FIRST AID FOR THE NBDE PART II

Dental Caries 12 ETIOLOGY 12 RESPONISBLE ORGANISMS 12 PATHOGENESIS 12 Examination and Diagnosis 15 CLINICAL EXAMINATION 16 CARIES DETECTORS 17 RADIOGRAPHIC EVALUATION 17 Cavity Preparation 17 CAVITY CLASSIFICATION 17 Operative Instruments 19 HAND CUTTING INSTRUMENTS 19 Restorations 20 DENTAL MATERIALS AND BIOMATERIAL SCIENCE 20 DIRECT ESTHETIC MATERIALS 24 CEMENTS/BASES/LINERS/TEMPORARY RESTORATION 26 11 Copyright © 2008 by The McGraw-Hill Companies, Inc. Click here for terms of use.DATABASE OF H IG H-YI E LD FACTS: DISC I PLI N E-BASE D COM PON E NT OPE RATIVE DE NTISTRY 12 DE NTAL CARI ES Perhaps the most common chronic disease in the world, an infectious microbiologic disease of the teeth that results in localized demineralization and destruction of the calcified tissues, leading to loss of tooth structure. Etiology Carious lesions occur when a mass of bacteria adhere to the tooth surface (dental plaque) → plaque bacteria feast on refined carbohydrates → metabolize the sugars and produce acid byproducts → the acid lowers the pH of the plaque adherent to the tooth → the critical pH is reached at which demineralization of the adjacent tooth takes place. ■ Critical pH: 5.5 (Some sodas have a pH of 3.5.) ■ Nonspecific plaque hypothesis: All plaque cause caries. ■ Specific plaque hypothesis: Only those that cause caries are pathogenic. ■ Fluoridation: It has significantly decreased the number of caries, especially in children. ■ Saliva is carioprotective: It acts as a buffer, carries minerals important for remineralization (Ca, PO4, and F), has antimicrobial properties, and washes away food. PAIN THEORY There have been different thoughts on the production of pain secondary to carious or other insult. The current accepted school of thought is the hydrodynamic theory. ■ When the tooth is subjected to insult, fluid movement through the tubules increases and the greater flow deforms the nerve endings in the pulp leading to pain response. ■ Cold conductivity increases both the volume and the flow in the tubules resulting in pain stimulus. Responisble Organisms ■ Streptococcus mutans and Lactobacilli are the most common cariogenic bacteria in coronal caries. ■ Actinomyces viscus is the most common cariogenic bacteria in root surface or smooth surface caries. ■ Dental plaque organisms—Streptococcus sanguis found earliest ■ Other offenders: Actinomyces naeslundi, Veillonella, Streptococcus salivarious Pathogenesis ENAMEL CARIES Caries in enamel have different properties than those in dentin. ■ Acidogenic or physiochemical progression of structural destruction of enamel → demineralization due to lowered pH. ■ Early lesions are capable of remineralizing or arresting, if pH is in favor of building and mineral content like fluoride is abundant. Cariogenic bacteria = SALIVA S. mutans, sanguis, mitis, salivarius A. viscus Lactobacilli Veillonella A. naeslundiDATABASE OF H IG H-YI E LD FACTS: DISC I PLI N E-BASE D COM PON E NT OPE RATIVE DE NTISTRY 13 ■ Incipient caries describes caries that have not progressed farther than enamel, they are reversible or able to remineralize. ■ Frank caries describe caries that have progressed just into the dentinoenamel junction (DEJ). PIT AND FISSURE CARIES The shape of pits and fissure make these caries the most prevalent variant. ■ Mostly S. sanguis and other strep. ■ Narrow at the enamel surface and spreads wide at the DEJ (inverted V). ■ Rapid destruction as many dentinal tubules are involved and undermining takes place. ■ Actual lesion is often much larger than clinically presentable. ■ Lesion progression parallels enamel rods. ■ Prevent with fissurotomy and sealant. SMOOTH SURFACE CARIES Interproximal or cervical are the second most prevalent of all caries and are usually found just gingival to the proximal contact. ■ Start wide at the surface and converges toward the DEJ (V shape). ■ Slower progression as less tubules are affected and undermining is less. ■ Prevent with fluoride. ZONES OF CARIOUS ENAMEL Also referred to as “zones of incipient lesion,” four zones have been characterized in a sectioned incipient lesion. 1. Translucent zone → the deepest zone, is termed accordingly due to its absent or composition-less appearance seen under polarized light. 2. Dark zone → represents remineralization and is termed so due to its inability to transmit polarized light. 3. Body zone → the largest zone, represents a demineralizing phase. 4. Surface zone → outermost zone, seems unaffected by the caries. DENTIN CARIES Acidogenic progression to the dentin layer results in a different pattern of destruction than that of enamel. The structure of dentin contains less mineralized tissue and instead more tubular structures, which allows for spread of the acidogenic destruction. ■ Faster progression than enamel caries, because less mineral content. ■ V-shaped caries with broad base at DEJ and the apex toward the pulp. ■ Infected dentin → tubules are infected with many acid-producing bacteria, and acidogenic and proteolytic activity result in degradation. ■ Affected dentin → bacteria present, but in smaller amounts. Demineralization occurs but still can be reversed if favorable environment assumes and infected layer is removed. The DEJ provides the least resistance to caries and allows for rapid spread once approximated.DATABASE OF H IG H-YI E LD FACTS: DISC I PLI N E-BASE D COM PON E NT OPE RATIVE DE NTISTRY 14 ZONES OF CARIOUS DENTIN Five zones have been characterized in carious dentin from innermost to outermost. Only the first three zones are capable of remineralization. Zone 2 and 3 are termed affected and 4 and 5 are infected. 1. Normal dentin → no bacteria or byproducts present in this deepest unaffected area. 2. Subtransparent dentin → demineralization from acidogenesis, but no bacteria found in dentinal tubules. 3. Transparent dentin → softer than normal, further demineralization—yet still no bacteria found. 4. Turbid dentin → the zone of bacterial invasion: bacteria present in the dentin tubules. Must remove this zone. 5. Infected dentin → many bacteria found in this outermost carious zone. Must remove dentin to treat successfully. ROOT SURFACE CARIES Destruction of cementum and radicular or root dentin is more often found in older individuals (senile caries) with clinical recession and resultant exposure to plaque and acid-producing bacteria. ■ Occurs when the root has been exposed to the oral environment and contaminated with plaque. ■ Cementum surface is rougher than enamel and has greater mechanical advantage of acquiring plaque. ■ Often associated with decreased salivary flow and decreased ability to provide adequate hygiene as seen in aging population. ■ Spreads shallow along the surface, is ill-defined as characterized by a U shape. ■ The relatively thin cementum provides little resistance to attack and results in a rapid progression, and progresses more rapidly than other lesions. ■ The pathway of initial demineralization is along the Sharpey’s fibers of the cementum. ■ The shallow nature of these lesions lend to the finding than many of these lesions are associated with remineralization. Generally very dark lesions have been remineralized to some degree. ■ Often asymptomatic. ■ Difficult to restore. RESIDUAL CARIES Infected or cavitated tooth structure remaining after attempted removal in a completed cavity preparation. ■ Can be intentional such as in indirect pulp capping procedures. RECURRENT CARIES Also known as secondary caries, is decay that remains in a completed cavity. ■ Radiolucent bases or liners can be mistaken for recurrent decay on radiographic presentation.15 RAMPANT CARIES Rapidly progressing wide-spread caries are often the result of histological disadvantages, poor hygiene, drug abuse, radiation, high-sugar diets, or decreased salivary conditions. ■ Acute onset ■ Often associated with pain ■ Deep and narrow presentation result in large cavitation ARRESTED CARIES Describes lesions that have remineralized. ■ Hard ■ Black or brown discoloration, a result of trapped debris and metallic ions ■ Asymptomatic EXAM I NATION AN D DIAG NOSIS The successful diagnosis of caries involves a good history, risk assessment, clinical evaluation, and radiographic analysis. The goal of examination is to diagnose caries activity before it becomes obvious on presentation. If found in premature or even incipient stages, a treatment approach to arrest and remineralize the faulty tooth structure is optimal. Only when changes are irreversible must we intervene with the infamous “drill and fill.” ■ A good history and caries risk assessment is important and can determine the course of action taken; for example, a small carious lesion in a low-risk patient may not need any restoration, whereas the same lesion in a highrisk patient may necessitate one. ■ Risk factors include history of prior caries, frequent sucrose intake, low fluoride intake (communities with nonfluoridated water), young or old age, poor oral hygiene, existing restorations, high concentrations of cariogenic bacteria, and salivary deficits. Table 1–1 shows risk factors for caries. Table 1–2 shows common drugs that affect salivary function. DATABASE OF H IG H-YI E LD FACTS: DISC I PLI N E-BASE D COM PON E NT OPE RATIVE DE NTISTRY T A B L E 1 – 1 . Caries Risk Factors MODERATE RISK FACTORS HIGH RISK