Dental Caries - PDF

Dental Caries Prof. Avijit Banerjee Professor of Cariology & Operative Dentistry / Hon Consultant / Clinical Lead, Restorative Dentistry Assoc Director of Education (Undergraduate) Head, Conservative & MI Dentistry, St Paul’s ICC King’s College London Dental Institute...

Dental Caries Prof. Avijit Banerjee Professor of Cariology & Operative Dentistry / Hon Consultant / Clinical Lead, Restorative Dentistry Assoc Director of Education (Undergraduate) Head, Conservative & MI Dentistry, St Paul’s ICC King’s College London Dental Institute @ Guy’s Hospital.  Caries What is it ? – Causes, what, when, where, why, how….? What do we do ? – Detection, diagnosis, treatment rationale, excavation techniques…………  Why caries management is important in modern dentistry? The disease is still prevalent in the UK Pts are prioritising aesthetics, but implants / porcelain are not always indicated….. Aesthetic restorations are an essential part of the rehabilitation of medium / high caries risk pts – motivation………… Manufacturers producing high quality direct, adhesive aesthetic materials / cements  What is “M.I.” Dentistry ? The concept of “Minimum Intervention Dentistry” involves the holistic approach to individualised patient care, where disease management involves all members of the dental team and the patient, using developments in caries detection R&D, tailored prevention / control regimes and treatments to maintain long- term oral health… “Minimally Invasive Dentistry” accepts that active lesions can be “sealed & healed”, with residual caries-affected dentine retained with a peripheral adhesive seal. The surgical excisional, mechanistic approach to caries removal, dictated by the restorative material, is no longer recommended. Oral physician’s biological approach vs. Oral surgeon’s mechanistic approach… Anusavice, 1988; Featherstone, 2000; Mount & Hume, 2000; Tyas et al, 2000; White et al., 2000; Mickenautsch, 2005; Dennison et al., 2005; Moncada et al., 2008; Banerjee & Watson 2011; Banerjee, 2011…  Dental caries “A reversible disease process of dental hard tissues, instigated by action of bacteria upon fermentable carbohydrates in the plaque biofilm at tooth surfaces, leading to acid demineralisation and ultimately proteolytic destruction of the organic component of dental tissues.”  Definition Caries - Latin for “decay”. Progressive disease initiated at the tooth surface, that is reversible up to a point. Results in softening and ultimate destruction of tooth substance.  Definition Caries – Carious process – the histopathological metabolic interactions occurring in the plaque biofilm causing disease. – Carious lesion – The signs of the disease on dental hard tissues, i.e. early lesions / discolouration / opacities, cavities etc. Causative factors – acidogenic theory Bacteria – Strep Tooth Mutans surface CARIES carbohydrate time  Plaque, carbohydrate, time ⇒ low pH Sound Carious enamel enamel high pH ⇐ saliva, oral hygiene, diet, fluoride  Stephan curve – acid attack pH Normal pH 7.0 Critical pH 6.2 (dentine) 5.5 Critical pH (enamel) 0 10 20 30 40 50 60 mins  Caries Diagnostic Regime Remove calculus, plaque & stains Scaling - SONICflex Polishing - PROPHYflex 2 Drying the tooth 3/1 syringe Early clinical detection Inspecting the tooth surface Diagnosis Consider treatment plan options Observation & monitoring Preventative measures Invasive preparation Recall & re-diagnose Monitor success Control of residual caries  Visual Detection “Sharp” eyes ± magnification Good illumination Clean, dryable tooth surface Dental explorer (blunt) Time Detection Methods for Incipient Enamel Lesions……………….  OPTICAL / FLUORESCENCE LIGHT MINERAL TISSUE SCATTERING DENSITY POROSITY Modified ICDAS QLF ECM classification Radiography Dye-enhanced AC Impedance FOTI RVG laser IN – UV illumination fluorescence DELF Computer (DELF). VIVO Quantitative laser Tomography Dye penetration fluorescence (QLF) (CT) scans UV illumination (iodide) DiagnoDent DiagnoDent? Ultrasound ? SEM Polarised, Quantitative Confocal, PTLM transmitted light BSE-SEM laser-scanning microscopy (PTLM) Microradiography fluorescence Acoustic microscopy microscopy Microfocal CT IN - Spectroscopy VITRO X-ray Reflected light microtomography confocal microscopy X-ray microanalysis  Caries Diagnosis Caries history / risk assessment Signs - detection Symptoms, i.e. pain history Special investigations – vitality tests – radiographs Evaluation of caries risk Factors contributing to increased risk: – Medical: drug therapy, sucrose-based medication – Social: stress, lifestyle change – Dietary: prolonged breast feeding, “grazing” – Host resistance: previous caries experience, lesions on certain tooth surfaces, soft, light coloured lesions – Salivary: low secretion and buffering – Microbiology: high numbers S. mutans and lactobacilli  Caries management strategies At the population level…….. – Efficiency At the individual level: – Efficacy (more relevant for these pts) – Prevent new disease – Operatively manage existing lesions Caries risk / activity categories Caries inactive / controlled (LOW) – 0-1 active lesion / no history of recent restorations Caries active / modifiable risk factors (MEDIUM) – >1 active lesions – ≥2 new / prog / filled lesions in last 2-3 yrs Caries active / unmodifiable or unidentifiable risk factors (HIGH) – >1 active lesions – ≥2 new / prog / filled lesions in last 2-3 yrs Control of caries risk / activity Caries inactive / controlled (LOW) – OH, F- Caries active / modifiable risk factors (MEDIUM) – OH, supplementary F- m/w, gels. – Dietary modification Caries active / unmodifiable or unidentifiable risk factors (HIGH) – Control at individual pt level. – As medium plus salivary flow stimulation, CHX Bitewing Radiography  Development of the incipient enamel lesion  Effects on tissues - biochemical Enamel – Mature: >95 % mineral (CO3, Mg- substituted hydroxyapatite), 5 secs). No enamel demineralisation or a narrow surface zone of opacity (edge phenomenon). Opacity or discolouration hardly visible on a wet surface, but 1 distinctly visible after air drying. Enamel demineralisation limited to the outer 50% of the enamel layer. Opacity or discolouration distinctly visible without air drying. No 2 clinical cavitation detectable. Demineralisation involving between 50% of the enamel and the outer third of dentine. Localised enamel breakdown in opaque or discoloured enamel 3 +/- greyish discolouration from underlying dentine. Demineralisation involving the middle third of dentine. Cavitation in opaque or discoloured enamel exposing the 4 underlying dentine. Demineralisation involving the inner third of dentine.  Identify: Examination - radiography Enamel lesions mICDAS E1 Outer half of enamel 0, 1 E2 Inner half of enamel 1,2 Dentine lesions mICDAS D1 Outer third of dentine 2 D2 Middle third of dentine 3 D3 Inner third of dentine 4 11 months later…… Tyas et al., 2000  Evidence shows that surface plaque stagnation is one critical indicator for potential lesion activity.  Enamel EDJ Sound dentine 1 2 3 4 Pulp 5 6 MI caries treatment rationale... Outer Inner Sound Caries-infected Caries-affected inner dentine dentine dentine Future T Current Treatment.... Treatment R A N Zone of high S bacterial load I T I Translucent O zone N Grossly infected; Less infected; unremineralisable remineralisable Non-vital Vital Ogawa et al. (1983) taken from Thylstrup, Fejerskov (1994) Textbook of Clinical Cariology, Munksgaard  Features of D1 & D2 Histology D1 early subsurface demineralisation D3 D2 early porosity ? bacterial penetration ? tertiary dentine Clinical signs white spot lesion, frosty chalky, roughened surface arrested brown spot lesion A schematic depicting D1, D2 Symptoms and a non-cavitated (closed) minimal D3 carious lesion. slight sensitivity to H/C/S if at EDJ Treatment Monitor OHI, fluoride, diet ? Fissure seal / PRR  Features of a D3 lesion Histology D1 enamel demineralisation increased porosity D3 D2 bacterial penetration organic / inorganic dentine / tubular destruction translucent dentine tertiary dentine Signs A schematic depicting the cavitated (open) / non-cavitated tertiary dentine laid down by (closed) the dentine-pulp complex as a defence reaction to the discolouration / opacities advancing D3 lesion. Symptoms ? Acute, reversible pulpitis Treatment Monitor / OHI / F / diet minimal cavity prep sealed restoration  Features of a D4 lesion Histology D1 gross demineralisation / bacterial penetration D4 D2 tubular destruction with pulp exposure Signs cavitation gross discolouration visible necrotic pulp ? A schematic depicting the progress Symptoms of the D3 lesion into a cavitated chronic, irreversible pulpitis D4 lesion involving the pulp. loss of function Treatment pulp capping sealed, layered, complex restorations pulp extirpation & RCT