Abstract. Root caries is a distinct clinical entity arising on cementum and root dentin exposed by gingival recession, and its burden is increasing as more adults retain natural dentition into later life. A pooled meta-analysis of 74 studies estimated global root caries prevalence in middle-aged and older adults at approximately 41.5%. Root surfaces demineralize at a higher critical pH than enamel, progress circumferentially rather than axially, and are frequently subgingival or juxtagingival, which complicates both detection and restoration. Because attachment loss is a prerequisite, root caries sits at the intersection of periodontology and cariology; a 2023 systematic review and meta-analysis reported approximately 38% greater odds of root caries among individuals with periodontal disease. Contemporary management prioritizes non-operative arrest. Randomized controlled trials support 5,000 ppm fluoride dentifrice for prevention and arrest of root lesions, and annual application of 38% silver diamine fluoride for arresting active lesions in community-dwelling elders. This review summarizes current evidence on epidemiology, etiology, diagnosis, and management, with attention to the practical implications for general practice.
Epidemiology
Root caries prevalence has risen in parallel with improvements in tooth retention. Populations that once became edentulous in the sixth or seventh decade now present with substantial numbers of retained teeth, longer periodontal attachment loss histories, and correspondingly more exposed root surface at risk.
Pentapati and colleagues pooled 74 publications in a systematic review and meta-analysis and reported a global root caries prevalence of 41.5% (95% CI 36.9–46.1) among middle-aged and older adults, with wide between-study heterogeneity attributable to differences in case definition, examiner calibration, setting, and population age structure [1]. Reported prevalence in community-dwelling cohorts spans a broad range across countries, and institutionalized populations consistently demonstrate higher disease burden than community-dwelling counterparts.
Because exposure of the root surface is a necessary precondition, the epidemiology of gingival recession bounds the epidemiology of root caries. Kassab and Cohen, reviewing survey data, reported that approximately 88% of adults aged 65 years and older and 50% of adults aged 18–64 years exhibit one or more sites of recession [6]. The at-risk surface population is therefore very large, and the relevant clinical question in older patients is generally not whether root surfaces are exposed but how many, and under what cariogenic conditions.
Etiology and Pathogenesis
Root caries is a biofilm-mediated, diet-modulated demineralization process, but several substrate properties distinguish it from coronal caries.
- Higher critical pH. Cementum and root dentin begin to demineralize at approximately pH 6.2–6.7, compared with roughly pH 5.5 for enamel. Acid challenges insufficient to damage enamel are therefore cariogenic at the root.
- Higher organic content. Root dentin contains a substantially greater proportion of organic matrix than enamel. Lesion progression involves both mineral dissolution and proteolytic degradation of collagen, with host matrix metalloproteinases and cysteine cathepsins implicated in matrix breakdown.
- Lesion geometry. Root lesions characteristically spread laterally along the cementoenamel junction and around the root circumference rather than penetrating axially, producing shallow, saucer-shaped defects that may be extensive before pulpal involvement occurs.
- Proximity to the pulp. The reduced dentin thickness at the cervical region means comparatively shallow lesions can approach the pulp, particularly on narrow interproximal root surfaces.
The associated microbiota is polymicrobial. Streptococcus mutans and Lactobacillus species are recovered from root lesions, but Actinomyces species and a broader acidogenic and aciduric consortium are also consistently implicated, and root caries is best conceptualized ecologically rather than as a single-pathogen disease.
Salivary hypofunction is among the most important modifiers. Polypharmacy is near-universal in older cohorts, and xerostomia-inducing agents — anticholinergics, antihypertensives, antidepressants, diuretics, antihistamines — reduce buffering capacity, clearance, and remineralization potential. Head and neck radiotherapy and Sjögren syndrome produce the most severe presentations, with rapidly progressive circumferential cervical lesions.
The Periodontal–Cariologic Interface
Gavriilidou and Belibasakis have argued that root caries should be understood as a cross-boundary periodontal–cariological condition rather than as a variant of coronal caries [2]. Periodontal attachment loss creates the substrate; periodontal therapy, by resolving inflammation and inducing tissue shrinkage, frequently increases the extent of exposed root surface; and the plaque-retentive anatomy of treated root surfaces, furcations, and restorative margins sustains the biofilm challenge.
The epidemiologic association has been formally examined. Nazário and colleagues conducted a systematic review and meta-analysis of observational studies and found that individuals with periodontal disease had approximately 38% greater odds of presenting with root caries [3]. The authors graded the certainty of evidence as low, which is expected given the observational designs, and residual confounding by age, smoking, socioeconomic position, and oral hygiene behavior cannot be excluded. The finding is nonetheless clinically coherent and argues for integrating caries risk assessment into periodontal maintenance rather than treating the two disciplines as parallel tracks.
Diagnosis and Risk Assessment
Detection depends primarily on careful visual–tactile examination of dried, isolated root surfaces, since buccal and lingual root lesions are poorly represented on bitewing radiography and interproximal lesions may be obscured by the adjacent contact.
The clinically decisive judgment is lesion activity, not lesion presence. Active lesions are typically yellowish or light brown, soft or leathery to gentle probing with a blunt explorer, and plaque-covered. Arrested lesions are dark brown to black, hard, and often glossy — a discolored but hard root surface generally represents successfully controlled disease and should not be restored on esthetic grounds alone. Excessive probing force on a demineralized surface can cavitate a lesion that would otherwise have remineralized, and a blunt probe used with light pressure is preferred to a sharp explorer.
Risk assessment should be explicit and should capture the factors with the strongest predictive weight:
- Number of exposed root surfaces and history of periodontal therapy
- Past root caries experience — the single strongest predictor of future lesions
- Objective and subjective salivary status, and a full medication reconciliation
- Removable partial denture wear, which is repeatedly identified as a risk indicator through plaque retention against abutment roots
- Fermentable carbohydrate intake frequency, with particular attention to sipping and grazing behaviors
- Manual dexterity, cognitive status, visual acuity, and the availability of caregiver assistance
- Fluoride exposure, including water source and current dentifrice concentration
Management
Contemporary management is non-operative wherever the lesion is accessible to plaque control and not frankly cavitated. Restoration of a root lesion in a high-risk mouth without modifying the underlying risk profile predictably produces recurrent marginal disease.
High-fluoride dentifrice
Ekstrand and colleagues randomized elderly nursing home residents with existing root lesions to 5,000 ppm versus 1,450 ppm fluoride dentifrice and reported superior lesion control in the high-concentration arm [4]. Subsequent randomized work in independently living older adults has supported both preventive and arresting effects of 5,000 ppm F dentifrice. Twice-daily use with a spit-don’t-rinse protocol is the standard instruction; adherence is the principal limiting factor, and dependency status materially affects delivery.
Silver diamine fluoride
Li and colleagues randomized community-dwelling elders with active root lesions and found that application of 38% silver diamine fluoride arrested significantly more lesions than placebo, with annual application effective and treated lesions becoming dark [5]. The staining is the principal patient-facing limitation and requires informed consent, but in posterior and non-display surfaces, in patients with limited access to operative care, and in care-dependent populations, the risk–benefit balance is frequently favorable. Potassium iodide has been investigated as a means of mitigating discoloration, with variable results.
Adjunctive and operative measures
Professionally applied 5% sodium fluoride varnish at recall, chlorhexidine varnish, and salivary substitutes or sialogogues in appropriate candidates have supporting evidence of varying strength. Recall intervals should be risk-stratified rather than uniform. Where operative intervention is indicated — cavitation, pulpal proximity, inability to clean the lesion, or unacceptable esthetics — glass ionomer and resin-modified glass ionomer materials are commonly selected for subgingival and moisture-challenged margins on the basis of chemical adhesion to dentin and fluoride release, though comparative evidence on restorative material longevity in root lesions remains limited and heterogeneous.
Clinical Implications
Three practical points follow from the evidence. First, root surface examination should be a discrete, deliberate step in the periodontal maintenance appointment, not an incidental finding. Second, the primary therapeutic goal for a non-cavitated active lesion is arrest, and the tools that achieve it — high-concentration fluoride and silver diamine fluoride — are inexpensive and low-morbidity. Third, medication review and salivary assessment are not optional adjuncts in this population; in many older patients the dominant driver of root caries risk is pharmacologic rather than behavioral.
For a plain-language summary of this material written for patients, see our companion article, Root Cavities: Why Receding Gums Change Your Cavity Risk After 50. Related reviews on this site include our discussions of xerostomia and salivary gland hypofunction and mechanical plaque control.
References
- Pentapati KC, Siddiq H, Yeturu SK. Global and regional estimates of the prevalence of root caries — systematic review and meta-analysis. Saudi Dental Journal. 2019;31(1):3–15.
- Gavriilidou NN, Belibasakis GN. Root caries: the intersection between periodontal disease and dental caries in the course of ageing. British Dental Journal. 2019;227(12):1063–1067.
- Nazário RMF, Frazão DR, Peinado BRR, et al. Is there an association between periodontal disease and root caries? A systematic review and meta-analysis. PLOS ONE. 2023;18(11):e0285955.
- Ekstrand KR, Poulsen JE, Hede B, et al. A randomized clinical trial of the anti-caries efficacy of 5,000 compared to 1,450 ppm fluoridated toothpaste on root caries lesions in elderly disabled nursing home residents. Caries Research. 2013;47(5):391–398.
- Li R, Lo ECM, Liu BY, Wong MCM, Chu CH. Randomized clinical trial on arresting dental root caries through silver diammine fluoride applications in community-dwelling elders. Journal of Dentistry. 2016;51:15–20.
- Kassab MM, Cohen RE. The etiology and prevalence of gingival recession. Journal of the American Dental Association. 2003;134(2):220–225.
This article is provided by Fridman Family Dental Care in Valencia, CA for general educational purposes. It summarizes published research and is not a substitute for individualized clinical judgment, diagnosis, or treatment. Patients with questions about their own oral health should consult a licensed dental professional. Call (661) 254-3700 or request an appointment online.
