•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
THE LEGEND OF THE WORMS
• EARLIEST REFERENCE TO TOOTH DECAY & TOOTH PAIN CAME FROM ANCIENT SUMERIAN TEXT KNOWN
AS THE ‘LEGEND OF THE WORMS’
• TOOTHACHE – A WORM THAT DRANK BLOOD OF TEETH & FED ON ROOTS OF JAWS
• DISCOVERED ON A CLAY TABLET NEAR
NIFFER, UR & OTHER CITIES IN
EUPHRATES VALLEY OF LOWER
MESOPOTAMIAN AREA (5000 BC)
• REMEDY READ AS FOLLOWS: “ MIX
BEER, THE PLANT SA-KIL-BIR AND OIL TOGETHER, REPEAT THEREON THE INCANTATION THRICE (AND)
PUT IT ON HIS TOOTH”
HUMORAL THEORY
• GREEK PHYSICIANS – 4 ELEMENTAL HUMORS ARE:
BLOOD – SANGUINE
PHLEGM – PHLEGMATIC
BLACK BILE – MELANCHOLIC
YELLOW BILE – CHOLERIC
• GALEN – ‘DENTAL CARIES IS PRODUCED BY INTERNAL ACTION OF ACID & CORRODING HUMORS’.
AN IMBALANCE RESULTS IN DISEASE
• AT THE END OF EIGHTEENTH CENTURY UP TO MIDDLE OF NINETEENTH.
• DENTAL CARIES – ORIGINATED IN TOOTH ITSELF LIKE BONE GANGRENE
• CARIES IS CHARACTERIZED BY EXTENSIVE PENETRATION INTO DENTIN, EVEN TO PULP
CHEMICAL(ACID) THEORY
• ROBERTSON (1835): DENTAL DECAY – ACID FORMED BY FERMENTATION OF FOOD AROUND TEETH
• REGNART (1938): INORGANIC ACIDS CORRODED ENAMEL & DENTIN
• ERDL (1843): DESCRIBED FILAMENTOUS PARASITES – IN MEMBRANE FROM TEETH
• FICINUS (1847): OBSERVED FILAMENTOUS MICROBES IN CARIOUS LESIONS – DENTICOLAE
• CARIES – INFILTRATION > DECOMPOSITION OF ENAMEL AND DENTIN
• MECH. BY WHICH MICROBES CAUSE DECAY WAS NOT EXPLAINED
• W D MILLER (1890): ACIDS & MICROORGANISMS – DECAY
• PASTEUR: DISCOVERED MICROBES TRANSFORMS SUGARS TO LACTIC ACID BY FERMENTATION
• MILLER SUMMARIZED DENTAL DECAY IS A CHEMOPARASITIC PROCESS
CONSISITING OF TWO STAGES: DECALCIFICATION OF THE TISSUES AND
DISSOLUTION OF THE SOFTENED RESIDUE.
• INSTEAD OF CLASSICAL CHEMO-PARASITIC THEORY IT HAS BEEN PROPOSED THAT ORGANIC OR
PROTEIN ELEMENTS ARE INITIAL PATHWAY OF INVASION
• ACCORDING TO THEORY – ORGANIC COMPONENT IS MORE VULNERABLE & IS ATTACKED BY
HYDROLYTIC ENZYMES
• GOTTLIEB (1944): INITIAL ACTION DUE TO PROTEOLYTIC ENZYMES ATTACKING LAMELLAE, ROD
SHEATHS, TUFTS & WALLS OF DENTINAL TUBULES
- STAPHYLOCOCCUS AUREUS WAS INVOLVED BECAUSE OF YELLOW PIGMENTATION CONSIDERED
PATHOGNOMIC OF DENTAL CARIES
•
• SCHATZ ET AL (1955): SIMULTANEOUS MICROBIAL DEGRADATION OF ORGANIC COMPONENTS
(PROTEOLYSIS) & DISSOLUTION OF MINERALS OF TOOTH (CHELATION)
• THEORY CONSIDERS CARIES TO BE A BACTERIAL DESTRUCTION OF TEETH WHERE INITIAL ATTACK IS
ESSENTIALLY ON ORGANIC COMPONENTS OF ENAMEL. BREAK DOWN PRODUCTS OF THIS ORGANIC
MATTER HAVE CHELATING PROPERTIES & THERE BY DISSOLVE MINERALS IN ENAMEL
• DECALCIFICATION IS MEDIATED BY VARIETY OF COMPLEXING AGENTS – ANIONS, AMINO ACIDS,
PEPTIDES, POLYPHOSPHATES, & CARBOHYDRATE DERIVATIVES
SULFATASE THEORY: PINCUS (1950) BACTERIAL SULFATASE HYDROLYZES MUCOITIN SULFATE OF
ENAMEL & CHONDROITIN SULFATE OF DENTIN PRODUCING SULFURIC ACID CAUSING
DECALCIFICATION
COMPLEXING & PHOSPHORYLATION THEORY: LURA (1967) HIGH BACTERIAL UTILIZATION OF
PHOSPHATES IN PLAQUE CAUSES A LOCAL DISTURBANCE IN PHOSPHATE EQUILIBRIUM RESULTING IN
LOSS OF INORGANIC PHOSPHATE FROM ENAMEL
- SOLUBLE CALCIUM COMPLEXING COMPOUNDS PRODUCED BY BACTERIA – FURTHER TOOTH
DISINTEGRATION
•
•
•
1.
2.
3.
•
•
•
•
•
•
•
•
•
CARIES IS MULTIFACTORIAL DISEASE:
A) ESSENTIAL FACTORS – BACTERIA, TOOTH STRUCTURE & DIETARY
CARBOHYDRATES
B) SECONDARY FACTORS – SALIVA, PLAQUE CONSTITUENTS, TIME, TRACE
ELEMENTS, ORAL HYGIENE ETC..
TOOTH STRUCTURE
• UNDERGOES CONTINUOUS CHANGES IN BOTH PHYSIOCHEMICAL AND MORPHOLOGICAL
PROPERTIES
• HEALTHY ENAMEL IS RESULT OF RELATIVELY STABLE OR FAVORABLE EQUILIBRIUM; & DISTURBANCE –
DISSOLUTION
• CARIES IS RESULT OF SERIES OF BACK & FORTH SHIFT IN CHEMICAL EQUILIBRIUM OF TOOTH
STRUCTURE WHICH IN SUMMATION DICTATES CONDITIONS MORE FAVORABLE TO INORGANIC
DISSOLUTION THAN RECRYSTALIZATION
• FUEL FOR CARIES PROCESS
• DEGRADABLE CARBOHYDRATES AS SOURCE OF BACTERIAL FERMENTATION TO ORGANIC ACIDS & AS
SUBSTRATE FOR ATP SYNTHESIS, FOR BACTERIAL SURVIVAL & PROLIFERATION
• DIETARY CARBOHYDRATES TO BE ACTIVE AS CARIOGENIC SUBSTRATES, IT MUST BE - IN READILY
USABLE MONOSACCHARIDE FORM
- EASILY BROKEN DOWN TO BACTERIAL METABOLITES
• DISACCHARIDE – GLUCOSE + FRUCTOSE
• MAJOR DIETARY FOOD STUFFS
• NEWBRUN CALLED SUCROSE AS “ ARCH CRIMINAL OF DENTAL CARIES “
• BECAUSE SUCROSE SERVES AS THE SUBSTRATE FOR EXTRACELLULAR
POLYSACHARIDE SYNTHESIS OF CERTAIN MICROBIAL ORGANISMS IMPLICATED IN
DENTAL CARIES.
- STUDIES HAVE SUPPORTED THIS INCRIMINATION (VIPEHOLM STUDY)
- SUCROSE CONDUCTIVE TO BOTH PLAQUE FORMATION & CARIES
• SO SUCROSE STANDS AS SINGLE MOST IMP. PREDISPOSING FACTOR IN CARIES PROCESS
• MICROORGANISMS ARE ESSENTIAL FACTOR FOR CARIES
• FERMENT DIETARY CARBOHYDRATES TO ACIDS > DEMINERALIZATION
AT BIRTH
- STREPTOCOCCUS MITIOR,STREPT SALIVARIUS,
NIESSERIA, STAPHYLOCOCCI, LACTOBACILLI.
- ANAEROBIC -- VEILLONELLA ALCALESCENS,
FUSOBACTERIA
- STRP MUTANS FOUND –NON-DESQUAMATING SURFACE.
- STRP MUTANS, STRP SANGIUS, A VISCOSUS– ONLY AFTER ERUPTION OF TEETH.
SALIVA
 HAS INHIBITORY EFFECT
 ACTS BY:
- MECHANICAL VIA CLEANSING
- CHEMICAL VIA SPECIFIC INTERACTIONS
 SALIVARY FLOW: INVERSELY PROPORTIONAL TO DEGREE OF CARIES ACTIVITY
 BICARBONATE BUFFERING CAPACITY
 SALIVARY GLYCOPROTEIN: LUBRICATION
 INORGANIC CONSTITUENTS: NA+, CL-, HCO3
-, K+, F-
– INHIBITION OF CARIES
 SECRETORY IMMUNOGLOBULIN (SIGA)
 PROTEINS: AMYLASE – CLEAVE MALTOSE
LYSOZYME – NON SPECIFIC ANTIBACTERIAL AGENT
•
• LYSOSYME
• LACTOPEROXIDASE
• LACTOFERRIN
• UNSTIMULATED SALIVARY FLOWRATE- 0.3ML/MIN
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•

CARIOLOGY.pptx

  • 2.
  • 3.
  • 4.
  • 5.
  • 6.
  • 7.
  • 8.
  • 9.
  • 10.
  • 11.
  • 12.
    THE LEGEND OFTHE WORMS • EARLIEST REFERENCE TO TOOTH DECAY & TOOTH PAIN CAME FROM ANCIENT SUMERIAN TEXT KNOWN AS THE ‘LEGEND OF THE WORMS’ • TOOTHACHE – A WORM THAT DRANK BLOOD OF TEETH & FED ON ROOTS OF JAWS • DISCOVERED ON A CLAY TABLET NEAR NIFFER, UR & OTHER CITIES IN EUPHRATES VALLEY OF LOWER MESOPOTAMIAN AREA (5000 BC) • REMEDY READ AS FOLLOWS: “ MIX BEER, THE PLANT SA-KIL-BIR AND OIL TOGETHER, REPEAT THEREON THE INCANTATION THRICE (AND) PUT IT ON HIS TOOTH”
  • 13.
    HUMORAL THEORY • GREEKPHYSICIANS – 4 ELEMENTAL HUMORS ARE: BLOOD – SANGUINE PHLEGM – PHLEGMATIC BLACK BILE – MELANCHOLIC YELLOW BILE – CHOLERIC • GALEN – ‘DENTAL CARIES IS PRODUCED BY INTERNAL ACTION OF ACID & CORRODING HUMORS’. AN IMBALANCE RESULTS IN DISEASE
  • 14.
    • AT THEEND OF EIGHTEENTH CENTURY UP TO MIDDLE OF NINETEENTH. • DENTAL CARIES – ORIGINATED IN TOOTH ITSELF LIKE BONE GANGRENE • CARIES IS CHARACTERIZED BY EXTENSIVE PENETRATION INTO DENTIN, EVEN TO PULP
  • 15.
    CHEMICAL(ACID) THEORY • ROBERTSON(1835): DENTAL DECAY – ACID FORMED BY FERMENTATION OF FOOD AROUND TEETH • REGNART (1938): INORGANIC ACIDS CORRODED ENAMEL & DENTIN
  • 16.
    • ERDL (1843):DESCRIBED FILAMENTOUS PARASITES – IN MEMBRANE FROM TEETH • FICINUS (1847): OBSERVED FILAMENTOUS MICROBES IN CARIOUS LESIONS – DENTICOLAE • CARIES – INFILTRATION > DECOMPOSITION OF ENAMEL AND DENTIN • MECH. BY WHICH MICROBES CAUSE DECAY WAS NOT EXPLAINED
  • 17.
    • W DMILLER (1890): ACIDS & MICROORGANISMS – DECAY • PASTEUR: DISCOVERED MICROBES TRANSFORMS SUGARS TO LACTIC ACID BY FERMENTATION • MILLER SUMMARIZED DENTAL DECAY IS A CHEMOPARASITIC PROCESS CONSISITING OF TWO STAGES: DECALCIFICATION OF THE TISSUES AND DISSOLUTION OF THE SOFTENED RESIDUE.
  • 18.
    • INSTEAD OFCLASSICAL CHEMO-PARASITIC THEORY IT HAS BEEN PROPOSED THAT ORGANIC OR PROTEIN ELEMENTS ARE INITIAL PATHWAY OF INVASION • ACCORDING TO THEORY – ORGANIC COMPONENT IS MORE VULNERABLE & IS ATTACKED BY HYDROLYTIC ENZYMES • GOTTLIEB (1944): INITIAL ACTION DUE TO PROTEOLYTIC ENZYMES ATTACKING LAMELLAE, ROD SHEATHS, TUFTS & WALLS OF DENTINAL TUBULES - STAPHYLOCOCCUS AUREUS WAS INVOLVED BECAUSE OF YELLOW PIGMENTATION CONSIDERED PATHOGNOMIC OF DENTAL CARIES
  • 19.
  • 20.
    • SCHATZ ETAL (1955): SIMULTANEOUS MICROBIAL DEGRADATION OF ORGANIC COMPONENTS (PROTEOLYSIS) & DISSOLUTION OF MINERALS OF TOOTH (CHELATION) • THEORY CONSIDERS CARIES TO BE A BACTERIAL DESTRUCTION OF TEETH WHERE INITIAL ATTACK IS ESSENTIALLY ON ORGANIC COMPONENTS OF ENAMEL. BREAK DOWN PRODUCTS OF THIS ORGANIC MATTER HAVE CHELATING PROPERTIES & THERE BY DISSOLVE MINERALS IN ENAMEL • DECALCIFICATION IS MEDIATED BY VARIETY OF COMPLEXING AGENTS – ANIONS, AMINO ACIDS, PEPTIDES, POLYPHOSPHATES, & CARBOHYDRATE DERIVATIVES
  • 21.
    SULFATASE THEORY: PINCUS(1950) BACTERIAL SULFATASE HYDROLYZES MUCOITIN SULFATE OF ENAMEL & CHONDROITIN SULFATE OF DENTIN PRODUCING SULFURIC ACID CAUSING DECALCIFICATION COMPLEXING & PHOSPHORYLATION THEORY: LURA (1967) HIGH BACTERIAL UTILIZATION OF PHOSPHATES IN PLAQUE CAUSES A LOCAL DISTURBANCE IN PHOSPHATE EQUILIBRIUM RESULTING IN LOSS OF INORGANIC PHOSPHATE FROM ENAMEL - SOLUBLE CALCIUM COMPLEXING COMPOUNDS PRODUCED BY BACTERIA – FURTHER TOOTH DISINTEGRATION
  • 22.
  • 23.
  • 24.
  • 28.
    CARIES IS MULTIFACTORIALDISEASE: A) ESSENTIAL FACTORS – BACTERIA, TOOTH STRUCTURE & DIETARY CARBOHYDRATES B) SECONDARY FACTORS – SALIVA, PLAQUE CONSTITUENTS, TIME, TRACE ELEMENTS, ORAL HYGIENE ETC..
  • 29.
    TOOTH STRUCTURE • UNDERGOESCONTINUOUS CHANGES IN BOTH PHYSIOCHEMICAL AND MORPHOLOGICAL PROPERTIES • HEALTHY ENAMEL IS RESULT OF RELATIVELY STABLE OR FAVORABLE EQUILIBRIUM; & DISTURBANCE – DISSOLUTION • CARIES IS RESULT OF SERIES OF BACK & FORTH SHIFT IN CHEMICAL EQUILIBRIUM OF TOOTH STRUCTURE WHICH IN SUMMATION DICTATES CONDITIONS MORE FAVORABLE TO INORGANIC DISSOLUTION THAN RECRYSTALIZATION
  • 30.
    • FUEL FORCARIES PROCESS • DEGRADABLE CARBOHYDRATES AS SOURCE OF BACTERIAL FERMENTATION TO ORGANIC ACIDS & AS SUBSTRATE FOR ATP SYNTHESIS, FOR BACTERIAL SURVIVAL & PROLIFERATION • DIETARY CARBOHYDRATES TO BE ACTIVE AS CARIOGENIC SUBSTRATES, IT MUST BE - IN READILY USABLE MONOSACCHARIDE FORM - EASILY BROKEN DOWN TO BACTERIAL METABOLITES
  • 31.
    • DISACCHARIDE –GLUCOSE + FRUCTOSE • MAJOR DIETARY FOOD STUFFS • NEWBRUN CALLED SUCROSE AS “ ARCH CRIMINAL OF DENTAL CARIES “ • BECAUSE SUCROSE SERVES AS THE SUBSTRATE FOR EXTRACELLULAR POLYSACHARIDE SYNTHESIS OF CERTAIN MICROBIAL ORGANISMS IMPLICATED IN DENTAL CARIES. - STUDIES HAVE SUPPORTED THIS INCRIMINATION (VIPEHOLM STUDY) - SUCROSE CONDUCTIVE TO BOTH PLAQUE FORMATION & CARIES • SO SUCROSE STANDS AS SINGLE MOST IMP. PREDISPOSING FACTOR IN CARIES PROCESS
  • 32.
    • MICROORGANISMS AREESSENTIAL FACTOR FOR CARIES • FERMENT DIETARY CARBOHYDRATES TO ACIDS > DEMINERALIZATION AT BIRTH - STREPTOCOCCUS MITIOR,STREPT SALIVARIUS, NIESSERIA, STAPHYLOCOCCI, LACTOBACILLI. - ANAEROBIC -- VEILLONELLA ALCALESCENS, FUSOBACTERIA - STRP MUTANS FOUND –NON-DESQUAMATING SURFACE. - STRP MUTANS, STRP SANGIUS, A VISCOSUS– ONLY AFTER ERUPTION OF TEETH.
  • 33.
    SALIVA  HAS INHIBITORYEFFECT  ACTS BY: - MECHANICAL VIA CLEANSING - CHEMICAL VIA SPECIFIC INTERACTIONS  SALIVARY FLOW: INVERSELY PROPORTIONAL TO DEGREE OF CARIES ACTIVITY  BICARBONATE BUFFERING CAPACITY  SALIVARY GLYCOPROTEIN: LUBRICATION  INORGANIC CONSTITUENTS: NA+, CL-, HCO3 -, K+, F- – INHIBITION OF CARIES  SECRETORY IMMUNOGLOBULIN (SIGA)  PROTEINS: AMYLASE – CLEAVE MALTOSE LYSOZYME – NON SPECIFIC ANTIBACTERIAL AGENT
  • 34.
    • • LYSOSYME • LACTOPEROXIDASE •LACTOFERRIN • UNSTIMULATED SALIVARY FLOWRATE- 0.3ML/MIN
  • 35.
  • 37.
  • 38.
  • 39.
  • 40.
  • 41.
  • 42.
  • 43.
  • 44.
  • 47.
  • 48.
  • 49.
  • 50.
  • 51.