Preclinics of Conservative Dental Medicine · MU Sofia

32. Tooth caries – etiology and pathogenesis; examination methods.

Covers the causes and development of tooth caries, starting with the definition as a biofilm-mediated, sugar-driven loss of mineral and the Keyes triad with time. It then explains the roles of saliva, fluoride, sugar frequency and bacteria, including the ecological plaque hypothesis. Pathogenesis follows through the Stephan curve and critical pH, the four zones of the white-spot lesion and spread into dentin. Examination methods come last, with a table of ICDAS codes 0 to 6, plus bitewing radiographs, transillumination, laser fluorescence and caries risk assessment.

Inside: 5 sections · 1 labelled picture · 1 table · 17 flashcards · 7 min

Topic 32 of 53 in the MU Sofia syllabus for Preclinics of Conservative Dental Medicine (Dental Medicine, Year 3). The free AceMed note covers it in 5 sections, about 929 words (7 min of reading), with 17 flashcards.

In this note

  1. Introduction
  2. Definition and etiology
  3. Pathogenesis
  4. Examination methods
  5. Key points

Introduction

Dental caries (Latin caries, “decay”) is the commonest disease of the dental hard tissues. This note covers its causes, how a lesion develops and how it is detected and graded – the basis of prevention and treatment.

Definition and etiology

Caries is a biofilm-mediated, sugar-driven, multifactorial, dynamic disease that results in net mineral loss from the dental hard tissues. Periods of demineralisation (acid dissolves apatite) alternate with remineralisation (salivary calcium and phosphate redeposit). A carious lesion appears when loss outweighs repair for long enough.

Keyes triad and time

Keyes described three essential, overlapping factors; Newbrun added time (Figure 1B):

  • host – the teeth (deep fissures, crowding, enamel quality) and saliva;
  • microflora – dental plaque, a biofilm;
  • substrate – fermentable carbohydrates, sucrose above all;
  • time – how long and how often the three act together.

Modifying factors tip the balance:

  • Saliva – flow, bicarbonate buffering, sugar clearance, calcium and phosphate supply. Hyposalivation (head-and-neck radiotherapy, Sjögren syndrome, many drugs) leads to rampant caries.
  • Fluoride – slows demineralisation, speeds remineralisation and makes the new mineral more acid-resistant (fluorapatite, critical pH about 4.5).
  • Frequency of sugar intake – matters more than the total amount: every intake starts a new acid attack.
  • Oral hygiene and socioeconomic status (education, diet, access to care).

Bacteria

  • Mutans streptococci (Streptococcus mutans, S. sobrinus) initiate lesions: they are acidogenic (ferment sugar to lactic acid), aciduric (survive low pH) and make sticky extracellular glucans from sucrose that bind plaque to the tooth.
  • Lactobacilli drive progression, not initiation: they thrive in cavities and dentin; high counts reflect high sugar intake.
  • Actinomyces species are linked to root caries.

Ecological plaque hypothesis (Marsh): caries is not a specific infection but the result of a shift in the resident plaque flora caused by frequent low pH. Acid-tolerant species take over and lower the pH further, so prevention targets the environment – sugar frequency, plaque, fluoride – not one bacterium.

Continue reading free

The whole note, all 5 sections, is free with an AceMed account, with its 17 flashcards. Premium adds flashcard recall, highlights and Ask AI.

Start freeAlready a member? Open the note