Rezaei, Masih DDC OP Dr.

Gutierrez

Dental Caries
Def Decalcification of hard dental tissue (E, D, C) Word meaning Latin word meaning dry not Susceptibility to Caries: 1. Crown Pits & fissures Occlusal surface Area below CP along PS 2. Tooth classification More likely Lower 1st M 3. Age periods More likely Childhood upto 20yo 4. Saliva More likely Thick & ropy Immunizing Factors from caries: 1. Diet 2. Fluorine in saliva 3. Agglutinin Titer What AB Kills Lactobacillus Acidophilus Streptococcus mutants How Reduce the # of bacterium 4. Bacterium Lactase Acidogenase What Enzyme Location Saliva How Renders the pH of saliva neutral Odontitis Def The bacteria & caries attack from outside & tissue reaction inside as defensive measures Lines of defense 1. 1st reaction o Known as Walling Off o Process Sclerosed dentine walls off carious area Secondary dentine is formed 2. 2nd line of defense o Known as Pulp inflammation o Process Pulp is infiltrated with Leukocytes Lymphocytes 3. 3rd line of defense o Known as Apical inflammation o Process The whole pulp succumbed to infection Apical periodontal tissue inflame Sclerotic dentine Calcified tissue fills up DT Dead tracks Become empty Clinical Classification of Dental Caries A. According to location 1. Pits & fissure caries Occlusal surface M & PM Buccal surface M Lingual surface Max I 2. Smooth surface caries Bu & Li surface PS below CP on G B. According to the rapidity of the process 1. Acute crown Depth Deep Destruction rate Rapid

Symptoms Constant pain Pulp involvement Yes Secondary dentine development No o Why not? Pulp has no chance due to process rapidity Age group Kids & young adults o Why more in this age group? 1. More organic matter in dentine 2. Wide open DT 3. Young teeth greater permeability 2. Acute Root Depth Shallow Common infection site IPS Age group Post mid age o B/c exposure duo to gingival atrophy Destruction rate Rapid o B/c Retained permeability even in old age Cavity formation duo to Cementum decal 3. Chronic crown & root Destruction rate Slow Pulp involvement Yes ( much later than acute) Secondary dentine formation Yes o Why yes Slow process enough time for DT sclerosis & deposition of secondary dentine Color Brown o Duo to Slow superficial destruction Age groups adults Quantity Few teeth Exhibits less enamel & cementum undermining Arrested Caries o Def A stationary form of caries duo to exposure to cleaning excursion of the food Eburrnated Dentine o Def Occlusal caries w/ extensive destruction o Characteristics Hard Polished Stained brown Eburnation of denting The process of dentin eburnation Acute Acute Chronic Crown Root Root & Crown Depth Deep Shallow Destruction rate Rapid Rapid Slow Symptoms Pain Pulp involvement Yes Yes Secondary dentine No Yes involvement Age group Kid / Young adults Post mid age Adults C. According to the nature of the lesion (New vs. Recurrent) 1. Primary Starts from Intact surfaces Ex Smooth area, Pits & fissures NEVER OCCURS ON THE ANTERIOR 2. Secondary Recurrent Central

DT Dentinal Tubules; DC Dental Caries; G Gingival , PS Proximal Surfaces; IPS Interproximal Surfaces; CP Contact Point;

Rezaei, Masih DDC OP Dr. Gutierrez 1. Recurrent Def A secondary caries resulted from faulty odontherapy Location Along immediate vicinity of resto Faulty therapy 1. Inadequate cavity filling 2. Marginal caries leaky margin duo to poor adaptation of filling mat margins to the cavity 3. Incomplete eradication of infected tissue in the 1st trt 4. Poor adaptation of prosthetic appliances 5. Ineffective sterilization of the prepared cavity Central o Def A secondary caries caused by sever attrition or breakage of crown w/ exposed pulp Location Deep aspect of the lesion Appearance Dense opaque zone Extends Over the whole body of lesion May be separated from the body of lesion by Enamel 3. Translucent Zone o A.K.A. Inner recrystallization zone Hypercalcified o Location Beneath the dark zone o o o o B. Smooth Area Characteristics Early stages o Morphology Flame-like Apex towards the interior Base On enamel surface o Color Faint white opacity o Outline Well defined w/ loss of structure continuity Progressing stage o Enamel prism change Disintegrate o Enamel rod change Loss of structure Cervical carious lesion o Morphology Crescent-shaped o Starts as Roughened chalky area o Progresses into Excavated area o Decalcification pattern Wider surface than interior B/c Bacterial colony spreads laterally

2.

Caries of Enamel
Enamel Structure: 1. Enamel Rod Prism 2. Enamel Rod Sheath Prism sheath 3. Interrod Substance Inter-prismatic Enamel Characteristics 1. Composition Organic 2-4% Inorganic 96-98% 2. Vitality Non-vital 3. Color Translucent 4. Healthy enamel Smooth surface 5. Carious enamel No more translucency (White opacity) Peptonization Responsible for foul smell Indole & Skatole Location of Caries of Enamel A. Pits & fissure B. Smooth surface Pits & Fissures Characteristics Early stages o Color Stained brown / black o Hardness Soft & catch a fine explorer Undermining stage o Color Opaque bluish white Progression stage o Shape / Morphology Conical / Tent-like Apex Towards surface (Bottom of the pit) Base Towards the DEJ 3 zones (Histopathological changes) 1. Body of the lesion (Main Bulk) o The most de-mineralized & effected area 1. Band of Retzius 2. Striations 3. Prism Core o Extends From Surface To Enamel o Mark structures Retzius lines Striations o Appearance Translucent than normal enamel o Area near zone 2 Undergoes recrystallization Hypercalcified 2. Dark Zone (Boundary) o Zone of Active demineralization Hypocalcified o What A border-line band separating 1st & 3rd zone

Caries of Dentine
4 Zones (Histopathological changes ) 1. Zone of complete decalcification o Matrix Decalcified walls then decomposed o DT Decalcified walls 2. Zone of incipient decalcification o Beginning of dentin decalcification 3. Zone of transparency o DT Obliterated Du to Tomes fiber calcification 4. Zone of fatty degeneration o Formation of fatty materials o Ca droplets precipitation in Tomes fiber protoplasm 3 stages on Advanced Changes in Carious Dentine: A. MO Involvement o MO invades the DT o MO spreads to side branches o Decalcification of matrix(forms DT walls) o Beaded appearance When Mo multiplies & distends the DT irregularly Spreading duo to Softened surrounding matrix B. Disintegration of DT walls o Distended DT walls are destroyed o Matrix transform into soft crumbly mass o Transverse Cleft Direction Perpendicular to DT Location Near the periphery Hypocalcified structures Contour lines of Owen Interglobular areas Lateral branching of DT o Oblong cavities When Matrix collapse & affected DT coalesced

A.

DT Dentinal Tubules; DC Dental Caries; G Gingival , PS Proximal Surfaces; IPS Interproximal Surfaces; CP Contact Point;

Rezaei, Masih DDC OP Dr. Gutierrez Direction Parallel to DT C. Coalescing o Individual areas coalesce o Dentine is transformed into soft structureless mass 3 Types of MO in Dentine Caries: 1. Cocci 2. Bacilli (Rods) 3. Filaments After being acted upon by Lactobacillus Acidophilus Acid is strong enough to destroy the tooth tissue but not the bacteria Dietary Theory 1. By James H. Shaw 2. Proposed The food consumed in a life time could directly & indirectly affect the susceptibility of the tooth through definite channels o o

Changes in the Structure of Enamel & Dentine in Case of Active (Protective Reaction) A. Reaction of Enamel to Caries o Sclerosis (transparent enamel) Hardening of enamel o 3 sources of inorganic sub for sclerosis (Why hardening) 1. Dissolved inorg subs precipitate on bottom & hardens 2. From saliva settle on the bottom of carious lesion 3. From blood circulation goes to enamel & settle B. Reaction of Dentine o Dead tract Area of dentine that becomes sclerotic in w/c DT contents becomes calcified DT contents may degenerate & DT empties C. Reaction of Pulp o Initial reaction Secondary dentine formation Morphologic reaction o Secondary reaction Inflammation Occurs when Caries get close to pulp

Essential Etiological Factors in Dental Caries

General Predisposing Factors: 1. Race 2. Diet 3. Heredity 4. Nutrition 5. Endocrine disturbance 6. Physical condition of the px Local Predisposing Factors: 1. Structural quality of a tooth 2. Developmental defects 3. Malposition of teeth 4. Attrition 5. Composition of saliva 6. Poor oral hygiene 7. Physical nature of food 8. Occupational influences Exciting Factors (Different type of bacteria) 1. Acidogenic type Acid producing bacteria 2. Acidophylic type Acidic environment loving bacteria 3. Proteolytic type o Bacteria capable of Splitting protein into diffusible body Digesting & liquefying calcified dentine 4. Protective type Filament producing bacteria for attachment

Proteolytic Theory By Bernard Gottlieb Proposed Caries is a proteolytic process involving the invasion of MO into the tissue thru organic channels. 1st organic subs destruction by Proteolytic bacteria 2nd inorganic subs destruction by Acidogenic bacteria Proteolysis-Chelation Theory Simultaneous destruction of organic & inorganic components Theory of Dr. Pincus Sulfate ions are bound to a polysaccharide w/c is a CHO part of the organic part of the tooth Sulphatase enzyme acts on the polysaccharide & releases the sulfate ion Sulfate ion combines w/ water & forms sulphuric acid Sulfuric acid combine w/ calcium salt to form CaSO4 Theory of I.I. de Varis Proposed The process of caries starts in the pulp A lymphatic infarct is formed duo to circulatory problem The section of enamel & dentine w/c corresponds to a group of odontoblast w/o vitality becomes defenseless to bacterial invasion Circulatory disturbance causes nutritional disturbance; therefore the dentine & enamel becomes low in resistance against bacterial attack Theory of Henrick Egyedi Proposed DC is caused by bacteria w/c grows in org subs of enamel The excess amount of CHO & glycogen stored serve as nutrition for the bacteria Atkinson & Mathews Proposed Proteolytic enzymes elaborated most likely by the bacteria on the tooth surface liberate aspartic & Glutamic acid from the tooth proteins as they pass down organic channels The liberated acids cause dissolution of enamel rods

Fluoride & Dental Caries

2 mechanism of fluoride: 1. Fluoride lower the solubility o enamel to acid 2. Fluorides inhibit specific bacterial enzyme

Caries Susceptibility Tests

Lactobacillus Count More candies more count Calcium dissolution test 1. Miligrams of powdered enamel + Glucose + Saliva 2. Calcium Phosphate is measured after 4 hrs Wach test 1. Saliva + Glucose broth culture incubated for 4 hrs 2. Amont of produced acid is measured Snyders test 1. Assesses Acidogenic ability of bacteria 2. The rate of color change of the indicator bromocresol green is measured 3. Medium acidity of 5pH for 24-48 hrs

Theories on Etiology of Dental Caries

Acidogenic Theory A.K.A. Miller-Black-Williams Chemico-parasitic theory DC is o Result of Decalcification tooth structure o By Acid o Derived from Refined fermentable CHO

DT Dentinal Tubules; DC Dental Caries; G Gingival , PS Proximal Surfaces; IPS Interproximal Surfaces; CP Contact Point;

Rezaei, Masih DDC OP Dr. Gutierrez o 24 hrs Yellow-grean (High susceptibility o 48 Moderate susceptibility Hydrogen ion concentration 1. The pH is measured 2. Saliva + glucose + enamel incubation for 4 hrs

DT Dentinal Tubules; DC Dental Caries; G Gingival , PS Proximal Surfaces; IPS Interproximal Surfaces; CP Contact Point;