Histopathology & microbiology of dental cariesAshish Karode
The document summarizes the histopathology of dental caries. It describes how dental caries is a microbial disease that causes demineralization of tooth enamel and dentin. It discusses the role of bacteria like Streptococcus mutans in producing acid that dissolves tooth structure. The summary describes the microscopic appearance of carious lesions in enamel and dentin, including the formation of zones of demineralization and bacterial invasion of dentin tubules over time. Advanced caries can ultimately lead to tooth cavitation and pulp involvement if left untreated.
Dental caries and periodontal diseases.pptFyslZargary
1. Dental plaque is a biofilm that develops on teeth and comprises living and dead bacteria and their products embedded in an organic matrix. The microbial composition of plaque varies between individuals and locations in the mouth.
2. Gingivitis is a reversible form of periodontal disease caused by dental plaque. It involves inflammation of the gingiva without loss of attachment to the tooth. The gingiva become red, swollen and bleed easily but are not painful. Early plaque is dominated by streptococci while established lesions contain increased levels of anaerobic bacteria like Porphyromonas and Prevotella.
3. Dental caries is caused by acid-producing plaque bacteria metabolizing ferment
Dental caries is caused by acid-producing bacteria in dental plaque that metabolize sugars from the diet. As the bacteria lower the pH, minerals are dissolved from tooth enamel and dentin, leading to cavitation. The primary bacteria involved are mutans streptococci. Risk factors include frequency of sugar consumption. Early lesions appear as white spots on smooth surfaces or pits and fissures. Untreated, caries progresses through enamel and into dentin, forming zones of demineralization and bacterial invasion.
Dental caries is caused by acid-producing bacteria in dental plaque that metabolize sugars from the diet. As the bacteria lower the pH, minerals are dissolved from tooth enamel and dentin, leading to cavitation. The primary bacteria involved are mutans streptococci. Risk factors include frequent sugar consumption. Early lesions appear as white spots on smooth surfaces or pits and fissures. Untreated, caries progresses through enamel and into dentin, forming zones of demineralization and bacterial invasion.
The document provides an introduction to dental caries (tooth decay) as a disease. It defines dental caries according to various authors and organizations. Caries results from an imbalance between tooth mineral and biofilm fluid that causes demineralization of enamel and dentin. Key factors that contribute to this imbalance are the host tooth surface, carbohydrates as a substrate for oral bacteria, the oral biofilm, and time. However, not all individuals with teeth and a biofilm who consume carbohydrates will develop caries, as several risk and protective factors can modify the caries process, such as saliva composition and flow, oral hygiene, fluoride exposure, and diet.
Dental Caries ; A Presentation by- MunabbiRMunabbir31
Dental caries, or tooth decay, is a microbial disease caused by bacteria in the mouth that leads to demineralization of tooth enamel and dentin. Key factors for development of caries include cariogenic bacteria, bacterial plaque, fermentable carbohydrates, and susceptible tooth surfaces. Symptoms may include tooth sensitivity, pain, and visible cavities. Diagnosis involves visual examination and sometimes x-rays. Treatment depends on the severity but may include fillings, root canals, extractions, or replacements like bridges or implants. Maintaining good oral hygiene through regular brushing and cleanings can help prevent caries.
Histopathology & microbiology of dental cariesAshish Karode
The document summarizes the histopathology of dental caries. It describes how dental caries is a microbial disease that causes demineralization of tooth enamel and dentin. It discusses the role of bacteria like Streptococcus mutans in producing acid that dissolves tooth structure. The summary describes the microscopic appearance of carious lesions in enamel and dentin, including the formation of zones of demineralization and bacterial invasion of dentin tubules over time. Advanced caries can ultimately lead to tooth cavitation and pulp involvement if left untreated.
Dental caries and periodontal diseases.pptFyslZargary
1. Dental plaque is a biofilm that develops on teeth and comprises living and dead bacteria and their products embedded in an organic matrix. The microbial composition of plaque varies between individuals and locations in the mouth.
2. Gingivitis is a reversible form of periodontal disease caused by dental plaque. It involves inflammation of the gingiva without loss of attachment to the tooth. The gingiva become red, swollen and bleed easily but are not painful. Early plaque is dominated by streptococci while established lesions contain increased levels of anaerobic bacteria like Porphyromonas and Prevotella.
3. Dental caries is caused by acid-producing plaque bacteria metabolizing ferment
Dental caries is caused by acid-producing bacteria in dental plaque that metabolize sugars from the diet. As the bacteria lower the pH, minerals are dissolved from tooth enamel and dentin, leading to cavitation. The primary bacteria involved are mutans streptococci. Risk factors include frequency of sugar consumption. Early lesions appear as white spots on smooth surfaces or pits and fissures. Untreated, caries progresses through enamel and into dentin, forming zones of demineralization and bacterial invasion.
Dental caries is caused by acid-producing bacteria in dental plaque that metabolize sugars from the diet. As the bacteria lower the pH, minerals are dissolved from tooth enamel and dentin, leading to cavitation. The primary bacteria involved are mutans streptococci. Risk factors include frequent sugar consumption. Early lesions appear as white spots on smooth surfaces or pits and fissures. Untreated, caries progresses through enamel and into dentin, forming zones of demineralization and bacterial invasion.
The document provides an introduction to dental caries (tooth decay) as a disease. It defines dental caries according to various authors and organizations. Caries results from an imbalance between tooth mineral and biofilm fluid that causes demineralization of enamel and dentin. Key factors that contribute to this imbalance are the host tooth surface, carbohydrates as a substrate for oral bacteria, the oral biofilm, and time. However, not all individuals with teeth and a biofilm who consume carbohydrates will develop caries, as several risk and protective factors can modify the caries process, such as saliva composition and flow, oral hygiene, fluoride exposure, and diet.
Dental Caries ; A Presentation by- MunabbiRMunabbir31
Dental caries, or tooth decay, is a microbial disease caused by bacteria in the mouth that leads to demineralization of tooth enamel and dentin. Key factors for development of caries include cariogenic bacteria, bacterial plaque, fermentable carbohydrates, and susceptible tooth surfaces. Symptoms may include tooth sensitivity, pain, and visible cavities. Diagnosis involves visual examination and sometimes x-rays. Treatment depends on the severity but may include fillings, root canals, extractions, or replacements like bridges or implants. Maintaining good oral hygiene through regular brushing and cleanings can help prevent caries.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can greatly reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque allows demineralization.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque enables demineralization.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky carbohydrates increase caries risk as they prolong acid exposure. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. Local acid drops below the critical pH of 5.5 cause subsurface demineralization and eventual cavities.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. The rate of decay depends on the type of carbohydrate, frequency of consumption, and how long sugars remain stuck to teeth. It also discusses factors like microorganisms, acids, dental plaque, and tooth structure that influence the caries process according to Miller's chemico-parasitic theory.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque allows demineralization.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky carbohydrates increase caries risk as they prolong acid exposure. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable alternatives like sorbitol and xylitol reduces caries.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque enables demineralization.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque enables demineralization.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky carbohydrates that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. Local acid production below pH 5.5 causes subsurface enamel demineralization and below pH 4-5 leads to surface enamel loss.
Dentine, unlike enamel, has the ability to react to the progression of caries due to the presence of odontoblasts. Odontoblasts can respond to irritation by depositing minerals in the dentinal tubules
Dental caries is the most prevalent disease affecting humans, spreading to almost all populations worldwide regardless of socioeconomic status or age. It is caused by bacteria in the mouth that feed on sugars, producing acids that demineralize tooth enamel and dentin over time. If left untreated, it can progress from white spot lesions to cavities, and eventually to tooth pain, abscesses, and tooth loss. The document provides detailed information on the histopathological stages and presentation of dental caries in enamel, dentin, and cementum.
Dental caries is the most common microbial disease affecting the tooth. Even through extensive studies over the years, the pathogenesis remains questionable. Hence a fundamental understanding of caries and its theories is essential as data from the past serves as the most vital evidence in the unavoidable quest to figure out the pathogenesis.
For more content check out my blog www.rkharitha.wordpress.com - "a little about everything dental"
This document provides information about dental caries (tooth decay). It defines dental caries, describes the carious process and pathological changes involved. It discusses the epidemiology of dental caries, including prevalence, incidence, and indices used to measure caries activity. Risk factors for dental caries like location and surface of teeth are presented. The roles of microorganisms, substrates, teeth susceptibility, and time in the development of caries are explained. Details about dental plaque as the medium for caries development are provided.
This document provides information on the etiology and classification of dental caries. It discusses the multifactorial nature of caries, involving bacteria, susceptible tooth surfaces, and diet playing major roles. It describes theories of caries development including Miller's chemoparasitic theory involving acid production by bacteria leading to demineralization. It also discusses host factors like tooth composition, plaque, diet and its effects on bacteria, the role of time and saliva, and systemic and genetic factors in caries development and susceptibility.
This document discusses dental caries, including its etiology, clinical characteristics, and histopathology. It describes how caries is caused by an interaction between host factors, such as tooth composition and saliva, and environmental factors like diet and bacteria. It also summarizes the typical progression and appearance of caries in different locations, such as pits and fissures, smooth surfaces, and root surfaces. Caries develops when acids produced by bacteria in dental plaque from sugars in the diet break down tooth minerals over time. The document provides details on the role of various microorganisms involved at different caries stages.
Dental caries is caused by demineralization of tooth structure due to acid produced by oral bacteria. It is characterized by loss of both inorganic and organic components of the tooth. Dental caries has been defined and classified in various ways based on factors such as the anatomical site, severity, tissue involvement, number of surfaces affected, and chronology. The key etiological factors include the presence of cariogenic bacteria in dental plaque, a susceptible tooth substrate, and a cariogenic diet. Secondary factors like time, the dynamic process of demineralization and remineralization, and saliva also influence the development of dental caries.
Dental_caries2020.pptjhjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjjRishi M
This document discusses dental caries (tooth decay). It describes caries as a multifactorial, sugar-dependent infectious disease caused by an interaction between bacteria in dental plaque and fermentable carbohydrates. Certain bacteria like Streptococcus mutans are especially adept at producing acid from sugars, which demineralizes tooth enamel over time if remineralization does not match demineralization. Factors that influence the development of caries include diet, oral hygiene, fluoride exposure, tooth structure, and flow of protective saliva. The document provides details on the etiology, pathogenesis, and risk factors involved in the development of dental caries.
Dental caries is caused by an interaction between oral bacteria, fermentable carbohydrates, and tooth surfaces over time. Miller's chemico-parasitic theory is the most widely accepted explanation of the etiology. It states that acids produced by oral bacteria from carbohydrates lead to enamel demineralization and destruction. Clinical presentation varies and includes pit and fissure caries, smooth surface caries, and root caries. Histologically, caries progresses through zones of demineralization and remineralization in both enamel and dentin. Prevention focuses on modifying the oral environment, bacteria, and substrate to reduce acid production and demineralization.
Dental caries is caused by acid-forming bacteria in dental plaque that metabolize fermentable carbohydrates. The process involves alternating periods of demineralization and remineralization of tooth enamel based on the pH level in the mouth. Streptococcus mutans is the primary cariogenic bacteria. Risk factors include frequent sugar consumption, poor oral hygiene, fluoride deficiency, and low saliva flow. Caries can be detected clinically, radiographically, and newer methods involving electrical resistance, light illumination, and digital imaging. Remineralization through fluoride and controlling bacteria and diet can prevent or reverse early caries.
Common Terms in Parasitology 22-02-2017 (1).pptxssuser12303b
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The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can greatly reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque allows demineralization.
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The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. The rate of decay depends on the type of carbohydrate, frequency of consumption, and how long sugars remain stuck to teeth. It also discusses factors like microorganisms, acids, dental plaque, and tooth structure that influence the caries process according to Miller's chemico-parasitic theory.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque allows demineralization.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky carbohydrates increase caries risk as they prolong acid exposure. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable alternatives like sorbitol and xylitol reduces caries.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque enables demineralization.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky sugars that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. The acidogenic theory proposes that the localized pH drop facilitated by plaque enables demineralization.
The document discusses the role of carbohydrates in dental caries (tooth decay). It states that fermentable carbohydrates like glucose, fructose, and sucrose are easily fermented by bacteria like Streptococcus mutans in dental plaque, producing acids that demineralize tooth enamel and lead to cavities. Frequent sugar intake and sticky carbohydrates that remain on teeth increase caries risk. Starches carry less risk as they are slowly broken down. Replacing sucrose with non-fermentable sugars can reduce caries. Local acid production below pH 5.5 causes subsurface enamel demineralization and below pH 4-5 leads to surface enamel loss.
Dentine, unlike enamel, has the ability to react to the progression of caries due to the presence of odontoblasts. Odontoblasts can respond to irritation by depositing minerals in the dentinal tubules
Dental caries is the most prevalent disease affecting humans, spreading to almost all populations worldwide regardless of socioeconomic status or age. It is caused by bacteria in the mouth that feed on sugars, producing acids that demineralize tooth enamel and dentin over time. If left untreated, it can progress from white spot lesions to cavities, and eventually to tooth pain, abscesses, and tooth loss. The document provides detailed information on the histopathological stages and presentation of dental caries in enamel, dentin, and cementum.
Dental caries is the most common microbial disease affecting the tooth. Even through extensive studies over the years, the pathogenesis remains questionable. Hence a fundamental understanding of caries and its theories is essential as data from the past serves as the most vital evidence in the unavoidable quest to figure out the pathogenesis.
For more content check out my blog www.rkharitha.wordpress.com - "a little about everything dental"
This document provides information about dental caries (tooth decay). It defines dental caries, describes the carious process and pathological changes involved. It discusses the epidemiology of dental caries, including prevalence, incidence, and indices used to measure caries activity. Risk factors for dental caries like location and surface of teeth are presented. The roles of microorganisms, substrates, teeth susceptibility, and time in the development of caries are explained. Details about dental plaque as the medium for caries development are provided.
This document provides information on the etiology and classification of dental caries. It discusses the multifactorial nature of caries, involving bacteria, susceptible tooth surfaces, and diet playing major roles. It describes theories of caries development including Miller's chemoparasitic theory involving acid production by bacteria leading to demineralization. It also discusses host factors like tooth composition, plaque, diet and its effects on bacteria, the role of time and saliva, and systemic and genetic factors in caries development and susceptibility.
This document discusses dental caries, including its etiology, clinical characteristics, and histopathology. It describes how caries is caused by an interaction between host factors, such as tooth composition and saliva, and environmental factors like diet and bacteria. It also summarizes the typical progression and appearance of caries in different locations, such as pits and fissures, smooth surfaces, and root surfaces. Caries develops when acids produced by bacteria in dental plaque from sugars in the diet break down tooth minerals over time. The document provides details on the role of various microorganisms involved at different caries stages.
Dental caries is caused by demineralization of tooth structure due to acid produced by oral bacteria. It is characterized by loss of both inorganic and organic components of the tooth. Dental caries has been defined and classified in various ways based on factors such as the anatomical site, severity, tissue involvement, number of surfaces affected, and chronology. The key etiological factors include the presence of cariogenic bacteria in dental plaque, a susceptible tooth substrate, and a cariogenic diet. Secondary factors like time, the dynamic process of demineralization and remineralization, and saliva also influence the development of dental caries.
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Dental caries is caused by an interaction between oral bacteria, fermentable carbohydrates, and tooth surfaces over time. Miller's chemico-parasitic theory is the most widely accepted explanation of the etiology. It states that acids produced by oral bacteria from carbohydrates lead to enamel demineralization and destruction. Clinical presentation varies and includes pit and fissure caries, smooth surface caries, and root caries. Histologically, caries progresses through zones of demineralization and remineralization in both enamel and dentin. Prevention focuses on modifying the oral environment, bacteria, and substrate to reduce acid production and demineralization.
Dental caries is caused by acid-forming bacteria in dental plaque that metabolize fermentable carbohydrates. The process involves alternating periods of demineralization and remineralization of tooth enamel based on the pH level in the mouth. Streptococcus mutans is the primary cariogenic bacteria. Risk factors include frequent sugar consumption, poor oral hygiene, fluoride deficiency, and low saliva flow. Caries can be detected clinically, radiographically, and newer methods involving electrical resistance, light illumination, and digital imaging. Remineralization through fluoride and controlling bacteria and diet can prevent or reverse early caries.
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3. HISTOLOGY : Study of microscopic anatomy
of cells and tissues of plants and animals.
HISTOPATHOLOGY: Microscopic
examination of tissues in order to study the
manifestations of disease.
DENTAL CARIES: Microbial disease of
calcified tissues of teeth characterised by
demineralisation of inorganic portion and
destruction of organic portion.
4. Dental Caries
It is a microbial disease of the calcified tissues of the teeth,
characterized by demineralization of the inorganic portion
and destruction of the organic substance of the tooth.
Many researches/investigations for more than a hundred years have
been done, still, many aspects of the etiology of this disease is
obscure and efforts at prevention are only partly successful.
5. ►Dental caries or tooth decay is one of the most common of all
disorders, second only to common cold.
►Dental caries has afflicted more humans longer than any other
disease. It was first appeared about 1400 BC years ago. From
that time to the present, dental caries affected almost all
human populations, at all socioeconomic levels, and at all ages.
►Some isolated populations like Eskimos, some African natives,
and inhabitants of rural India are “immune” to dental caries
because they are not exposed to western food habits.
6. o The word ‘caries’ is derived from the Latin word ‘rot’.
It is the most prevalent disease affecting the human race,
o Practically spread all over the world,
oAffects both sexes and all races, all socio-economic strata
and people of all ages,
o Starts soon after teeth erupt into the oral cavity
9. OF ENAMEL: Hard translucent tissue covering
the anatomical crowns.
COMPOSITION: Inorganic matter 96%
Organic matter 0.2-0.8%
Water 1.2-4%
STRUCTURE: Hydroxyappatite crystals laid in
form of rods, Striae of Retzius, rod sheath etc.
10. OF DENTIN: Semi transparent calcified connective
tissue penetrated by small canals containing
protoplasmic processes belonging to cell which remain
outside the tissue in pulp cavity.
COMPOSITION: Inorganic matter 61-73%
Organic matter 20.2-22.8%
Water 10.8-15.4%
STRUCTURE: Hydroxyapatite crystals laid in form of
dentinal tubules, dentin matrix and Tomes fibres etc.
11. DENTINO ENAMEL JUNCTION:
Has more interprismatic substance, crossing
and branching of dentinal tubules, enamel
spindles and enamel lamellae.
12. OF CEMENTUM: Bone like tissue arranged in
layers present around the anatomical root
COMPOSITION: Inorganic matter 65-70%
Organic matter 35-40%
STRUCTURE: Acellular cementum and cellular
cementum.
13. Causative Factors
• Presence of caries pathogens (MS, LB)
• Frequent or prolonged exposure to
fermentable carbohydrates
Potentiating Factors
• Low fluoride exposure level
• Inadequate salivary flow
14. Causes of dental caries
• Pre-microbiology era
– Dental caries is the death (decay) of a
tissue
• Microbiology period era
– Dental caries is a microbe related disease
15. The first microbes
observed
•Anton Van Leeuwenhoek
(1632-1723) developed
the microscope and was
the first to discover oral
bacterial flora: “I didn’t
clean my teeth for three
days and then took the
material that had lodged
in small amounts on the
gums above my front
teeth…. I found a few
living animalcules..”
16. Re-isolation of “Mutans streptococci”:
• Streptococcus mutans (human) (same
species Clark isolated in England in 1924)
• Streptococcus sobrinus (human)
• Streptococcus rattus (rats)
• Streptococcus cricetus
• Streptococcus ferus
• Streptococcus macacae
• Streptococcus downeii
17. 1. Acid production (acidogenicity)
• Lower the pH to below 5.5, the critical pH. Drives
the dissolution of calcium phosphate (hydroxyapatite)
of the tooth enamel
• Inhibit the growth of beneficial bacteria, promote the
growth of aciduric bacteria.
• Further lower the pH, promote progression of the
carious lesion
18. 2. Acid tolerance (aciduricity)
•Allows the cariogenic bacteria to thrive under acidic
conditions while other beneficial bacteria are
inhibited. This results in dominance of the plaque
by cariogenic bacteria
3. Glucan formation
• Glucan mediated biofilms are more resistant to
mechanical removal
• Bacteria in these biofilms are more resistant to
antimicrobial treatments
Allows the cariogenic bacteria to stick onto the teeth
and form a biofilm
19. Ecological niche: Human oral cavity
■“Intentionally designed … to be a cariogenic
organism” (Coykendall 1976)
Carciogenic properties
■Ability to produce acid
(acidogenicity)
■Ability to withstand acid
conditions (aciduricity), at
the expense of benign flora
■Ability to adhere to teeth
20.
21.
22. Both pathogenic and commensal (nonharmful) bacteria exist in a
natural plaque.
At sound site, the pathogenic bacteria may exist in low numbers
to cause any clinical effect, or they may exist in higher numbers,
but the acid produced is neutralized by the action of other
bacteria.
Disease is a result of a shift in the balance of the residence micro
flora driven by a change in the local environment (frequent
sugar intake etc).
24. Lesion Initiation
• MS present in low numbers in plaque (carrier state)
• Frequent sugar supply gives MS competitive advantage
• ECP helps adhere them firmly to tooth surface
• Metabolism of sugar to acid by products lowers pH
• Few organisms can survive in low pH (aciduric)
• MS proportions increase
• This lowers the pH further and decreases the number of
competing organisms
• Once the pH low enough (critical pH, 5.0-5.5) tooth
mineral begins dissolving
• Mineral loss follows down the grain of the enamel rods
25. • Saliva dilutes & buffers acid & contains concentrated
calcium & phosphate ions
• When sugar present, net demineralization rapidly
occurs
• Between sugar episodes, remineralization slowly occurs
• If remin periods exceed demin periods, subsurface
lesion will mineralize & arrest
• If demin periods exceed remin periods, cavitation will
occur
• Demin periods exceed remin periods when sugar Intake is
increased in intensity
26.
27.
28. The surface of a tooth i. e. covered by plaque,
which consists mainly of bacteria. Plaque is often
found close to the gum, in between teeth, in
fissures and at other "hidden" sites.
Demineralization:
When sugar and other fermentable
carbohydrates reaches the bacteria, they form
acids which start to dissolve the enamel - an
early caries lesion occurs due to loss of Calcium
and Phosphates
Remineralization:
When sugar consumption has ceased, saliva
can wash away sugars and buffer the acids.
Calcium and Phosphates can again enter the
tooth. The process is strongly facilitated by
fluorides
A CAVITY occurs if the Demineralization "wins" over the Remineralization over time
29. The first indication of tooth decay are
white spots on the enamel caused by the
loss of calcium.
If the demineralization process
outruns the natural remineralisation
process, the lesion grows and a cavity
is formed.
The bacteria may invade the pulp of
the tooth,
causing a consistent tooth pain,
especially during the night.
The bacteria may also
produce an abscess,
and eventually the tooth
may be extracted by the
dentist.
30. SLOWLY PROGRESSING LESIONS GO
THROUGH MORE DEMIN/REMIN CYCLES
LEADING TO DARK SHALLOW LESIONS
RAPIDLY PROGRESSING LESIONS GO
THROUGH FEWER DEMIN/REMIN CYCLES
LEADING TO LIGHTER-COLORED, MORE
AGGRESSIVE LESIONS
31. 1. A tooth surface without caries.
2. The first signs of demineralization.
3. The enamel surface has broken down.
4. A filling has been made but the demineralization has not been stopped.
5. The demineralization proceeds and undermines the tooth.
6. The tooth has fractured.
32.
33. ENAMEL CARIES
The early lesion is a white spot which appears
on the surface of the enamel. Caries spreads in
zones which are as follows.
Translucent zone
Dark zone
Body of the lesion
Surface zone
34. The zones seen before complete disintegration of enamel are:
Zone 1: Translucent zone,
-lies at the advancing front of the lesion,
-slightly more porous than sound enamel,
-it is not always present
Zone 2: Dark zone,
-this zone is usually present and referred
to as positive zone
-formed due to demineralization.
Zone 3: Body of the lesion,
-found between the surface and the dark zone,
-it is the area of greatest demineralization,
Zone 4: Surface zone,
-relatively unaffected area,
-greater resistance probably due to greater degree of mineralization and
greater F concentration.
35.
36. Pit And Fissure Caries:
-lesion begins beneath plaque, with decalcification of enamel
-pit and fissures are often deep, with food stagnation,
-enamel in the bottom of pit or fissure is very thin, so early dentin involvement
frequently occurs.
-here the caries follows the direction of the enamel rods.
-It is triangular in shape with the apex facing the surface of tooth and the
base towards the DEJ.
-when reaches DEJ, greater number of dentinal tubules are involved.
-it produces greater cavitation than the smooth surface caries and there is
more undermining of enamel.
37.
38.
39.
40.
41. Smooth surface Caries:
The earliest manifestation of incipient caries (early caries) of enamel is usually
seen beneath dental plaque as areas of decalcification (white spots).
The first change seen histologically is the loss of inter-rod substance of
enamel with increased prominence of the rods.
-this is followed by the loss of mucopolysaccharides in the organic substance.
-presence of transverse striations of the enamel rods,
- accentuated incremental lines of Retzius
as it goes deeper, the caries forms a triangular pattern or cone shaped lesion
with the apex towards DEJ and base towards the tooth surface.
Finally, there is loss of enamel structure, which gets roughened due to
demineralization, and disintegration of enamel prisms.
44. Early lesion with intact
enamel
5-10% mineral loss, zone
of intact enamel
Lesion body 60%
or more mineral loss
translucent zone – 5-10%
mineral loss
normal enamel
45.
46.
47.
48.
49.
50. The events of the dentinal caries are as follows:
1.
2.
3.
Defense reaction of the pulpodentinal complex
Seclerosis
Reactionary dentine formation
Sealing of the dead tracts
Carious destruction
1. Demineralization
2. proteolysis
51. RIES OF DENTIN
gins with the natural spread of the caries process along the DEJ and rapid
olvement of the dentinal tubules. The dentinal tubules act as tracts leading to
pulp (path for micro-organisms).
rly Dentinal Changes:
itial penetration of the dentin by caries dentinal sclerosis,
lcification of dentinal tubules and sealing off from further penetration by
cro-organisms,
ore prominent in slow chronic caries.
Dentinal
sclerosis
54. Behind the transparent sclerotic zone, decalcification of dentin appears.
In the earliest stages, when only few tubules are involved, microorganisms may
be found penetrating the tubules Pioneer Bacteria.
55. This initial decalcification
involves the walls allowing
them to distend as the
tubules are packed with
microorganisms. Each tubule
is seen to be packed with pure
forms of bacteria, eg., one
tubule packed with coccal
forms the other tubule with
bacilli.
56. As the microorganisms proceed further they are distanced from the
carbohydrates substrate that was needed for the initiation of the caries.
Thus the high protein content of dentin must favour the growth of the
microorganisms.
Therefore proteolytic organisms might appear to predominate in the
deeper caries of dentin while acidophilic forms are more prominent in
early caries.
57. Advanced Dentinal Changes ;
-decalcification of walls, confluence of the dentinal tubules,
-tiny “liquefaction foci”, described by Miller are formed by the focal coalescing
and breakdown of dentinal tubules. These are ovoid areas of destruction parallel
to the course of the tubules which filled with necrotic debris and increase in size
by expanding.
The adjacent tubules are distorted and their course is bent due to this
expansion.
58.
59.
60. The destruction of dentin by decalcification and then proteolysis occurs in
numerous focal areas- leading to a necrotic mass of dentin of a leathery
consistency.
-clefts present in the carious dentin that extends at right angles to the
dentinal tubules, accounts for the peeling off of dentin in layers while
excavating.
61.
62. Shape of the lesion is triangular with the
apex towards the pulp and the base
towards the enamel.
Zone 1; Zone of Fatty Degeneration of
Tome’s Fibers,(next to pulp)
-due to degeneration of the
odontoblastic process. This occurs
before sclerotic dentin is formed and
makes the tubules impermeable.
Zone 2; Zone of dentinal sclerosis,
-deposition of Ca salts in the tubules.
Zone 3; Zone of decalcification of dentin
Zone 4; Zone of bacterial invasion
Zone 5; Zone of decomposed dentin due to
acids and enzymes.
63. Root Caries
Root caries as defined by HAZEN, is a soft, progressive lesion
that is found anywhere on the root surface that has lost its
connective tissue attachment and is exposed to the environment.
-the root surface must be exposed to the oral environment before
caries can develop here.
-Plaque and micro-organisms are essential for the cause and
progression of the lesion, mostly Actinomyces,
64. -micro-organisms invade the cementum either along the Sharpey’s
fibers or between the bundles of fibers.
-spread laterally, since cementum is formed in concentric layers.
-after decalcification of cementum, destruction of matrix occurs
similar to dentin with ultimate softening and destruction of this
tissue.
-invasion of micro-organisms into the dentinal tubules, finally
leading to pulp involvement.
-the rate is slower due to fewer dentinal tubules than crown area
65.
66. Dark brown pigmented carious lesion , insensitive
to painful stimuli in which caries progression is
halted.
67. ZONE 1: Surface layer- Brown in colour and of
leathery consistency.
ZONE 2: Pigmented zone- Hard, dark brown in
colour, forming main bulk with presence of
coalesced bacteria bodies
ZONE 3: Sclerotic layer-Hard, white zone
having highly calcified tubules with absence of
bacteria.
68. Caries occuring beneath or around the existing
restoration.
Histologically can occur as:
1. Outer lesion 20%
2. Wall lesion 11.9%
3. Both leisions 60% cases
69.
70. IN ENAMEL: A triangular outer lesion is seen which
continues with the dentinal lesion along the dentinal
wall. Both lesions are walled by dark zone.
IN DENTIN: Appearance can be-
1. Superficial demineralization of cavity walls
2. Subsurface demineralization without visible changes of
wall surface
3. Subsurface demineralization with increased
mineralization of surface layer
4. Alternating zones of demineralization and
remineralization.
71.
72.
73. Dental caries is the result of the metabolic activities of bacteria in
microbial communities on teeth termed dental biofilms (often
referred to as dental plaque)
Hence, the presence of microbial communities on the
tooth surface is a prerequisite for caries lesions to
develop
Although there are different opinions as to how and which
microorganisms produce carious lesions, it is agreed that caries
cannot occur without microorganisms
73
74. The prevalence of dental caries (i.e., the
percentage of persons with >1 decayed, missing,
or filled teeth) in permanent teeth increases with
age, from 26% among persons aged 5--11 years to
67%among persons aged 12--17 years and 94%
for dentate adults (with >1 natural teeth) aged
>18 years.
75.
76. Complex ecology of the oral cavity.
■ 300 – 400 species are indigenous oral flora.
■ History:
▪ Miller (1880): Little knowledge about bacteria.
▪ Clarke (1924): First who associate bacteria with dental caries
oFirst to isolate MS from human dental caries
oFirst to produce caries in extracted teeth.
▪ Orland (1955):Used animals to induce dental caries using
MS.
77. 1924: Clark recovered Gram-positive cells
1960:Fitzgerald & Keyes found caries-
conducive streptococci to be Streptococcus
mutans
78. What is virulence?
The ability of a bacterium to cause infection.
Virulence factors: Two types:
▪ Those that promote bacterial colonization and
invasion of the host tissue
▪ Those that cause damage of the host tissue.
79. The bacterium should be found in people with
the disease
The bacterium should be isolated from the
lesions of infected person
Pure culture, inoculated into a susceptible
individuals or animals should produce the
disease
Same bacterium should be re-isolated from
intentionally infected animals or humans.
80. Virulence is within the bacterium and is
independent of the host
Isolation and growth of bacterium is necessary:
Yet, some pathogens not yet cultured
Nos. 2 & 4: assume that all members of the
same species are virulent
No. 3: Ethics with human subjects, Yet some
pathogens from humans can not cause the
same effect in animals.
84. An organism must be acidogenic
An organism must be aciduric
An organism must exhibit tropism for teeth
An organism must utilize refined sugar
(sucrose)
(Newburn, 1983)
89. Mutans Streptococci
S. mutans
S. sobrinus
Viridans Streptococci
S. mitis
S. salivarius
S. sanguinis
90. 90
Pit and fissure caries-
most common carious lesions found in humans
Fissures provide mechanical retention for the
bacteria. S mutans, S salivarius, S sanguis, L
acidophilus, L casei, A viscous, A nalsundii,
Actinomyces israelii develop fissure lesions
91. Smooth surface caries-
A limited number of organisms have proved
able to colonize smooth surfaces in large
enough numbers to cause decay in test animals.
Streptococcus mutans is very significant in this
respect.
91
92. Root caries-
In rodents, gram – positive filamentous rods, including
actinomyces species have been associated with this type of
lesion
Strains of Nocardia and S. sanguis may also cause root caries
In cross-sectional studies of plaque overlying carious root
surfaces, mutans streptococci, alone or in combination with
lactobacilli, have been isolated more frequently or in higher
proportions than on sound root surfaces
(Billings etal., 1985;Brown etal., 1986;Fure etal., 1987;Keltjens etal., 1987;
Bowden et al., 1990; van Houte et al., 1990)
92
93. Deep dentinal caries-
Because the environment in deep dentinal
lesions is different from that at other
locations the flora here is also different
The predominant microbe- lactobacillus
93
94. Secondary caries resembles Pit & Fissure caries
3 associated microbes-
■
■
■
S. mutans
Lactobacillus
Actinomyces viscous
The presence in significant nos. of these bacterias in
dentin of Secondary caries indicates their role in
formation & development of Secondary carious lesions
(Gonzalez- Cabezas; 1999).
Definite relationship between S. mutans & Secondary
caries
(Fontana et al;1996)
94
95. Irrespective of the age of plaque and the diet, the
predominant organisms are gram-(+)ve cocci of the
genus streptococcus which form about 50%of the
total CFU recovered from young plaque
These streptococci have been divided into various
groups based on their colonial morphology and
physiological characteristics
Oral streptococci are isolated on Mitis-Salivaris
Agar, a selective medium that permits isolation from
mixed flora
95
96. In 1924Clarke isolated a streptococcus that
predominated in many human carious lesions
He named them streptococcus mutans because
of its varying morphology
Characteristics of S. mutans include
■
■
■
■
■
■
Nonmotile
Catalase negative
Gram positive
Cocci in short or medium chains.
Opaque, cushion shaped colony on Mitis–
Salivarius bacitracin Agar
Colony surface resembles frosted glass 96
98. TYPES: (Coykendall, 1989)
■ S. anginosus : important in purulent infections
■ S. bovis : found in patients with colon cancer
■ S. mitis : similar to sanguis but doesn’t ferment any
sugar
■ S. mutans : seven species (9 species – recent data)
■ S. salivarius : in saliva, rare in infections
■ S. sanguis : causes endocarditis
■ S. vestbularis : new species from oral cavity.
99. Species Serotype Arg Raf Mel H2O2 Aero Baci Source
Human
S mutans c, e, f - + + - + -
S rattus b + + + - + -
S cricetus a - + + - - +
S sobrinus d, g - - - + + -
S ferus c - - - - - +
S macacae c - + - - - +
S downei h - - - - - +
Rats
Rats
Human
Rats
Monkey
Monkey
101. Three factors:
▪ Ability to adhere to other bacteria and tooth surface
▪ Ability to rapidly metabolize nutrients (CHO)
▪ Ability to tolerate acidic environment.
103. PBP*
(Adapted from Slots & Taubman,
1992)
*PBP: Pellicle Binding Protein
Initial Attachment
Pellicle glycoprotein
S. mutans
104. Sucrose Glucose Fructose
+
GTF-S** GTF-I*
GTF Binding Glucans
Glucans
*Insoluble form (-1,3-linked) “Mutan” – polymerized by GtfB
**Soluble form (-1,6-linked) “Dextran” – polymerized by GtfD
GtfC responsible for a mixture of -1,3 & -1,6
(Adapted from Slots & Taubman,
1992)
105. (Adapted from Slots &
Taubman, 1992)
Pellicle Glycoprotein
Glucan
Binding
Protein
Glucans
Aggregation
S. mutans
S. mutans
S. mutans
106. Through cell membrane, extrusion of protons:
▪ Membrane ATPase hydrolyze ATP molecules
▪ Hydrolysis of one ATP, results in extrusion of three
protons
▪ This results in elevation of cytoplasmic pH.
▪ When pH decreases, ATPase activity increases 4-
folds.
107. Based on ability of S. mutans to synthesize
insoluble glucan.
S. mutans have 3 genes:
▪ gtfB encodes GTF-I enzyme: insoluble glucan
▪ gtfC encodes GTF-SI enzyme: insoluble glucan
▪ gtfD encodes GTF-S enzyme: soluble glucan
109. Sterile mouth at birth
S. sanguis and S. mutans colonize teeth
Number of bacteria increases in the presence
of:
▪ Sucrose
▪ Caries
▪ Teeth
110. ACQUISITION OF S. mutans
Birth 5 Year
19 33
First Tooth
6.8 +/- 1.4 mo.
MS
26
N=38
Caufield et al., J Dent Res. 72:37-45, 1993.
111. Important facts:
▪ Difficult to change S. mutans strain(s)
▪ High number of S.mutans strains and isolates.
▪ One (or more) strain (isolates) is/are present in the
mouth.
113. Lactobacilli are -
Gram (+)ve
Non-spore forming
Rods
Grow best under microaerophilic conditions.
Represents about 1% of the oral flora.
Favorite habitat of lactobacilli is in the dentin
of deep carious lesions.
Relatively low affinity for tooth surface.
113
114. Preferentially colonize the dorsum of the
tongue
Does NOT play a major part in initiation,
but important in progression
With established low pH the number of
lactobacilli increases and the number of S.
mutans decreases
Contribute to the demineralization of the
teeth once lesions are established
114
115. 115
It is a gram positive, non motile, non spore
forming organism occurring as rods and
filaments. It is a good plaque former
All species of actinomyces ferment glucose,
producing mostly lactic acid, lesser amounts of
acetic and succinic acid, and traces of formic acid.
Most interest has centered on A viscosus and A
naeslundii because of their ability to induce root
116. 116
All species of actinomyces ferment
glucose, producing mostly lactic acid,
lesser amounts of acetic and succinic
acid, and traces of formic acid
117. Anaerobic bacteria
Taxonomically distant from streptococci but
have very similar sugar metabolism and can
produce lactic acid.
Although well-known as gut inhabitants, it is
only quite recently that their occurrence in the
mouth and possible association with caries has
been recognized
This change in viewpoint is because
■ introduction of molecular detection methods
■ the development of a selective medium using
mupiromycin to suppress growth of other bacteria 117
118. S.Mutans has the central role in etiology
of dental caries
If We understand the dental caries microbiology well, we
will be able to treat patients differently
It is of paramount value that the term “dental caries” not be
equated with “cavities” by dentists. The lesion is not the
disease, but the effect of the disease. The disease does not
occur without infection by cariogenic bacteria
To prevent, detect, and manage caries throughout life one
must not be restrictively focused on the end result of the
disease, cavities 118