Dental caries – Etiopathogenesis, progression dynamics, and contemporary treatment and prevention strategies

Dental caries is a multifactorial bacterial infectious disease affecting the calcified tissues of the teeth. It arises from the dynamic demineralization of dental enamel and dentin induced by organic acids produced by microbial biofilm during carbohydrate fermentation. Recognized by the World Health Organization (WHO) as a pervasive global public health challenge, dental caries impacts nearly 100% of adults and over 50% of school-aged children globally. Untreated carious lesions result not only in localized pain and eventual tooth loss, but also pose severe risks of systemic focal infections, potentially impacting cardiovascular, renal, and musculoskeletal systems.

The primary driver of cariogenesis is a state of dysbiosis within the oral microbiome. The cariogenic biofilm is predominantly colonized by acidogenic and aciduric bacterial species, chief among them Streptococcus mutans, Streptococcus sobrinus, and Lactobacillus spp. These pathogens synthesize insoluble extracellular glucans from dietary sucrose, facilitating strong adherence to the enamel pellicle. The indispensable substrate for this process is fermentable carbohydrates—most notably refined sucrose, glucose, and fructose. Following carbohydrate intake, rapid bacterial fermentation triggers a steep drop in plaque pH along the Stephan curve below the critical threshold of 5.5, initiating the dissolution of hydroxyapatite crystals.

The carious process unfolds in well-defined clinical phases and remains entirely asymptomatic in its earliest stage. The initial diagnostic manifestation is subsurface enamel demineralization, presenting clinically as a chalky white spot lesion. At this point, the outer anatomical surface remains intact, rendering the pathology completely reversible. If the acid challenge persists without remineralizing therapy, the structural integrity of the enamel collapses, yielding an irreversible cavitation. Once bacterial penetration breaches the dentino-enamel junction into dentinal tubules, hypersensitivity to thermal, osmotic, and sweet stimuli ensues. Continued untreated invasion triggers irreversible pulpitis, severe spontaneous odontogenic pain, and tissue necrosis requiring endodontic therapy.

Modern dentistry prioritizes minimally invasive management, biological remineralization, and rigorous preventive protocols. In early incipient lesions, clinical therapy centers on remineralization using concentrated fluoride vehicles (dentifrices with 1,450–5,000 ppm F, professional varnishes), which convert susceptible hydroxyapatite into acid-resistant fluorapatite. Adjunctive therapies such as casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) and non-fermentable polyols like xylitol actively impair Streptococcus mutans proliferation and biofilm metabolism. When structural cavitation occurs, modern biomimetic composites and glass ionomer restorations are employed. Uncompromising daily plaque control (twice-daily brushing, interdental flossing) combined with dietary restriction of fermentable snacking frequency forms the non-negotiable cornerstone of lifelong caries prevention.