2.1 Cariology & Caries Diagnosis
Key Takeaways
- Dental caries is a dynamic, biofilm-mediated disease driven by frequent fermentable carbohydrate exposure, not simply a structural defect in a tooth
- ICDAS codes 0-6 stage lesion severity; ICCMS merges these into Initial (codes 1-2), Moderate (3-4), and Extensive (5-6) categories for management
- Lesion activity (active vs inactive/arthrested) is assessed independently of severity and directly drives the decision between non-operative and operative care
- Bitewing radiographs only detect interproximal caries once demineralisation reaches the inner enamel or the enamel-dentine junction; early enamel lesions are radiographically invisible
- Reversible pulpitis produces brief pain triggered by thermal stimuli that resolves on stimulus removal; irreversible pulpitis produces lingering (>10 seconds) or spontaneous pain
The Caries Process: Aetiology
Dental caries is a localised, dynamic disease of the hard tissues of the teeth caused by acidogenic dissolution of enamel and dentine. The classical acidogenic theory (Miller, 1890) holds that cariogenic bacteria within the dental biofilm metabolise fermentable carbohydrates, producing organic acids (principally lactic acid) that lower the plaque pH below the critical threshold of approximately pH 5.5 for enamel, driving hydroxyapatite dissolution.
Key Microorganisms
The biofilm is polymicrobial, but certain species are strongly associated with caries initiation and progression:
| Species | Role |
|---|---|
| Streptococcus mutans | Primary caries initiator; highly acidogenic and aciduric; adheres to enamel via glucan production |
| Streptococcus sobrinus | Co-associated with S. mutans, particularly in smooth-surface caries |
| Lactobacillus species | Predominate in advanced dentine caries; tolerant of low pH |
| Actinomyces species | Associated with root surface caries |
The Caries Balance
Caries is best understood as a demineralisation-remineralisation equilibrium. Each acid challenge demineralises tooth structure; periods of resting pH allow remineralisation by calcium, phosphate, and fluoride from saliva. Disease occurs when the frequency of acid challenges overwhelms the repair capacity of the oral environment.
- Pathological factors: cariogenic biofilm, frequent sugar intake, reduced saliva flow, low fluoride exposure
- Protective factors: adequate saliva, fluoride (toothpaste, water, varnish), calcium and phosphate reservoirs, sensible dietary frequency
Lesion Activity vs Severity
A critical concept for the MFDS candidate: activity and severity are independent dimensions. A small white spot can be actively progressing, while a large cavitated lesion can be arrested and hard. The ICCMS framework explicitly separates these:
- Active lesions: surface is opaque, whitish/yellowish, rough to probe, in a plaque-stagnation area; dentine feels soft or leathery
- Inactive (arrested) lesions: surface may be whitish/brownish/black, shiny, hard and smooth to probe; dentine is shiny and hard
ICDAS and ICCMS Classification
The International Caries Detection and Assessment System (ICDAS) uses a 0-6 visual scale:
| ICDAS Code | Clinical Finding |
|---|---|
| 0 | Sound surface, no evidence of caries |
| 1 | First visual change in enamel (opacity visible only after prolonged air-drying, ~5 seconds) |
| 2 | Distinct visual change in enamel (white spot or brown discolouration visible when wet) |
| 3 | Localised enamel breakdown with no visible dentine |
| 4 | Underlying dark shadow from dentine (grey/blue/brown shadow beneath intact enamel) |
| 5 | Distinct cavity with visible dentine |
| 6 | Extensive distinct cavity with visible dentine |
The International Caries Classification and Management System (ICCMS) merges these into three management-oriented stages:
| ICCMS Stage | ICDAS Codes | Typical Management |
|---|---|---|
| Initial | 1-2 | Non-operative care (fluoride, sealants, diet modification) |
| Moderate | 3-4 | Tooth-preserving operative care if cavitated; otherwise non-operative |
| Extensive | 5-6 | Tooth-preserving operative care |
Radiographic Detection
Bitewing radiographs are the standard projection for detecting interproximal caries, but they significantly underestimate lesion depth compared to histological extent. A radiolucency is only visible once approximately 40-50% demineralisation of enamel has occurred.
ICCMS Radiographic Scoring (Posterior Teeth)
| Radiographic Score | Finding |
|---|---|
| R0 | No radiolucency |
| RA1 | Radiolucency in outer half of enamel |
| RA2 | Radiolucency in inner half of enamel (may reach EDJ) |
| RA3 | Radiolucency limited to outer third of dentine |
| RB4 | Radiolucency reaching middle third of dentine |
| RC5 | Radiolucency in inner third of dentine |
| RC6 | Radiolucency extending to the pulp |
Clinical implication: A radiolucency confined to enamel on a bitewing is likely already into dentine histologically. The enamel-dentine junction (EDJ) is the critical radiographic threshold; once a radiolucency crosses into dentine, operative intervention is generally indicated.
EPR (Extended Parallel Radiography)
In high-caries-risk patients, horizontal bitewings may be supplemented by vertical bitewings or a full-mouth series to detect recurrent and root caries, particularly in adults with gingival recession.
Secondary and Root Caries
Secondary (recurrent) caries occurs at the margins of existing restorations. Detection requires careful visual inspection of margins (especially interproximal) and gentle probing. Radiographic detection is limited by the radiopacity of restorative materials.
Root caries affects exposed cementum and dentine following gingival recession. It is softer, progresses more rapidly than coronal caries, and is often lesion-active in older adults or patients with xerostomia. ICDAS root caries codes are separate from the coronal 0-6 scale.
Caries Risk Assessment
Structured caries risk assessment tools (e.g., CAMBRA, Cariogram) synthesise clinical, dietary, social, and microbiological factors into a risk stratification (low/moderate/high). The strongest single predictor of future caries is past caries experience.
| Factor | Increases Risk |
|---|---|
| Previous new lesions in last 3 years | Yes |
| High S. mutans / Lactobacillus counts | Yes |
| Frequent between-meal sugar consumption | Yes |
| Xerostomia (medication, Sjogren's, head and neck radiotherapy) | Yes |
| Socioeconomic deprivation | Yes |
| Adequate saliva flow and fluoride exposure | Decreases risk |
Distinguishing Reversible from Irreversible Pulpitis
Sensibility testing (thermal and electric pulp testing) is the clinical gateway to pulpal diagnosis:
| Feature | Reversible Pulpitis | Irreversible Pulpitis |
|---|---|---|
| Pain character | Brief, sharp, evoked | Lingering, dull, throbbing or spontaneous |
| Duration | Seconds; resolves on stimulus removal | >10 seconds after stimulus removal; may be spontaneous |
| Response to cold | Hypersensitive but settles | Lingering pain or exaggerated response |
| Percussion | Usually normal | May be normal or tender |
| Management | Remove irritant (caries, leaking restoration); restore | Endodontic treatment or extraction required |
Key MFDS point: A tooth that hurts spontaneously (without any stimulus) or that shows prolonged pain after a cold stimulus is removed is by definition in irreversible pulpitis and will not recover with simple restorative management alone.
A 28-year-old patient presents with a first permanent molar that gives a brief, sharp pain when exposed to cold water that resolves within 2 seconds of removing the stimulus. The tooth is not tender to percussion. What is the most likely pulpal diagnosis?
On a bitewing radiograph, an interproximal radiolucency is seen extending to the outer third of dentine but not reaching the middle third. Using the ICCMS radiographic scoring system, what is the correct radiographic code, and what is the likely histological extent compared to the radiographic appearance?
Which of the following clinical findings best indicates that an ICDAS code 2 white spot lesion on the buccal of an upper lateral incisor is ACTIVE rather than arrested?