Operative Dentistry I - Lesson 1: Introduction PDF

OPERATIVE DENTISTRY I Lesson 1: Introduction Transcribed by: Junamae T. Cariman College of Dentistry According to Sturdevant: Diagnosis The art and science of dentistry which deals with “The process of identifying a dise...

OPERATIVE DENTISTRY I Lesson 1: Introduction Transcribed by: Junamae T. Cariman College of Dentistry According to Sturdevant: Diagnosis The art and science of dentistry which deals with “The process of identifying a disease by its signs, diagnosis, treatment, and prognosis of defect of the symptoms, and results of various diagnostic teeth which do not require full coverage restorations for procedures” – Dr. Louis I. Grossman correction “Defined as the determination, discriminative Such treatment should result in the restoration of estimation and logical appraisal of conditions found proper tooth form, function and aesthetics, while during examination as evidenced by distinctive marks, maintaining the physiologic integrity of the teeth in signs, that are characteristic of health or disease” – harmonious relationship with adjacent hard and soft Derrick McGhee tissues. P Prevention Diagnosis, treatment, and prognosis of defects of tooth do Includes the procedures for prevention before the not require full coverage restorations for correction. manifestation of any signs and symptoms of disease. I Interception Procedures undertaken after the signs and symptoms FULL CROWN have appeared, in order to prevent the disease from developing into a more serious form. P Preservation Means preservation of the vitality and periodontal support of the remaining tooth structure is obtained by preventive and interceptive procedures R Restoration Procedures done to restore form, function, phonetics and aesthetics M Maintenance After restoration of the tooth is completed, it must be maintained to provide service for longer duration P Prognosis CLASS I : pit fissure Predicting the likely outcome of a disease based on the condition of the patient and action of disease Treatment results in; Restoration of proper tooth form Restoration of function restoration of esthetics Maintenance of physiologic integrity of the teeth in CLASS II proximal : of posterior teeth harmonious relationship with the adjacent hard and soft tissues. ➔ Enhance the general health welfare of the patient  INDICATIONS ❖ Dynamic – there’s constant change, activity or ➔ It is categorized into three primary treatment needs progress ❖ Preventable – can be stopped I Caries ❖ Chronic – persisting for a long time of consistently. recurring Caries → Cavity – a defect in enamel or in enamel and dentin resulting from a pathologic process which is dental caries. 4 GENERAL MECHANISMS OF DENTAL CARIES S Susceptible host S Suitable substrate M Microorganism I Time 2. Malformed, discolored, nonaesthetic, or fractured THEORIES OF DENTAL CARIES Various theories have been proposed trying to explain the etio-pathogenesis of dental caries, which are Early Theories 1. Exogenous Theories - Legend of worm - Chemical Theory - Parasitic or Septic Theory 3 Restoration replacement or repair. 2. Endogenous Theories - Humoral theory - Vital theory EXOGENOUS THEORIES The Worm Theory Dates back as far as 5000 BC referenced in a Sumerian text They believe tooth worm bore a hole through your teeth and hid beneath the surface; drank blood of teeth and fed on roots of jaws. Chemical Theory (acid theory) DENTAL CARIES (2020) Robertson 1835 – opined that caries was caused by - Dental caries is biofilm-mediated, diet-modulated, chemical disintegration of the tooth multifactorial, non-communicable, disease resulting in it was believed that putrefaction of protein led to formation net mineral loss of dental hard tissues. of ammonia which was subsequently oxidized to nitric acid. ❖ Biofilm – thin, slimy film bacteria (consortium of Parasitic or Septic Theory microorganisms) that adheres to the surface the first theory that related microorganisms with caries on ❖ Mediated – means of conveying/ in the middle of a causative basis accordingly, it was proposed that even though caries starts ❖ Disease purely as a chemical process BUT microorganisms ❖ Modulated – has controlling influence continued the disintegration in both enamel and dentin\ ❖ Non-communicable ENDOGENOUS THEORIES Humoral Theory the four-elemental fluid (humors) of the body-blood, phlegm, black bile, yellow bile - Pente imbalance in these 4 humors determines the person’s physical and mental constitution Vital Theory TWO THEORIES ON PATHOGENECITY OF PLAQUE proposed by Hippocrates, Celsus, Galen, and 1. Nonspecific plaque hypothesis Auicenna. 18th century. - Assumes that all plaque is pathogenic Postulated that tooth decay originated like bone gangrene from within the tooth itself. 2. Specific plaque hypothesis NEW THEORIES - Recognized that plaque is pathogenic only when signs of associated disease are present Theory (Willoughby Miller) WiM The theory said that caries is caused by acids produced by oral bacteria following fermentation of high frequency sucrose exposure may be the single sugar. most important factor in producing a cariogenic plaque Consists of 2 stages: frequent sucrose ingestion begins a series of changes 1. Decalcification of enamel, destruction of dentin in the local tooth environment that promotes growth pf (preliminary stage) PS highly acidogenic bacteria that leads to caries 2. Dissolution of the softened residue of enamel & dentin (subsequent stage) SS GENERAL MECHANISM OF DENTAL CARIES Miller advocated an essential role of 3 factors in the caries process: 1. The oral microorganisms, 2. The carbohydrate substrate, and 3. The acid → this theory is considered as the backbone of current knowledge and understanding of the etiology of dental caries Proteolytic Theory Heider and Bodecker 1878 and Abbot in 1879 HBA Morphology : · self cleansing of tooth Said that the organic portion of the tooth serves as 1. Host susceptible individual - surface Location : pathways for advancing microorganisms causing - Molars are more prone posterior teeth not : reachable demineralization of the teeth and therefore dental - Tooth is the primary factor composition : caries. caries susceptibility of tooth to its 2. Saliva is inversely proportional calcium content Pincus in 1949 fluoride , - High salivary phosphate content, less prone to caries Proposed that the first step in the carious process is the - pH breakdown of dental cuticle - Viscosity Nasmyth’s membrane and enamel proteins are acted - Flow upon by sulfatase enzyme producing sulfuric acid. This Mucous (viscous – thick and ropy, more viscous) → prone acid plus the calcium of hydroxyapatite crystals to caries destroys the inorganic component of enamel. Serous (low viscosity) – less decay RELATIONSHIP OF BIOFILM (PLAQUE) TO DENTAL CARIES pH Scale - Soft, translucent, and tenaciously adherent material accumulating on the surface of the teeth - A gelatinous mass of bacteria adhering to the tooth surface. idental plaquel  Critical pH → 5.5 – 5.7 3 DETRIMENTAL CHANGES Demineralization → Below 5.5 – 5.7 Remineralization → Higher than 5.7 1. Protective factor deleted from food materials during processing, storage & preparation Flow – decreased salivary flow/ production may have 2. Cariogenic factor added higher caries susceptibility 3. Frequency of meals - very important in controlling both the oral flora and mineral content of teeth 4. Time - flushes the oral cavity - It is not what you eat - stagnant when the person is asleep - It’s how many times (frequency) you eat and for how long (duration) the food stays in your mouth 3. Muscular Activity after eating, that causes the development of - Activities of tongue, cheek, lips, & muscles of the face cavities. will create & guide the self-cleansing activities w/ in the - The frequency of in between meals/ snacks counts oral cavity. CARIES RISK ASSESSMENT 4. Habits - Poor eating habits such as in between meals will be Soft drinks prone to caries - contains sugar and acid = erosion - acidity due to phosphoric acid and citric acid 5. Group Susceptibility - Females more susceptible pH of mouth – 6.2-7.0 - More civilized societies, more prone to caries than pH of soft drinks – 2.47 – 3.35 people from primitive areas. 6. Age 7. Environment - Examples would be areas with fluoridated water, less prone to caries. GENERAL MECHANISM OF DENTAL CARIES ❖ Host (susceptible tooth/ individual) ❖ Parasite (Bacteria) - Microorganisms brough into contact w/ the tooth surface via a bacterial plaque, creating Upon consumption of carbohydrates, pH level of a classic parasitic relationship plaque remains at a cariogenic level for 30 minutes Streptococcus mutans lenamel) CLINICAL SITES FOR CARIES INITIATION - the principal bacterial agent involved in the carious agent 1. Recesses of developmental pits and fissure - Enamel (coronal) Lactobacillus acidophilus = dentin Actinomyces viscosus = root caries ❖ Medium – Diet (suitable substrate) - Suitable substrate/ available nutrients to support bacterial growth - Carbohydrate is the most cariogenic of all 2. Smooth enamel surfaces that shelter plaque food materials Fermentable carbohydrates = the chief offenders insofar as food is concerned More fibrous and harder food increases masticatory activity = less caries  3. Root surface In enamel: cone shaped with the apex (smallest area) at the external opening Apex In dentin: cone shaped with the apex (smallest area) toward the pulp APCX In pit and fissure caries, the triangles of decay are positioned base to base In enamel: cone shaped with the apex (smallest area) at the dentino-enamel junction (DEJ) PROGRESSION OF CARIOUS LESION ▪ Smooth surface: 18 mos. ± 6 mos. ▪ Newly erupted tooth: 3 years ▪ Occlusal pit and fissure – less than smooth surface ▪ Frequent exposure to sucrose containing food: 3 weeks ▪ Poor oral hygiene: 3 weeks In dentin: cone shaped with the apex toward the pulp ▪ Radiation xerostomia (dry mouth): 3 mos. PATTERN OF DENTAL CARIES Enamel Rods - The basic unit of the enamel structure - It run perpendicularly from the surface of the tooth to the dentin - The structure of dentin is an arrangement of microscopic channels called dentinal tubules, which radiate outward from the pulp chamber to the exterior cementum or enamel border. Decay is apex to base Narrower as its progresses Proximal surface caries appears smaller in radiograph and wider/bigger clinically ➔ Demineralization of enamel by caries generally follows the direction of the enamel rods → The different triangles of decay patterns between pit and 2. Secondary (recurrent) caries fissure and smooth-surface caries develop in the enamel - Occurs at the junction of the restoration and because the orientation of enamel rods is different in the the tooth and may progress under the two areas of the tooth. restoration - Primary cause is microleakage’ CLASSIFICATION OF DENTAL CARIES ACCORDING TO THE LOCATION (NATURE OF LESION) 1. Primary caries - Original carious lesion of the tooth: 3 morphologic types: In enamel pits and fissures. On enamel smooth surfaces. On root surfaces (common in older populations). Caries originating in pits and fissures ACCORDING TO THE RAPIDITY OF THE PROCESS 1. Chronic (slow or arrested) Caries - may be slow or may be arrested following several active phases - slow rate resulting from episodic demineralization and remineralization due to changes in the oral environment - lesion is discolored/dark and hard - the slow rate allows time for extrinsic pigmentation Caries originating on smooth surfaces hence the black color - an arrested enamel lesion is brown to black, hard - common in adults ACCORDING TO NUMBER OF SURFACES INVOLVED a. Simple – involving only one surface Caries originating on root surfaces - Occurs on a root that has been exposed to the oral environment and habitually covered with plaque. - Prevalent in the older population b. Compound – involving two surfaces of tooth - Usually more rapid than other forms of caries. c. Complex – involving three or more surfaces of a tooth  - on smooth surface enamel it appears opaque white CLASSIFICATION BY SURFACE NAME when air-dried and will seem to disappear - it is a demineralized enamel that has not extended to Single Surface the DEJ. Surface Name Abbreviation - enamel surface hard and still intact Occlusal O - no cavitation Mesial M - lesion can be remineralized through plaque removal Lingual L and control and fluoridization Distal D Incisal I Buccal B Facial F Combination Surface Surface Name Abbreviation Mesio-occlusal MO Mesio-incisal MI Linguo-occlusal LO Disto-lingual DL 2. Cavitated Caries (Nonreversible) Disto-incisal DI - enamel surface is broken Bucco-occlusal BO - lesion has advanced into dentin Mesio-occlusodistal MOD - remineralization not possible Mesio-occlusodistobuccal MODB - treatment by tooth preparation and restoration are indicated. ACCORDING TO DEPTH Shallow Cavity Depth: has 2.0 mm or more of remaining dentin Moderate Cavity Depth: less than 2.0 mm, but greater than 1.0 mm of ACCORDING TO G.V. BLACK remaining dentin Class I – pit and fissure cavities (occlusal of posterior, lingual of anterior) Deep Cavity Depth: less than 1.0 mm of remaining dentin Class II – cavities on the proximal surfaces of posterior teeth ACCORDING TO SEVERITY (EXTENT OF CARIES) (premolars and molars) 1. Incipient Caries (reversible) - It is the first evidence of caries activity in the enamel. Class III – cavities on the proximal surfaces of incisors and canines that do not involve the incisal angle Forward Caries Class IV – cavities on the proximal surfaces of incisors and - when the caries in the enamel is larger or at least the canines that involve the incisal angle same size as dentin. Class V - Cavities on the gingival 1/3 of facial and lingual surfaces of all teeth (not on the pit and fissure Residual Caries - caries that remains in a completed tooth preparation, whether by intention or by accident. - it is not acceptable if at the DEJ or on the prepared enamel tooth wall. - It is acceptable when it is affected dentin. Class VI - (This was only added to G. V. Black’s Classification). Cavities on the incisal edges or cusps of all teeth due to attrition, abrasion or erosion. INFECTED DENTIN VS. AFFECTED DENTIN Carious dentin consists of 2 layers 1. Outer layer – infected dentin 2. Inner layer – affected dentin INFECTED DENTIN AFFECTED DENTIN Backward Caries Contains bacteria Has no bacteria - it is a condition when the spread of caries along the Not remineralized Can be remineralized DEJ exceeds the caries in the contiguous enamel Must be removed Should be preserved  In tooth preparation, it is desirable that only dentin be removed, leaving the affected dentin which then may be Separation of Teeth remineralized in a vital tooth following the completion of - use wood or plastic wedge for mechanical separation restorative treatment of teeth to visualize whether or not contacting tooth have cavity. DIAGNOSIS OF DENTAL CARIES 1. Explorer Transillumination 2. Radiograph – caries appears radiolucent - checks for cracks or caries - light source located lingually while the teeth are a. Bitewing radiograph viewed from the facial direction - Proximal caries b. Periapical x-ray - Helps assess the proximity of the carious lesion to the pulp - Helps assess the periapical condition of the tooth Discoloration – pits and fissures discoloration Patient’s complaint Sensitivity within the dentin DIAGNOSIS OF DENTAL CARIES Dental Floss - The floss is inserted in contact area & dragged occlusally or incisally may show shredding.