooth replacement in large animals beyond proof-of-concept in mice.^[158] Limitations include incomplete amelogenesis and root development, necessitating refined signaling pathways like Wnt and Shh for clinical viability.^[159] Pharmacological interventions targeting developmental suppressors, such as anti-USAG-1 antibodies, seek to reactivate dormant tooth buds in adults or congenitally missing teeth by enhancing BMP signaling. Preclinical ferret and mouse studies demonstrated supernumerary tooth eruption following USAG-1 inhibition, with antibodies blocking the protein's interaction with BMP to promote bud initiation without tumorigenesis.^[151]^[160] In Japan, Phase I trials of the anti-USAG-1 drug (TRG-035) commenced on October 18, 2024, at Kyoto University Hospital, enrolling 30 adults with oligodontia to evaluate safety and tolerability through 2025, with broader efficacy trials projected for 2030.^[161] Initial dosing via intravenous administration showed no severe adverse events in early cohorts, but regenerative outcomes—such as measurable tooth growth—require Phase II data, as current evidence is confined to safety endpoints.^[152]^[162] This approach holds potential for edentulous regions but risks off-target effects on craniofacial bones, underscoring the need for precise dosing informed by genetic profiling.^[163]

Historical Context

Ancient Beliefs and Practices

In ancient Mesopotamia, Sumerian texts dating to approximately 5000 BC attributed tooth decay and associated pain to mythical "tooth worms" burrowing into enamel, a belief reflected in incantations invoking deities to expel the creatures.^[164] This pre-scientific etiology prompted rudimentary interventions, including the use of sharpened flint tools for drilling into affected teeth, with archaeological evidence of such practices emerging around 3000 BC in regions encompassing Sumeria and early Egyptian sites.^[165] These efforts, however, lacked efficacy against actual pathology, as artifacts reveal that pre-agricultural populations exhibited minimal dental caries prevalence—often below 5% of teeth affected—due to diets low in fermentable carbohydrates.^[166] By around 3000 BC in ancient Egypt, similar worm-centric views persisted, documented in medical papyri like the Ebers Papyrus (circa 1550 BC), which prescribed ineffective herbal remedies such as honey mixtures, ground bones, and incantations to alleviate toothache without addressing underlying decay.^[167] Egyptian practitioners, termed "tooth-doctors," performed drilling and extractions using copper tools, but skeletal remains indicate that caries rates remained low until the Neolithic dietary shift toward agriculture increased starch consumption, elevating decay incidence to 10-20% in early farming communities.^[168] This causal link from fermentable substrates to bacterial proliferation was unrecognized, perpetuating mythological treatments over empirical observation. In classical Greece, Hippocrates (circa 460-370 BC) cataloged dental symptoms like suppuration and mobility but did not fully endorse the tooth worm theory, instead advocating extractions and cauterization for loose teeth, though without knowledge of microbiology to explain suppuration as infection rather than parasitic activity.^[169] Roman practices, building on Greek foundations, emphasized extractions as a primary response to advanced caries or abscesses, with tools like forceps evidenced in archaeological finds from sites such as the Roman Forum (circa 1st century AD), where extracted teeth were discarded in drains.^[170] Narcotics like opium were employed for pain relief during procedures, yet overall ancient caries burdens—higher post-agriculture but still far below modern levels—stemmed from dietary carbohydrates fostering acid-producing bacteria, not worms, as later debunked by microscopic evidence absent in these eras.^[171]

Evolution to Modern Scientific Understanding

In the late 17th century, Antonie van Leeuwenhoek's microscopic observations of microbial life in dental plaque marked an early shift toward recognizing biological agents in oral pathology, challenging prevailing notions of decay as merely chemical or humoral imbalances.^[172] His 1683 descriptions of "animalcules" in scrapings from his own teeth provided the first empirical evidence of bacteria in the mouth, laying groundwork for later microbial theories of caries and periodontal destruction.^[173] The 19th century's adoption of germ theory, propelled by Louis Pasteur and Robert Koch, extended to dentistry through antisepsis practices introduced by Joseph Lister in 1867, which significantly curtailed postoperative infections following extractions and surgeries previously prone to iatrogenic tooth loss.^[174] Dentists like Ashley W. C. in 1876 applied carbolic acid and sterilization techniques, reducing sepsis rates in oral procedures and preserving teeth that might otherwise have been extracted prophylactically amid rampant inflammation.^[174] The mid-20th century brought transformative interventions: widespread antibiotics from the 1940s, including penicillin's clinical use post-1941, combated bacterial abscesses and osteomyelitis that historically necessitated extractions, while community water fluoridation trials beginning in Grand Rapids in 1945 demonstrated a 60% reduction in childhood caries rates, contributing to a broader decline in adult tooth loss from over 50% edentulism in the 1950s to near 10% by century's end.^[95]^[175] Concurrent public health campaigns promoting toothbrushing and flossing, amplified by fluoride toothpaste in the 1960s, further halved caries prevalence in monitored populations by enhancing plaque control alongside chemical remineralization.^[176] By the 1960s, research solidified periodontitis as a polymicrobial infection driven by specific pathogens like Porphyromonas gingivalis, with epidemiological studies linking gingival inflammation to alveolar bone loss and tooth mobility, prompting scaled-up preventive protocols.^[177] Post-2000 genomic advancements, including genome-wide association studies identifying loci like those near AMBN for caries susceptibility and NIN for aggressive periodontitis, enabled personalized risk assessment by quantifying host genetic vulnerabilities interacting with microbial and environmental factors.^[178]^[179]

Current Research Directions

Advances in Tooth Regeneration

In 2024, researchers at Kyoto University Hospital initiated Phase 1 human clinical trials for an antibody drug targeting the USAG-1 protein to stimulate tooth regrowth in adults with partial tooth loss, marking the first such trial globally.^[180] The trials, involving approximately 30 healthy participants aged 30-64 with at least one missing tooth, aim to assess safety and preliminary efficacy by inhibiting USAG-1, which suppresses bone morphogenetic protein (BMP) signaling essential for tooth development; preclinical data indicate this could activate latent tooth-forming potential akin to a third dentition set.^[152] Developers project potential clinical availability by 2030 if trials succeed, contrasting with prosthetic replacements by regenerating functional, biologically integrated teeth.^[162] Animal models have demonstrated USAG-1 inhibition's causality in tooth regeneration through enhanced BMP and Wnt pathway activation in dental epithelial and mesenchymal stem cells. In mice and ferrets engineered for congenital tooth agenesis, anti-USAG-1 antibodies induced supernumerary teeth with proper enamel, dentin, and periodontal ligament formation, restoring alveolar bone without systemic side effects observed in broader genetic knockouts.^[181] These findings, derived from controlled knock-in models rather than observational data, underscore epithelial-mesenchymal reciprocity as the core mechanism, where USAG-1 blockade reactivates dormant primordia during targeted embryonic or postnatal windows, providing ethical preclinical evidence from non-human mammals before human extrapolation.^[182] Bioengineered tooth organoids advanced in 2024-2025 by recapitulating these interactions in vitro, using stem cell-derived epithelial and mesenchymal aggregates within biomaterial scaffolds to form tooth-like structures with vascularized roots. Techniques involving bioorthogonal crosslinking hydrogels supported organoid maturation, yielding prototypes with odontoblastic differentiation and innervation potential, as validated in mouse implantation models.^[157] By 2025, progress in human dental pulp stem cell organoids enabled scalable production for drug screening, addressing root-cause regeneration over symptomatic prosthetics while highlighting scalability challenges in achieving full-size human teeth.^[150] This biologics-focused paradigm prioritizes causal restoration of odontogenic competence, informed by verifiable animal efficacy data.^[183]

Technological and Pharmacological Innovations

Cone beam computed tomography (CBCT) provides three-dimensional imaging for early detection of periodontal bone loss, a key precursor to tooth loss, outperforming traditional periapical radiographs in identifying and localizing alveolar defects.^[184] Integrated with artificial intelligence (AI), CBCT enables automated diagnosis of gingival bone defects via intraoral scans, replacing invasive probing and achieving high accuracy in tooth numbering and defect classification as demonstrated in studies from 2025.^[185]^[186] Machine learning models predict tooth loss risk by analyzing clinical datasets, including behavioral factors and radiographic data, with AI-based approaches showing performance comparable to or exceeding clinician predictions in specific risk categories.^[187]^[188] For instance, models trained on electronic dental records forecast periodontal disease progression, aiding preventive interventions.^[189] Pharmacological host-modulation therapies, such as subantimicrobial-dose doxycycline (typically 20 mg daily), inhibit matrix metalloproteinases in periodontitis without exerting strong antibacterial effects, leading to significant reductions in probing pocket depth when adjunctive to scaling and root planing.^[190] Clinical evaluations confirm its efficacy in modulating destructive host responses, with sustained benefits observed over nine months in randomized trials.^[191] Emerging trends as of 2025 incorporate nanotechnology for antimicrobial delivery in periodontal management, including copper nanoparticles that promote bone growth while targeting pathogens, reducing infection risks that contribute to tooth loss.^[192] Hybrid strategies combine nano-enabled agents with microenvironment modulation to enhance surgical outcomes and preserve periodontal tissues, leveraging smart-responsive nanomaterials to address dysbiosis and oxidative stress dynamically.^[193]^[194] These approaches show promise in vivo for biofilm control and localized therapy, though long-term clinical data remain limited.^[195]

Key Controversies

Fluoride Supplementation and Mass Medication Ethics

Fluoride added to public water supplies at concentrations of 0.7 mg/L has been linked to a 25% reduction in tooth decay among children and adults, based on longitudinal studies and meta-analyses evaluating lifelong exposure.^[196] This benefit arises primarily from frequent, low-dose contact that promotes enamel remineralization and inhibits bacterial acid production.^[197] However, controlled trials and systematic reviews demonstrate that topical fluoride applications—such as varnishes, toothpastes, and gels—provide the dominant cariostatic effect, with systemic delivery contributing minimally beyond post-eruptive mechanisms on existing teeth.^[198]^[199] Excessive fluoride exposure during tooth development poses risks, including dental fluorosis, characterized by enamel hypomineralization and white opacities, which becomes visually apparent at water concentrations above 1.5 mg/L.^[200] Such cosmetic defects affect aesthetics and may predispose enamel to further wear, with prevalence rising dose-dependently in children under 8 years.^[201] Empirical data from non-fluoridated regions further indicate that low systemic fluoride intake does not independently drive caries escalation when rigorous oral hygiene—removing plaque and limiting fermentable carbohydrate retention—prevents acid demineralization at the tooth surface.^[202] Community water fluoridation exemplifies mass medication, compelling systemic fluoride ingestion without individualized informed consent or dosage adjustment for age, health, or total exposure from sources like diet and dentifrice.^[203] Proponents cite public health utility, yet ethical analyses contend this contravenes medical principles by treating populations as uniform, ignoring variability in fluoride pharmacokinetics and potential for overexposure in high-intake subgroups.^[204] Courts in fluoridating nations have upheld the practice against mass medication claims, but dissenters highlight the absence of pre-market toxicity data for additives like hydrofluorosilicic acid and the infeasibility of universal opt-outs, framing it as an infringement on bodily autonomy.^[205]^[206] Emerging dietary evidence supports reducing reliance on systemic fluoride, as low-carbohydrate regimens diminish cariogenic biofilm formation and acidogenic potential by curtailing substrate for Streptococcus mutans and related pathogens.^[207] A 2023 review of ketogenic interventions noted decreased periodontal and cariogenic bacterial loads, suggesting such patterns could obviate broad supplementation needs in adherent populations.^[208] This aligns with causal mechanisms of caries—wherein enamel erosion stems fundamentally from microbial fermentation of sugars—positioning fluoride as an adjunct rather than a panacea, particularly amid critiques of institutionalized promotion overlooking lifestyle alternatives.^[209]

Personal Agency Versus Socioeconomic Determinism

Empirical studies indicate that personal behaviors, such as oral hygiene practices and tobacco use, exert a stronger influence on tooth loss than socioeconomic status (SES) alone, with modifiable lifestyle factors mediating much of the observed disparities. For instance, inadequate tooth brushing emerges as the predominant behavioral risk factor for poor oral health outcomes, surpassing sociodemographic variables in predictive power across diverse populations.^[210] Similarly, analyses controlling for education and income reveal that self-reported oral health perceptions and preventive behaviors independently correlate with reduced tooth loss, underscoring individual agency in outcomes.^[211] Tobacco smoking exemplifies how volitional habits override SES gradients, as smokers exhibit elevated tooth loss rates—such as having fewer than 19 remaining teeth in 37.3% of cases—regardless of income or educational attainment.^[212] This association persists independently, with smoking contributing substantially to the overall burden of edentulism even after adjusting for economic confounders.^[213] Cessation mitigates risk over 9–12 years, further evidencing causality rooted in personal choice rather than immutable socioeconomic constraints.^[214] From an evolutionary standpoint, the sharp rise in dental caries aligns with dietary shifts to processed sugars and starches post-agricultural revolution, maladaptive to ancestral dentition evolved for coarser foods. Modern processed diets exacerbate decay through persistent adhesion and fermentation, a pattern individuals can counteract via dietary restraint, challenging narratives that frame tooth loss as predominantly deterministic. While SES influences access to education on these levers, causal pathways prioritize hygiene and consumption habits, as evidenced in cohorts where behavioral interventions yield outcomes decoupled from baseline affluence.^[217] Deterministic interpretations, often amplified in public discourse to emphasize systemic inequities, understate self-control's role, yet data affirm that barriers like cost or availability do not preclude agency; for example, in universal coverage contexts, persistent gradients trace to uptake of services and adherence rather than provision alone.^[218] This causal realism posits individual modifiable factors—diet, cessation, brushing—as proximal drivers, enabling agency to transcend socioeconomic origins without denying structural hurdles.^[219]

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School dental-sealant programs could prevent most cavities, lower ...
Research shows dental sealants to shield the back teeth could prevent up to 80 percent of cavities in school-aged children.
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May 15, 2024 · School sealant programs provide pit and fissure dental sealants to children using portable equipment in a school setting.
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Policy on Use of Fluoride - AAPD
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Occlusal changes following posterior tooth loss in adults. Part 2 ...
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Evaluation of alveolar process resorption after tooth extraction using ...
The alveolar ridge width can reduce by up to 50% in the first year after tooth loss, with two-thirds of this reduction occurring within the first three months.
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A retrospective cohort study of how alveolar ridge preservation ...
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Stage IV periodontitis is associated with an increased risk of tooth loss. Teeth with PPD ≥5 mm at the end of APT are at risk of periodontitis progression ...
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Periodontal disease appears to be associated with a 19% increase in risk of future cardiovascular disease. This increase in RR is more prominent (44%) in ...
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Periodontal diseases and cardiovascular events: meta-analysis of ...
The risk of developing cardiovascular disease was found to be significantly (34%) higher in subjects with periodontal disease compared to those without ...
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May 27, 2022 · Periodontitis Grade B/C was associated with higher cardiovascular risk than no periodontitis/Grade A (odds ratio [OR], 2.13; 95% confidence ...
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Our analysis found no evidence of a causal association between periodontitis and infective endocarditis, with odds ratios (ORs) of 0.992 (95% CI: ...
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Tooth loss, especially loss of occlusal pairs, can inevitably cause decreased masticatory function which in turn affects food intake and nutritional status (13) ...
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Feb 25, 2025 · This study aims to examine the relationship between tooth loss trajectories and all-cause mortality in Chinese adults aged 65 years and older.
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Tooth loss and mortality risk: the mediating role of hs-CRP in a ... - NIH
Apr 24, 2025 · Complete tooth loss is associated with higher mortality in the Chinese population, with systemic inflammation (hs-CRP) as a mediator.
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Tooth loss progression and mortality among older adults
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Sep 4, 2023 · Individuals with less than 20 teeth in the mouth could had higher odds of incident depression at 2- and 4-years follow-up, with differences between men and ...
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Association Between Mental Health and Oral Health Status ... - NIH
Greater risk for dental decay and tooth loss can lead to more frequent pain experience, social isolation, and low self-esteem, and reducing quality of life and ...
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Jan 4, 2022 · This study examines the association of tooth loss with self-rated health and psychological and subjective wellbeing among older adults in India.
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15-Year Retrospective Study on the Success Rate of Maxillary Sinus ...
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Long-term survival rate of implants placed in conjunction with 246 ...
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The pairwise meta-analysis showed implants placed in smokers had a higher risk of failure than implants placed in non-smokers, with an OR 2.402 (95% CI, 2.176, ...
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Anti-USAG-1 therapy for tooth regeneration through enhanced BMP ...
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Development of a new antibody drug to treat congenital tooth agenesis
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History of Dentistry - Flintlock Dental
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Dental Caries Prevalence as Evidence for Agriculture and ... - PubMed
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The Ancient Egypt and The Need for Dental Care
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May 21, 2015 · Teeth found in a floor drain in the Roman Forum suggest some ancient dentists had developed sophisticated extraction techniques.
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Dental caries as indicators of agricultural practices in the foothills of ...
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Sep 18, 2020 · Although not universally accepted for many years, the idea of antisepsis was taken up and reported on in 1876 by a London dentist, Ashley ...
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Why American Communities Began Adding Fluoride to Water
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[PDF] National Supervised Toothbrushing Program and Dental Decay in ...
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Current issues in periodontal research methodology - LWW
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Anti–USAG-1 therapy for tooth regeneration through enhanced BMP ...
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Organoids in the oral and maxillofacial region: present and future
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Periodontal therapeutics: Current host‐modulation agents and future ...
The most profound clinical outcome of subantimicrobial‐dose doxycycline therapy compared with placebo was a significant reduction of pocket depth, a benefit ...
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Jan 28, 2025 · Copper nanoparticles can promote bone growth to treat periodontal disease. A research group developed a novel chitosan-modified copper sulfide ...
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In the field of dentistry, nanotechnology has triggered a transformative shift, reshaping our understanding of oral health and revolutionizing the diagnosis and ...
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Biofilms and oral health: nanotechnology for biofilm control
Jul 16, 2025 · Recent advances in nanotechnology have demonstrated nanoparticles as a promising therapeutic alternative for controlling dental biofilms. In ...
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Community Water Fluoridation is Effective at Preventing Cavities
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An overview of oral health status, socio-economic and behavioral ...
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Globally, dental diseases disproportionately afflict low-income populations. Oral diseases can reduce employment opportunities and limit upward social mobility ...
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Oct 3, 2024 · We demonstrated that SEP is significantly associated with dental treatment seeking, oral health behaviors, and mental health.