Title | CARIOLOGY MODULE NOTES |
---|---|
Author | Beatrice Traballo |
Course | Dentistry |
Institution | Centro Escolar University |
Pages | 13 |
File Size | 534.3 KB |
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Cariology lecture notes for dentistry students...
CARIOLOGY M1Lesson 1: Definition of Dental Caries the Disease and Some Related Terminologies Caries- Latin meaning ‘dry rot’; slow disintegration of any biological hard tissue as a result of bacterial action ubiquitous - it is omnipresent in all populations and is as old as mankind definitions of caries:
WHO - defined it as a localized posteruptive, pathological process of external origin involving softening of the hard tooth tissue and proceeding to the formation of a cavity GV Black - the chemical dissolution of the calcium salts, first of the enamel then of the dentin by lactic acid Shafer - gave his definition as irreversible microbial disease of the calcified tissues of the teeth characterized by demineralization of the inorganic portion and destruction of organic substance of the tooth Kess and Ash- a disease involving hard portions of the teeth which are exposed in oral cavity and is characterized by disintegration of enamel, dentin and cementum forming open cavities. Last - an illness due to specific infectious agent or its toxic products that arises through transmission of that agent or its products from an infected person, animal or reservoir to a susceptible host. Sturdevant - defined it as an infectious microbiologic disease of the teeth that results in localized dissolution and destruction of calcified tissues. GJ Mount - is perceived to be a prolonged imbalance in the oral cavity such that the factors favoring demineralization
of enamel and dentin overwhelm the factors that favor remineralization and repair of those tissues. Cawson - progressive, irreversible bacterial damage to teeth exposed to the oral environment. Kidd and Smith - a disease of the calcified tissues of the teeth caused by the action of micro-organisms on fermentable carbohydrates. Lundeen - an infectious microbiological disease that results in localized dissolution and destruction of the calcified tissues of the teeth and progresses as a series of exacerbations and remissions. Ernest Newburn - tooth decay, is a pathological process of localized destruction of tooth tissues by microorganisms. Ostrom - a process of enamel or dentin dissolution that is caused by microbial action at the tooth surface and is mediated by physiochemical flow of water dissolved ions. Hume - essentially a progressive loss by acid dissolution of the apatite (mineral) component of the enamel then the dentin, or of the cementum, then dentin. Fejerskov and Nyvad - a complex disease caused by an imbalance in physiologic equilibrium between tooth mineral and biofilm fluid. Selwitz - a multifactorial disease that starts with microbiological shifts within the complex biofilm and is affected by salivary flow and composition, exposure to fluoride, consumption of dietary sugars and by preventive behaviours (cleaning teeth). Sikri - Dental caries is an infectious disease caused by imbalance of oral micro-organisms leading to acid production and subsequently dissolving the hard tissues of tooth.
definition of dental caries by unidentified authors:
Dental caries, also known as tooth decay/cavity, is a disease where bacterial processes damage hard tooth structure (enamel, dentin and cementum). These tissues progressively breakdown, producing dental cavities (holes in the teeth). A disease of the teeth resulting in damage to tooth structure. The bacterial disease that causes demineralization of teeth through exposure to sugars and starches. Decay of teeth due to penetration of bacteria through the enamel to the dentin. A disease of teeth in which micro-organisms convert sugar in the mouth to an acid that erodes the tooth, commonly called a cavity. A destructive process causing decalcification of tooth enamel and leading to continued destruction of enamel and dentin.
Related Terminologies Caries may be classified status and activity status.
based
on
Dentin caries- into dentin.
Coronal caries- in any surface of the anatomic tooth crown.
Root caries- in the root surface.
Primary caries- not adjacent to an existing restoration or crown.
Secondary or Recurrent caries- adjacent to an existing restoration, crown or sealant.
Residual caries- carious tissue that was not completely excavated prior to placing a restoration.
Cavitated caries lesion- results in the breaking of the integrity of the tooth, or a cavitation.
Non-cavitated caries lesion-has not been cavitated. In enamel caries, non-cavitated lesions are also referred to as “white spot” lesions.
Active caries lesion- considered to be biologically active which tooth demineralization is in frank activity at the time of examination.
Inactive caries lesion- considered to be biologically inactive at the time of examination, that is, in which tooth demineralization caused by caries may have happened in the past but has stopped and is currently stalled. Also referred to as arrested caries meaning that the caries process has been arrested but that the clinical signs of the lesion itself are still present.
Rampant caries- the presence of extensive and multiple cavitated and active caries lesions in the same person. Typically associated with “baby bottle caries,” “radiation
location, cavitation
Caries Lesion- Tooth demineralization as a result of the caries process. Other terms used are carious lesion or in layman’s term- cavity.
Smooth-surface caries- on a smooth tooth surface.
Pit-and-fissure caries- caries on a pit and fissure area
Occlusal caries- caries lesion on an occlusal surface.
Proximal caries- on a proximal surface.
Enamel caries- in enamel, typically indicating that the lesion has not penetrated into dentin.
therapy caries,” or “meth-mouth caries.” These terms refer to the etiology of the condition M-1 Lesson 2: Contributing Factors to the Development of Dental Caries Dental caries- a multifactorial because its development is dependent on the interaction of the four primary factors: the host (tooth surface), a substrate (carbohydrates), presence of oral bacteria (in the biofilm) and time Factors that cause caries according to Keyes Jordan diagram Personal factors:
sociodemographic status income dental insurance coverage knowledge attitude oral health literacy behavior: oral hygiene and smoking education
oral environment factors:
saliva- buffer capacity, composition, flow rate sugars- clearance rate, frequency protein Ca+2, PO4-3 Plaque ph, microbial species chewing gum fluoride dental sealants antibacterial agents
factors that directly contribute to caries development:
tooth time bacteria in biofilm diet- amount, composition, frequency
Caries balance the balance between demineralization and remineralization of the tooth. It is illustrated in terms of pathologic factors- or those favoring demineralization, and protective factors- or those favoring remineralization. At the tooth level, dental caries activity is characterized by localized demineralization and loss of tooth structure, the caries lesion. Some bacteria in the biofilm metabolize refined carbohydrates for energy and produceorganic acid by-products. These organic acids, if present in the biofilm ecosystem for extended periods, can lower the pH in the biofilm to below a critical level (5.5 for enamel, 6.2 for dentin). This low pH has effects both on the biofilm composition and at the tooth surface level. With extended periods of low pH there is a shift in the microbiome to bacteria that are acidogenic and acidophilic, causing a dysbiosis in the microbiome. This change in turn will lead to further acidification of the environment. The low pH drives calcium and phosphate from the tooth to the biofilm to reach equilibrium, hence resulting in a net loss of minerals by the tooth or demineralization. When the pH in the biofilm returns to neutral and the concentration of soluble calcium and phosphate is supersaturated relative to that in the tooth, mineral can then be added back to partially demineralized enamel in a process called remineralization. M1 Lesson 3: Etiology and Theories of dental caries
From powerpoint:
(1) Acidogenic Theory
Dental caries
(2) Proteolytic Theory (3) Proteolysis-chelation Theory
progressive
initially subsurface bacterial acid
one of the most common of all diseases
major cause of loss of teeth
considered a
biological process of tooth decay with mutifactorial etiology
demineralization of teeth by
disease of modern
civilization
microbial disease of calcified tissues of teeth
characterized by demineralization of inorganic portion
Etiology of Dental caries OLD THEORIES: Exogenous Theories: (1) Legend of worm (2) Chemical Theory (3) Parasitic or Septic Theory Endogenous Theories: (1) Humoral Theory (2) Vital Theory NEW THEORIES:
Old theory (Exogenous theory): Legend of the tooth worm
5000 BC ancient Sumerian text obtained from Mesopotamian area caused by worm that drank blood of teeth fed on roots of jaws
Old theory (Exogenous theory): Chemical Theory
1819 proposed by Parmly unidentified chemical agent responsible for caries stated that caries began on enamel surface where food putrefied acquired sufficient dissolving power to produce disease chemically Old theory (Exogenous theory): Parasitic or Septic Theory
1843 proposed by Erdl filamentous parasite in plaque he termed as “Denticolae” responsible for dental caries
Old Theories (Endogenous Theory): Humoral Theory 4 humors of body
blood phelgm black bile yellow bile any change in relative causes disease
proportion of these elements
Old Theories (Endogenous Theory): Vital Theory 18 century tooth decay originated within the tooth itself New Theories chemicoparasitic
(exogenous
like bone gangrene, from Theory):
Acidogenic/
1890 WD Miller dental decay is a chemoparasitic process consisting of 2 stages 2 stages: 1. Decalcification of enamel – results in total destruction 2. Decalcification of dentin as a preliminary stage. Followed by dissolution of softened residue Factors that cause decay: •
1) ― ― 2)
role of carbohydrates - Food substances act as substrate for microorganisms of dental plaque cariogenicity of carbohydrate varies with: frequency of ingestion Taken repeatedly in between 2 major meals Provides constant supply of carbohydrate to plaque bacteria for fermentation + production of acids physical form
― ― 3) ― ― ― 4) ― 5) ― • ― •
•
sticky solid carbohydrates chemical composition in the form of glucose, sucrose fructose rapidly diffuse into plaque make themselves easily available for fermentation by plaque bacteria route of administration Oral intake of sticky food presence of other food constituents Refined pure carbohydrates more caries producing role of microorganisms- caused by acid resulting from action of microorganisms on carbohydrates S. mutans has been proved for the initiation of caries role of acids- play most important role in pathogenesis of dental caries pH 5.5 is called critical pH below this pH demineralization of tooth substance begins role of dental plaque
― Found on unclean tooth surfaces ― Appear as tenacious, thin film ― May accumulate within 24-48 hours New Theories (exogenous Theory): Proteolytic theory proposed that enamel lamellae or rod sheath (proteins) may be lysed which means proteolysis as first event in further progression of bacterial invasion + demineralization = carious lesion New Theories (exogenous Theory): Proteolysis-chelation theory
suggests that caries is caused by simultaneous events of proteolysis + chelation proteolysis- destruction of organic portion of tooth by proteolytic microorganisms chelation- removal of calcium by forming soluble chelates M1 Lesson 4: Histological and Clinical features of dental caries Dental caries lesions- are the outcome or symptoms of innumerable metabolic events in biofilms which have covered the tooth surface three distinctly different clinical site for caries initiation:
Developmental pits and fissures of enamel, which are the most susceptible sites Smooth enamel surfaces that shelter cariogenic biofilm Root surfaces
M-2: PRE-TASK
The attempts to understand dental caries etiology started in 5000 BC, when the cause of dental caries was described as a tooth worm. This theory of the tooth worm was rejected by Pierre Fauchard, who is known as the father of modern dentistry. In the 1680s, van Leeuwenhoek discovered microorganisms in the tartar taken from his teeth. He drew the microbes in his notebook, which are known now as cocci, fusiform and spirochetes bacteria. (He and Shi, 2009) The development of caries was believed to be caused by only a few gram-positive bacterial species, such as Streptococcus mutans, Streptococcus sobrinus and lactobacillus. This understanding was based on cultivation studies by isolating
these bacteria and determining their cariogenic properties. This is called the specific plaque hypothesis. It became evident that a caries lesion could happen in the absence of these putative pathogens. Current evidence states that population groups and individuals are susceptible to dental caries with a low level of S. mutans, and vice versa. (Marsh, 2009)
M-2 Lesson 1: The Microbiology of Dental Caries THE RESIDENT MICROFLORA It has been estimated that the human body is composed of approximately 1014 cells, of which 105 are mammalian. The majority are the organisms that comprise the resident micrflora of the host. Acquisition of this resident microflora occurs from birth and is a natural process, during which all environmentally exposed surfaces of the body become colonized. The organisms that establish and predominate on particular surfaces vary, however, depending on the biological and physical properties of each site. The mouth is no exception during to this process, and distinct species of bacteria can be recovered from the mouth of infants only a few hours old. Once established, the resident microflora gas a diverse composition, consisting a wide range of Gram + and Gram bacterial species, as well as yeast and other types of microorganism. In addition, the composition of the oral microflora will change as the biology of the mouth alters over time.
Table 1: Microorganisms Present During Post- Natal Life (Newman and Carranza, 2018)
SITE AND DISTRIBUTION OF ORAL BACTERIA Although the mouth is highly selective for the microorganisms that are able to colonize and become established, more than 700 different types have been detected in the mouth. The mouth is not a homogeneous environment for microbial colonization. Distinct micro-habitats (niches) exists and these can serve as reservoir for many species commonly found in dental plaque. Figure 1: Ecosystem (Niches) of Oral Cavity According to a study conducted by Xiaojing et al. in 2000, the anatomic closeness of these microfloras to the blood stream can facilitate spread of bacterial products, components and immunocomplexes to the other parts of the body that may be associated with different systemic disease.
M-2 Lesson 2: Saliva and Caries Development
2. Direct antibacterial activity
What is saliva?
Salivary glands produce an impressive array of antimicrobial products.
Saliva is composed of more than 99% water and less than 1% solids, mostly electrolytes and proteins, the latter giving saliva its characteristic viscosity. The term ‘saliva’ refers to the mixed fluid in the mouth in contact with the teeth and oral mucosa, which is often called ‘whole saliva’. Normally, the daily production of whole saliva ranges from 0.5 to 1.0 liters. Ninety per cent of whole saliva is produced by three paired major salivary glands, the parotid, submandibular and sublingual glands. Secretions from the many minor salivary glands in the oral mucosa also contribute, although only somewhat less than 10%. Salivary protective mechanisms that maintain the normal oral flora and tooth surface integrity include: 1. Oral clearance An important function of saliva is to dilute and eliminate substances. This is a physiological process usually referred to as salivary clearance or, more commonly, oral clearance. The flushing effect of salivary flow is, by itself, adequate to remove virtually all microorganism not adherent to an oral surface. The flushing is most effective during mastication or oral simulation, both of which produce large volumes of saliva.
Lysozyme, lactoperoxidase, lactoferrin, and agglutinins possess antibacterial activity. These salivary components are not part of the immune system but are part of an overall protection scheme for mucous membranes that occur in addition to immunologic control. These protective proteins are present continuously at relatively uniform levels. The normal resident oral flora apparently has developed resistance to most of these antibacterial mechanisms. 3. Buffer Capacity The buffering capacity of the saliva is determined primarily by the concentration of bicarbonate ion. The benefit of buffering is to reduce acid formation. In addition to buffers, saliva contains molecules that contribute to increasing biofilm pH. These include urea and sialin, which is a tetrapeptide that contains lysine and arginine. Hydrolysis of either of these basic compounds results in production of ammonia, causing the pH to increase. Because saliva is crucial in controlling the oral flora and the mineral content of the teeth, salivary testing should be done on patients with high caries activity. 4. Remineralization Saliva and biofilm fluid are supersaturated with calcium and phosphate ions. Without a means to control precipitation of
these ions, the teeth literally would become encrusted with mineral deposits. Saliva contains statherin, a proline-rich peptide that stabilizes calcium and phosphate ions and prevents excessive deposition of these ions on teeth. This supersaturated state of saliva provides a constant opportunity for remineralizing enamel and can help protect teeth in times of cariogenic challenges. M-2 Lesson 3: Biofilm and Caries Development DENTAL BIOFILM: DEVELOPMENT, COMPOSITION AND PROPERTIES
STRUCTURE,
In order for the oral microorganisms to persist, they have to attach to a surface and grow: otherwise they will be lost from the habitat. An important relatively recent discovery is that the properties of microbial cells forming a biofilm are distinct from those expressed when microorganisms are growing as individual cells in a liquid culture. This has led to a novel interest in trying to understand the dental biofilm mode of growth. The development of dental biofilms can be divided into several arbitrary stages, as revealed by experimental studies in situ (Nyvad, 1993)
Figure 1: Schematic Diagram of Biofilm Formation I. Pellicle Formation Microorganisms do not colonize directly on the mineralized surface. The teeth are always covered by an acellular proteinaceous film (Pellicle), which ...