DENTAL CARIES REQUIRE:
-susceptible host
-bacteria
-food source (substrate)
-time
SPECIFIC vs. NON-SPECIFFIC PLAQUE HYPOTHESIS
Non-specific hypothesis
-all plaques are similar
-goal of treatment is removal of all plaque
-failure is the patient's fault-did not keep the plaque off
Specific plaque hypothesis
-the qualitative difference between plaques, i.e. the specific bacterial composition of the plaque, and the specific intraoral site that the plaque colonizes, determines which disease, if any, plaque will cause
Cariogenic bacteria
Strep mutans (SM) - the all around bad guy; virulence factors; aciduric (lives in an acidic
environment), produces insoluble glucans, homofermenter
Lactobacilli - the secondary invader of initiated lesions
Actinomycosis - associated with cemental caries
Clinical methods used in caries diagnosis
Visual
Tactile
Radiography
Transillumination
Cariescreen M
bacteriological screening test using a selective media for the estimation of salivary SM CFU's
Caries detectors Br Dent J 174: 245-248, 1993
-201 cavities were prepared under rubber dam. When caries removal was considered complete using
the conventional tactile and optical criteria, a caries detector dye (1% acid red in propylene glycol), which is claimed to stain 'infected' tissue red, was applied. Fifty-two per cent of cavities showed caries dye stain in some part of the DEJ. Subsequent microbiological sampling of dye-stained and dye-unstained sites resulted in the recovery of low numbers of bacteria and revealed no difference in the level of infection of the two sites. It was concluded that the conventional tactile and optical criteria are satisfactory assessments of the caries status of tissue during cavity preparation and that subsequent use of a caries detector dye on hard and stain-free dentin will result in unnecessary tissue removal.
Types of caries detectors
-0.5% basic fuchsin in propylene glycol "sleuth"
-1.0% acid red 52 in propylene glycol "caries detector"
Rampant caries
-sudden, widespread, rapidly progressing process resulting in early pulpal involvement and affecting those teeth usually immune to decay
Nursing caries
-etiology-prolonged bottle feeding containing substrate (baby sleeping with bottle in mouth)
-max. anterior teeth involved
-mand. anterior spared (covered by tongue during feeding)
Primary dentition deep caries
-EPT not reliable
-more extensive than radiographic presentation
-furcation radiolucency indicative of necrotic pulp
-no pulp therapy in chronically ill children (extract)
-indirect pulp cap with no exposure
-pulpotomy with exposure
Root caries
-geriatric or post-periodontal incidence
-distinguish between active and inactive root caries
-inactive: eburnated (sclerotic) dentin which is darkened by extrinsic staining and is firm to the touch of the
explorer
-limited access for isolation may preclude composite and glass ionomers
-frequent fluoride use (i.e. radiation patients) may degrade the surface of Glass ionomer restorations over time
-amalgam may be the material of choice due to ease of direct insertion, carving, finishing and durability
Caries control
-eliminate seeding lesions
gross excavation, indirect pulp caps, ZOE
replace questionable restorations
-use active/therapeutic restorations
fluoride releasing materials
antibacterial properties
-eliminate susceptible areas
seal remaining pits/fissures
-diet modification
reduce carbohydrate
xylitol products
-reduce oral flora
Chlorhexidine treatment
increase personal oral hygiene
high dose APF(1.23%)- office applied (bacteriocidal)
-more frequent recall
-induce remineralization - low dose daily F- home applied; rinses, dentifrice
-saliva analysis
buffering capacity (phosphate, bicarbonate)
clearance (quantity)
viscosity (quality)
-Peridex after completion of caries control (1/2 oz rinse b.i.d. for 16 days)
-S. mutans, lactobacillus culture on completion and recall
Assessment of caries risk and indicators of future problems with restoration longevity
Past dental history (DMF)
Salivary levels of S. mutans
Diet analysis
Salivary testing (flow rate, buffer capacity)
Fluoride
-reduction in caries 50%-60%
-enhancement of enamel remineralization
-water intake best vehicle
-dentifrices 1000 ppm (1450-2500 ppm) contain NaF or Na monofluorophosphate
-high dose topical F
2 % stannous F in water (mix daily, readily converts to stannous hydroxide)
APF 1.23 % F and .98% phosphoric acid (NaF, hydrofluoric acid, phosphoric acid) pH 3-3.5
-low dose rinses
.2% NaF once/week
.05% NaF daily
-Fluoride release curve and therapeutic benefit of F releasing restorative materials:
release curve: Initial high burst for a short period (1 week) followed by a rapid slow down
with a stable long-term low-dose release
therapeutic benefit: Low-dose fluoride release provides enamel/dentin protection via
remineralization mechanisms
| Caries risk (Adults) | Office therapy | Home therapy |
| Low | · topical APF annually | · Fluoride dentifrice (2-3x/day) |
| Moderate | · Topical APF or Fluoride varnish 2x/yr · diet modification | · Fluoride dentifrice 2-3x/day · Fluoride rinse 1 min/1x/day |
| High | · Topical APF or Fluoride varnish 2-4x/yr · Diet modification · Supress S mutans w/ 0.12% Chlorhexidine gluconate | · Fluoride dentifrice 2-3x/day · Fluoride gel APF or NaF (5 min, 1x/day) · Salivary substitute if xerostomic |
F releasing sealants have the potential to act as a slow release depot for F in the mouth to aid in the
remin/demin reaction occurring daily
DIAGNOSIS
Noncarious Cervical Lesions
Abrasion
Mechanical wear produced by the friction of exogenous material
Smooth, concave lesions with no sharp internal line angles
U-, or wedge-shaped ditch on the facial root surface in proximity to the CEJ
Oral-hygiene-related abrasions are usually concomitant with gingival lesions such as laceration,
hyperplasia and gingival recession, the latter being the most common
The gingival sulcus is usually shallow in proximity to abrasion lesions
Attrition
Incisal or occlusal wear resulting from tooth-to-tooth contact through functional or parafunctional
movements
Does not usually pertain to cervical lesions
Erosion
Loss of tooth structure from the action of dietary or gastric acids
May appear on facial and lingual surfaces
Usually involve a wide area of tooth destruction, with no sharp angles
Lingual surfaces - rule out bulimia or esophageal reflux
Abfraction
Cervical erosion lesions that are stress-induced
Lee and Eakle hypothesized that hyperocclusion can result in tooth flexure and tensile
stresses concentrated at the fulcrum, or cervical area of the tooth
Typically V- or wedge-shaped lesions
Usually supported by a stable periodontal housing: less tendency for abfractions to occur in
teeth that are periodontally mobile because the stress concentration is dissipated
Criteria for justifying replacement of restorations
1. The new restoration will significantly improve the situation
2. There is a fracture/continued decay risk
3. There is an unrepairable marginal void
4. There is poor proximal contour or gingival overhang
5. Marginal ridge discrepancy/tissue impingement
6. Unrepairable recurrent caries
7. Large voids/dark marginal staining
8. Ditching deeper than 0.5mm judged carious or caries prone
Dentin hypersensitivity
Odontoblast receptors are direct nerve endings near pulp
myelinated
A (alpha, beta, and delta) fibers differ in size and conduction
most are A-delta-responsible for brief, sharp and well-localized pain (low threshold-EPT
response)
non-myelinated
C fibers, >10% sympathetic nerves (high threshold-dull ache of irreversible pulpitis)
The most widely accepted theory of the mechanism of dentin hypersensitivity is Brannstrom’s
Hydrodynamic theory:
-movement of fluid within dentinal tubules transduces surface stimuli by deformation of
pulpal mechanoreceptors, via A-delta fibers
-hypersensitive dentin has 8 times as many open tubules as non-sensitive teeth
-diameter of dentin tubules can be twice that of non-sensitive teeth
-Poiseulle’s Law- multiply the diameter by 2 , the fluid flow increases by 16 times
Sherman and Jacobsen wrote an article in 1992 entitled “Managing dentin hypersensitivity: What
treatment to recommend to patients”. They recommended a conservative stepwise approach
to managing dentin hypersensitivity:
Step 1. perform thorough exam to rule out other pain sources and evaluate cause then recommend use of a desensitizing dentifrice with KNO3 for a 2-6 week trial period
Step 2. Seal dentinal tubules via in-office potassium oxalate treatment or fluoride iontophoresis (2-10 week trial) (or better yet, apply a DBA for immediate relief)
Step 3. If conservative treatment does not work, place a composite restoration w/ GI base (or DBA liner)
(Note: when this article was written, the jury was still out about DBA’s as desensitizers. Today, it would seem appropriate to try a desensitizing dentifrice initially, and if unsuccessful go immediately to a DBA alone or DBA under a restoration)
Cracked tooth syndrome
Factors Contributing to Etiology
Occlusal/parafunctional factors
Restorative factors
thermal cycling
Tooth morphology and position
most common in mand. molars; oblique ridge protects max. molars
Trauma
Third most common cause of tooth loss
DIAGNOSIS
Pt. Hx and symptoms
pain on biting/release
no pain on vertical pressure, but on lateral pressure
thermal sensitivity
sensitivity to sweets/sour
lost restoration
inability to localize the offending tooth
Transillumination
Provocative bite test (tooth sleuth)
Staining with dyes
Radiographs
Endodontic evaluation
Periodontal evaluation
Surgical evaluation
Treatment
Orthodontic band, copper band, occlusal equilibration
Cusp coverage amalgam alloy restoration
Full coverage temporary crown
10% of patients have continued symptoms
ISOLATION & ACCESS
Gingival surgical techniques for restorative procedures
Double vertical miniflap (aka. “Markley flap”): vertical incisions at line angles of tooth in attached gingiva for procedures not extending beyond line angles
Envelope miniflap: vertical incisions at line angles of adjacent teeth to reflect the gingival papilla for procedures extending beyond line angles of tooth
Double envelope miniflap: Buccal/lingual envelope miniflap with removal of interproximal tissue for class 2 restorations
Electrosurgery
Rate of incision- 7mm/sec
Cooling period- 8-15 sec
Contact on metallic restorations <0.4 sec
Contraindications to electrosurgery
all general contraindications
demand-type cardiac pacemakers
uncontrolled saliva or blood flow
recurrent apthous-type lesions
parotid gland biopsy
post radiation therapy treatment
Rubber dam isolation for a Class 5 lesion
Punch hole 1-3mm to facial and allow extra interproximal dam to minimize stretching
Use extra heavy or special heavy dam for greater retraction and tear resistance
Place retraction cord in sulcus
Use a modified #212 clamp if needed
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