1
DEFINITION AND ETIOLOGY OF DENTAL CARIES
Seminar By
Dr. S. HIMAGIRI Postgraduate Student
DEPARTMENT OF CONSERVATIVE DENTISTRY & ENDODONTICS SRI RAMACHANDRA DENTAL COLLEGE AND HOSPITAL CHENNAI
2
CONTENTS INTRODUCTION
1
DEFINITION OF DENTAL CARIES
2
THEORIES
3 EARLY THEORIES RECENT THEORIES HUMORAL THEORY VITAL THEORY ACIDOGENIC THEORY PROTEOLYTIC THEORY PROTEOLYTIC CHELATION THEORY
CONTRIBUTING FACTORS IN DENTAL CARIES
18
TOOTH FACTOR COMPOSITION MORPHOGENIC CHARACTERISTIC POSITION SALIVA COMPOSITION PH QUANTITY VISCOSITY ANTIBACTERIAL FACTOR DIET PHYSICAL FACTORS QUALITY OF DIET LOCAL FACTORS CARBOHYDRATE VITAMIN FLUORIDE CARIES PROCESS
30
3
INTRODUCTION Dental caries is the most prevalent chronic disease affecting the human races, and it affects persons of both sexes, and socio-economic data, and every age group.
Anthropologic studies of vanlenhossek
revealed that the dolichocephalic skulls of men from preneolithic periods (12000 BC) did not exhibit dental caries. But skulls from brachycephalic men of Neolithic period (12000 to 30000 BC) contain carious teeth. Thousand years ago Sumerian, and the Chinese offered worms as the cause of the disease. Incidence of caries of individual teeth. Upper and Lower I molar Upper and Lower II molar Upper II premolar Upper I premolar Lower II premolar Upper central and lateral Upper cuspid and lower I
= = = = = = =
95% 75% 45% 35% 35% 30% 10%
premolar Lower central and lateral Lower canine
= 3% = 3%
Dental caries the word derived from Greek ROT = Decay (Latin) KER = Death (Greek) Chinese employed mush ha, meaning Hallow = Dental caries. Benjimin and Franklin is said to have, stated that hot things, cold things, sharp things, sweet things, all rot the teeth, and make them look like old things.
DEFINITION OF DENTAL CARIES
4 According to Shafer, dental caries is a microbial disease of the calcified tissues of teeth, characterized by demineralization of organic portion, and destruction of the inorganic portion of the tooth. According to Radkie’s, he defines tooth as one that shows resistance to removal of a sharp dental explorer from the tooth surface after the application of moderate pressure such definition does not account for white spot lesion. According to Soben Peter it is a progressive, irreversible microbial disease affecting the hard parts of teeth, expose to the oral environment resulting
in
demineralization
destruction,
thus
leading
to
cavity
formation. According to Johnson and Beighton it is customally explained as a series of physiochemical phenomenon in which acids produced by metabolism
of
dental
plaque
by
bacteria,
produce
subsurface
demineralization of tooth tissue. According to Hairy Laurajansen, dental caries or tooth decay is localized destruction of teeth by microorganisms.
ETIOLOGY OF DENTAL CARIES Etiology of dental caries is generally to be a complex problem complicated by many indirect factors. However some chief theories have evolved through years of investigation and observation. Theories classified in two ways
I. EARLY THEORIES
5 The legend of Worm (5000 B.C)
According to this theory tooth decay due to the worms.
Treatment was acupuncture.
II. RECENT THEORIES Sub-classified in two ways. A) Endogenous
Humoral Theory
Vital Theory
B) Exogenous
Chemico parasitic
Proteolytic
Proteolytic chelation
ENDOGENOUS HUMORAL THEORY Four elements of the body were blood, phlegm, yellow bile, and black bile.
According to Gallen caries produced by internal action of
acrid and corroding humors. According to Hippocrates stated that stagnation of juices in the teeth was the cause of toothache, and also referred debris around the teeth and their corroding acids causes decay. VITAL THEORY Introduced in 18th Century According to Vital theory decay originated like bone gangrene from with in the tooth itself.
EXOGENOUS
6 ACIDOGENIC (OR) CHEMICO PARASITIC THEORY In 1882 W.D. Miller introduced Acidogenic theory.
According to
W.D. Miller he stated dental decay is Chemico-parasitic process consisting of two stages, the decalcification of enamel, which results in its total destruction and total decalcification of dentin as a preliminary state followed by dissolution of the softended residue.
The acid that
effects the primary decalcification of enamel dentin is released by fermentation of starch, sugar lodged in the retaining centers of the teeth. The bulk of scientific evidence does implicate, carbohydrates, oral microorganisms and acids. ROLE OF CARBOHYDRATES A carbohydrate is an important ecologic factor to produce dental caries.
The cariogenicity of a dietary carbohydrate varies with the 1. Frequency of ingestion. 2. Physical form 3. Chemical composition 4. Root of Administration.
Frequency of ingestion is directly proportional to development of caries
Sticky solid carbohydrates are more caries producing than those consumed as liquid.
Polysaccharides are less easily fermented by plaque bacteria, than mono and disaccharides.
Refined pure carbohydrates are more caries producing than crude carbohydrates.
ROOT OF ADMINISTRATION
7 Glucose or sucrose is fed entirely by stomach. contributes
to
dental
caries,
because
unavailable
I.V. dose not for
microbial
breakdown, if glucose (or) sucrose consumed through oral cavity it is readily fermented by bacteria. PATHOGENIC PROPERTIES OF CARIOGENIC BACTERIA Cariogenic bacteria is according to I.
Such bacterial rapidly ferments the carbohydrate compare to other plaque bacteria and it produce acids e.g. Streptococcusmutans.
II.
The production of extra cellular and intracellular polysaccharides. Extra cellular polysaccharides include glucans and Fructans it constitutes the formation of plaque, but latter are labile and it can be metabolized under carbohydrate-restricted condition. Intracellular polysaccharides are glycogen like storage compounds that can be used for energy production and converted into acid, when free sugars are not available.
III.
The pathogenic bacteria they can liable at low pH and preferentially it grows and metabolize. These
properties
make
cariogenic
bacteria
potentially
more
comparative than most other plaque species under conditions of high sugar and low pH and contribute for developing caries. In vitro studies Miller showed that when the teeth were incubated in saliva mixed with bread (or) sugar decalcification occur.
But
there was no effect when the teeth were incubated in saliva mixed with meat (or) fat, instead of carbohydrates.
ROLE OF MICROORGANISMS
8 Three basic groups of microorganisms predominate in dental caries.
Streptococcus mutans, sanguis, mitis, salivarious,
Gram-positive cocci.
Milleri.
Actinomyces ) A – Viscosus,
A – Nauslundi
Gram positive Bacilli
A - Israeli, Rothia denticariosa
Veillonellae, V.parvula,
Among these bacteria’s streptococcus mutans is the chief etiologic agent in human dental caries.
MECHANISM OF PRODUCING DENTAL CARIES The microorganisms that degrade carbohydrates and produce acids.
These acids are responsible for demineralization of enamel and
dentin. MICROBIAL COMPOSITION OF DENTAL PLAQUE IN HEALTH Bacteria
Fissure
Streptococcus (+ Ve) Actinomyces (+ Ve) Lactobacilli (+ Ve) Velionella Fusobacterium (- Ve) Spirochetes (- Ve) Gram – Ve Anaerobes
++++ +++ +/+/++ -
(-) (+/-) +
Proximal
Gingival
+++ ++++ +/+++ + +
Crevice +++ +++ +/++ ++ + ++
=
Indicate
not
= =
present Detected on occasions Present in low proportions
commonly
9 ++++
=
Present
in
high
proportions
In fissures predominate bacterial is gram +ve, streptococci.
But Gram – ve anaerobes are detected occasionally.
In
contrast
to
fissures
Gram-ve
anaerobes
are
more
predominant in gingival crevicular fluids.
Before they stated that lactobacilli are chief bacteria producing caries.
But now they believed that it does not cause the
disease but progress the disease.
E.g. L. Acidophilus, L.
Salivarious. MICROBIOLOGIC
ASPECTS
OF
DENTAL
PLAQUE
AND
DENTAL
CARIES Dental caries is the localized destruction of the tissues of the tooth by acids, particularly lactic acid produced by fermentation of dietary carbohydrates by bacteria in dental plaque. Later stages it involves the proteolytic break down of the collagen matrix in the deeper tissues such as the dentine. The microorganisms implicated in dental caries are located in the complex biofilm overlying the tooth surface.
This biofilm is termed
Dental Plaque.
FORMATION STRUCTURE AND ORGANIZATION OF DENTAL PLAQUE Microorganisms are never come into contact with a clean tooth surface immediately after tooth has been cleaned, molecules are derived from saliva, GCF, are absorbed to the enamel and cementum surface this
10 thin conditioning film is referred to as the “Acquired Pellicle� then microbes are interact with the polymeric layer. The development of dental plaque can be divided in to the several arbitrary stages. These stages are as follows. I.
The absorption of host and bacterial polymers to the tooth to form a surface conditioning film (the acquired pellicle).
II.
The transport of microorganisms to the polymer coated tooth surface generally this is passive process. Facilitated by salivary flow because of most of the bacteria are non motile.
III.
Long term physiochemical interactions between the microbial cell surface and pellicle coated tooth, the inter play of Vander walls attractive forces and electrostatic repulsion due to the interaction of charged molecules on the bacterial cell surface and conditioning film produce reversible adhesion.
IV.
They develop steriochemical interactions between adhesions on the microbial surface and receptors in the acquired pellicle. This interaction usually results in irreversible adhesion. Antigens like I / II found in streptococci mutans.
Eg.
These
antigens are capable of binding salivary glycoprotein and other microbial cells, calcium. V.
Co-aggregation After attachment to the tooth surface bacteria start to multiply to increase the diversity of the plaque microbial flora. But obligatory anaerobic bacteria not bind to acquired pellicle if attached to the other microorganisms.
Eg. Streptococci,
Actinomycetes. VI.
The multiplication of bacteria it produce confluent growth and biofilms.
Then bacteria synthesize extra cellular polymer
(Glucans) produced by fermentation of sucrose i.e., especially streptococcus
mutans,
glucans
microorganisms to tooth structure.
that
provide
adhesion
of
11 VII.
Detachment of cells from the biofilms in to saliva facilitating
colonization of fresh sites. CURRENT
HYPOTHESIS
TO
EXPLAIN
THE
ROLE
OF
PLAQUE
BACTERIA IN THE ETIOLOGY OF DENTAL CARIES. Role of plaque in dental caries is explained by two schools of hypotheses. 1. Specific plaque hypotheses 2. Non specific plaque hypotheses Specific plaque hypotheses propose that specific bacteria that present in the plaque they produce dental caries. This hypothesis given by “Hoesche� in 1976.
This proposal is valuable because it focuses
efforts on controlling disease by targeting preventive measures and treatment against a limited number of organisms. Non-specific plaque hypotheses stated that, disease is outcome of overall activity of the total plaque microbial flora. Recently alternative hypotheses have been proposed that they reconcile the key elements of the earlier two hypotheses in brief. The recent hypothesis is called ecological plaque hypotheses. This hypothesis proposes that the organisms associated with disease may also present at the sound sites but all level too low to be clinically relevant. Disease is a result of shift in the balance of the resident microflora driven by a change in local environmental condition.
Excessive Sugar
Acid Production
Neutral pH
S. Sangius S. Oralis
Remineraliz ation
Low
Lacto bacilli S. Cocci
Dental Caries Demineralization
pH
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STRUCTURE OF DENTAL PLAQUE Well-established plaque consists of mainly cocci and bacilli filamentary bacteria and fusiform bacteria.
The structure shows
accumulation of dead or metabolically inactive cells near the pellicle. The filamentous bacteria may orient themselves to enamel surface and producing “palisade effect sometimes cocci grown on the surface of filamentous microorganisms and gives “corn cob” appearance. Glycogen like storage granules also seen in scanning electron microscope. THE ROLE OF DENTAL PLAQUE It is also known as bacterial plaque (or) microbial plaque it plays a role in dental caries process, otherwise it initiate the dental caries process.
Williams recognize it in 1897, and he demonstrated in histologic preparation.
G.V. Black, he observed and stated that plaque as important in the carious process, and it is described as the gelatinous, thin, transparent film usually escapes observation, and which is revealed only by careful observation and tenaciously adherent to the tooth structure known as plaque.
It is also known as bacterial plaque,
because of it is completely composed of bacteria and their by products. PLAQUE COMMUNITIES AND HABITATS There are significant differences in the plaque communities found in various habitats.
13 Habitat Mucosa Tongue Tooth (Non carious) Gingival crevice Root caries Enamel caries
→ → → → → →
Predominant species S.mitis, S.sanguis, Salivarious (+ Ve) S.Salivarious, Mutans, Sangius (+ Ve) Stangius (+ Ve) Actinomyces, Spirochates Lactobacillus, Actinomyces (+ Ve) S.mutans
Many distinct habitats may be identified individual teeth, with each habitat containing unique plaque community.
Pit and Fissure on the grown may harbor a relatively simple population of streptococci.
The root surface of gingival sulcus may harbor a complex community dominated by filamentous and spiral bacteria.
But generally it
consists of salivary components such as mucin, desquamated epithelial cells, and of microorganisms. An important component of dental plaque is dental pellicle, which forms, just prior to the formation of bacterial colonization and may facilitate plaque formation. The pellicle is glycoprotein it is derived from the saliva absorbed on the tooth surface it serves as a nutrient for microorganisms.
The pH of plaque in different persons varied but
average about 7 in caries free persons, to 5.5 in person with extreme caries.
THE PROTEOLYTIC THEORY Theory claims that the organic portion of the tooth is attached first with certain lytic enzymes this leaves the inorganic portion without a matrix support.
14 According to this theory organic portion of tooth may play an important role in the carious process.
Bodecker and Heider they demonstrated certain structures with in enamel like enamel lamellae tuffs, Rod sheaths these structures may be important in the progress of dental caries, since they could serve as a pathway for microorganisms through the enamel many other workers done investigation on organic portion of the enamel and they concluded that enamel contains approximately 0.56%organic matter of which 0.18% is a type of keratin 0.17% soluble protein like Glycoprotein and the reminder citric acid and peptides.
Gottlieb and Gottlieb (1944) Diamond and Applebaum (1946) postulated that caries is essentially a proteolytic progress the microorganisms invade the organic pathways and destroy them in their advance, and they stated acid formation accompanied the proteolysis.
Gottlieb
held
that
yellow
pigmentation
was
characteristic of caries and this was due to pigment production by proteolytic organisms.
Drizen and co-workers reported that similar type of pigmentation could be produced in vitro by the action of inter-mediatory products of carbohydrates degradation on decalcified non-carious tooth crown.
Caries of dentin was demonstrated by Frisbie and Nuckolls (1945,1947) to be similar to that occuring in enamel, these investigators also pointed out that there may be softening of dentin even through the overlying enamel appears hard and intact they believed that acid would be neutralized before penetrating full thickness of enamel. Therefore they could not cause decalcification.
Pincus (1948,1949) he proposed that Nasmyth’s membrane and other enamel proteins are muco-proteins it releases sulfuric acid upon hydrolysis.
Lending support to this theory they isolated Gr -Ve Bacilli from the oral cavity and they capable by producing the enzyme from the oral cavity and they capable of producing the enzyme sulfatase.
This
15 enzyme releases H2So4 from the muco-protein and released acid dissolve the enamel combining with calcium to form “Calcium sulfate” this compound is found in caries enamel but not in sound enamel Wislocki (1950) pointed out that sulfatase has not been demonstrated at the carious lesion.
Manley and Hardwick (1951) attempted to reconcile the two chief theories they pointed out that while the Acidogenic and proteolytic mechanisms may be separate and distinct they need not to be. Thus many
bacteria
produce
acid
from
appropriate
carbohydrates
substrate some bacteria capable of degrading protein in the absence of carbohydrate producing acids. On this statement they proposed that they might be two types of carious lesion in one type microorganism invade enamel lamellae attack enamel and involve the dentin before there is clinical evidence of caries.
In the other no
enamel lamellae is present and this alteration of enamel prior to invasion by micro organisms this alteration of enamel prior to invasion of micro organism this alteration is produced through decalcification of the enamel by acids formed by bacteria in dental plaque overlying the enamel, they early lesion produce are those typically described as “Chalky Enamel”. PROTEOLYSIS – CHELATION THEORY DEFINITION Chelation is a process involving the completing of a metallic ion to a complex substance through a coordinate covalent bond which result in a highly stable, poorly dissociated or weakly ionized compound (Chelas = Claw). Two of the most widely occuring examples are: 1. In chlorophyll molecule of green plants when four pyrrole nuclei are linked by this type of bond to magnesium. 2. In hemoglobin when four pyrrole nuclei are linked to iron by a similar bond some other examples are Citrate Amino acids,
16 hydroxy and Ketoesters of EMF pathway of glyco lysis such evidence dose not lend great strength to the theory atleast dose not contradict it. Reduced caries incidence concomitant with administration of fluoride
might
occur
through
formation
of
fluoro-apetite,
which
strengthens the linkages between the organic and in organic phases of the enamel. The proteolysis – chelation theory of dental carries is proposed by Schartz states that bacterial attack on the enamel initiated by keratinolytic micro organisms leads to breakdown of the portion and other organic components of enamel chiefly “Keratin” this result in the formation of substance which may form soluble chelate with mineralized component of tooth and there by decalcify the enamel at a neutral or even alkaline pH. Micro biotic secretions or metabolic products of microorganisms have the ability to chelate calcium from tooth substances leaving the organic matrix to be disintegrated but several reconciliation must be made if the proteolysis chelation theory is to be accepted these includes. 1) Why the caries incidence increased with the increased consumption of sugar ? Carbohydrates stagnate on non-cleansable areas and causes.
Increased production of acids by bacteria.
Producing conditions which Keratinous proteins are less stable.
2) Why the count of lactobacilli increasing the high caries activity?
Proteolysis may provide ammonia, which prevents a pH drop that would tend to inhibit growth of lactobacilli.
Chelation may encourage the growth of lactobacilli
17
Ca++
it
produce
vitamin-sparing
action
on
some
lactobacilli. 3)
Why decreasing caries with topical or systemic administration of
fluoride? Flouride interact with hydroxyapatite to form fluoro apatite this form is very resistant to acids produced by bacteria and they’re by decreasing caries incidence. CONTRIBUTING FACTOR IN DENTAL CARIES
Micro organisms
Host Dental Decay
Substrate
Can represent of key’s ring or caries triad. Later this ring was surrounded by larger one, which was labeled saliva to emphasize the importance of saliva origin of the disease
Host
Micro organisms Decay Saliva Substra te
18
HOST (TOOTH FACTOR) Whenever discussing about caries Triad host tooth factor is very important to discuss its. 1. Composition 2. Morphologic characteristics COMPOSITION. Caries susceptibility Îą
1 _________________
Ca++, F content of teeth
MORPHOLOGY G.V. Black divided tooth surfaces into 1. Self cleansable 2. Non-self cleansable. NON-SELF CLEANSABLE Areas on the tooth surface where the food can stagnate are considered non-self cleansable areas and the areas on the tooth surface where food is moving continuously are considered as self-cleansable areas. E.g.
Non-Self cleansable. 1. Pits and Fissures 2. Gingival Embrasures 3. Contact areas
19 4. Areas of near approach 5. Buccal and lingual apical to the cervical ridge. SELF-CLEANSABLE E.g. 1. Tips of cusps 2. Marginal and crossing ridges 3. All inclined planes of cusps 4. Occlusal embrasure 5. Axial angles of teeth. MALPOSITION Leads to become non-cleansable areas and increased chances of caries occurrence. AGE OF THE PATIENT Decay activity is highest between the ages of 1 to 20 years a decline the decay after 20 years due to enhanced about proper diet and oral hygiene. TIME In oral cavity prior to ingestion of carbohydrate the pH is slightly acidic or alkaline immediately after exposure to carbohydrate plaque pH drops by 2 or more pH units indicating an increase in hydrogen concentration of 1000 folds or more and this pH slowly comes in to neutral by action of diffusion of salivary buffers in to plaque. So the length of the time that pH remains low is important factor for to damage the enamel and is extremely important in dental caries. CONTRIBUTING FACTORS IN DENTAL CARIES
20 Carries has remarkable variation in person to person with same age group race, and geographic area. A workshop conference on dental caries mechanics and control technique was held at the university of Michigan in 1947.
In this
meeting they listed number of indirect factors that might influence the etiology of caries as follows. A. Tooth (A) Composition (B) Morphogenic characteristics (C) Position B. Saliva (A) Composition 
Organic

Inorganic
(B) pH (C) Quantity (D) Viscosity (E) Antibacterial factors. C. Diet 1. Physical factors A) Quality of diet 2. Local factors A) Carbohydrate content B) Vitamin content C) Flouride content Additional factor is also important here is discuss in systemic factor. TOOTH FACTOR
21 Tooth is a hard tissue; consist of enamel, dentin, pulp and cementum. Are referred to collectively as ground substance. Enamel matrix is distinctive consisting of special protein group called amelogen and enamelin. INORGANIC COMPONENT Tissue consist of crystallites of biologic apatite is essentially a calcium phosphate salt approximately in composition to calcium hydroxyapatite [Ca10 [Po4]6[OH]2]. Armstrong and Malherbe and Ockerse are studied on chemical composition of teeth i.e. [Mg, Ca++ PO4 carbonate) But no differences are found in Mg, Ca++ PO4 carbonate content of enamel from sound and carious teeth but they found significance difference in flouride content of the sound enamel and carious enamel. However Malherbe and Ockerse found the fluoride content of enamel and dentin from sound teeth and carious teeth. Sound teeth to be 410 ppm – Enamel Sound teeth to be 873 ppm - Dentin But carious teeth Enamel - 139 ppm Dentin
- 223 ppm
Armstrong
reported
that
sound
enamel
teeth
contained
0.0111±0.0020% flouride. Whereas carious teeth 0.0069 ± 0.0011% flouride. Brude vold and his associates in 1965 in his studies they indicate that surface enamel is more resistant to caries than subsurface enamel
22 because surface enamel is more highly mineralized and tends to accumulate greater quantities of fluoride, zinc, lead and iron than the underlying enamel and the surface enamel is lower in Co 2 more organic material so dissolve at slower rate in acids. So, these factors apparently contribute to caries resistance than underlying enamel. MORPHOLOGIC CHARACTERISTICS OF TOOTH Morphologic characteristic that influence the initiation of the caries are;
Mellenby suggested that enamel hypoplasia predisposes to the development of dental caries.
And that the more severely a tooth is affected the more extensive will be the caries.
Deep marrow occlusal fissures or buccal or lingual pits such fissures tend to trap food bacteria, and debris and causes caries.
TOOTH POSITION Tooth position may play role in dental caries under certain circumstances teeth, which are malalligned out of position, rotated or otherwise not normally situated may be difficult to cleanse and tend to favor the accumulation of food and debris.
But position of the teeth
seems to be a minor factor in the etiology of dental caries. DIET FACTOR The role of the diet and nutritional factors develops special consideration because of the often-observed differences in caries incidence of various populations who subsist on dissimilar physical nature of the diet. If is one factor responsible for the difference in caries experience between primitive and modern man.
23
The diet of the primitive man consisted generally of raw unrefined foods containing a great deal of rough age, which cleanses the teeth of adherent debris during the usual masticatory excursion. The presence of soil and sand in incompletely cleansed vegetables in the primitive diet induced severe attraction of both occlusal and proximal surfaces of the teeth the flattening of teeth causing a reduction in the probability of decay. In the modern diet soft refined foods tend to cling tenaciously to the teeth and are not removed because of the general lack of roughage and causes collection of debris on the tooth surface cause caries. CARBOHYDRATE CONTENT OF THE TEETH Carbohydrate content of diet is one of the most important factors in the dental carious process. Because glucose converted into lactic acid by bacteria Glucose ↓ Glucose 6 – phosphate ↓ 2 – p – Glycerate ↓ Phaspho enal pyruvate ↓ Pyruvate ↓ Lactic acid. This acid decrease pH and favors bacterial growth leads to carries. VITAMIN CONTENT OF THE DIET
24 Vitamin D is probably greatest influence in relation to dental caries. There is a general agreement of the necessary of vitamin D for normal
development
of
teeth
malformation,
particularly
enamel
hypoplasia has described in the deficiency state. Vitamin K has been tested as a possible anti-carries agent by virtue of its enzyme inhibitory activity in the carbohydrate degradation cycle. Vitamin C deficiency leads every change in periodontal tissue and pulps of the teeth calcium phosphorus disturbance in calcium and phosphorus metabolism during the period of tooth formation may result in severe enamel hypoplasia and defects in dentin leads to high risk of dental caries. VITAMIN B COMPLEX Vitamin B complex deficiency may exert a caries protective influence on the tooth since several b- vitamin are essential growth factor for the oral acidogenic flora and also severe as component of the co enzyme involved in glyco lysis. SALIVA Specific gravity is1.0012 –1.012 pH 6.02 to 7.05
COMPOSITION
25 Water – 95.5% Solids – 0.5% ↓ ----------------------------Organic (0.3%) Inorganic (0.2%) Amylase
Salts like NaCl, Kcl,
Lysosime
Calcium carbonate
Carbonic anhydrase
Calcium phosphate
Anti-bacterial components
Alkaline sodium
Maltase
phosphate
NON-PROTEIN SUBSTANCES E.g., Urea, Xanine, Uricacid, creatinine saliva is important for the health of both oral soft and hard tissues. The sources of saliva are major and minor salivary glands secretary products of these glands can be divided into two major categories. 1. Water and Electrolytes 2. Macromolecules particularly protein and glycoprotein Secretion of saliva mainly controlled by autonomic nervous system. Postganglionic parasympathetic nerve Releases Acetylcholine Stimulates Muscuranic cholinergic receptors on secretary cells Is linked to Water and electrolyte secretion
Adrenergic nerve endings – sympathetic nervous system
26 Non-epinephrine released it stimulate Adrenergic receptors located in secretary cells. In general β-adrenergic receptor stimulation is linked to protein secretions. SYMPATHETIC NERVE SUPPLY Derived from I, II thoracic segments of spinal card.
When it
stimulate
There is secretion but less quantity.
But more thicker consistency.
PARA SYMPATHETIC Arises from
Inferior salivary nucleus for parotid gland.
Superior salivary nucleus for sub-mandibular and sub-lingual gland.
It stimulates there is more secretion, but more thin (water) consistency
functional
roles
of
individual
components
of
saliva
antibacterial properties and mineralization effects. LACTOFERRIN Is an iron binding protein it shows antibacterial properties by means it binds two iron molecules and prevent the iron from being used by microorganism that require it for metabolism. LYSOSIMES Lysosimes are an enzymatic protein that has direct antimicrobial effect. ACTION
27
Lysosimes are positively charged and bind to salivary anions like HCO3-- F-- Iodide nitrate, when combined with these anions the complex binds to cell wall of bacteria and destabilize by hydrolysis of glycoside bonds in the polysaccharide component of the cell wall and allowing autolysis to take place. ORIGIN OF LYSOSIMES 1. Major salivary gland 2. Crevicular Fluid. PEROXIDASE It is produced by acinar cells of some major salivary gland salivary peroxidase enzymes contain heme and uses thiocynates and H 2O2 produced produce by oral bacteria.
It catalyze the formation of
hypocynate and cyano sulfurous acid. 1. SCN + H2O2 →
OSCN + Water Hypothocynate is inhibitor of bacterial glycolysis.
2. H++ OSCN + H2O2 → HOOSCN + Water Cyanosulfuronic acid more toxic than OSCN. It forms
when
excess
H2O2
is
released
from
bacteria. SALIVARY IMMUNOGLOBULIN IgA is produced by plasma cells located in the major and minor salivary gland.
IgA is principle immunoglobulin found in saliva the
immunoglobulin exists in saliva in approximately equal amounts of two isoforms IgA1 and IgA2.
28 IgA is a defense protein inhibiting pathogens entering the GIT and secretary IgA has also been shown to inhibit bacterial adherence to dental enamel. IgA also shown to bind to mutans facilitating bacterial aggregation and removal from oral cavity.
IgA molecules contain multivalent
antibodies and can prevent the adverse effects of bacterial toxins and enzymes.
α - AMYLASE α - Amylase is an enzyme that metabolizes starch and other polysaccharides it is produced by acinar cells of the major salivary glands particularly serous type. It metabolizes polysaccharide → glucose + maltose glucose maltose are substrate for cariogenic bacteria, amylase promotes the adherence of streptococci to hydroxyapatite. FACTORS AFFECTING MINERALIZATION Statherin is low molecular weight protein with a molecular mass of 5300 Daltons, it contains high levels of proline, tyrosine, phosphoserine and it negativity charged protein, binds to hydroxyapatite, it inhibits the spontaneous
precipitation
of
calcium
phosphate
salts
form
supersaturated saliva and prevents crystal growth by so doing it favors re-mineralization
of
the
tooth
surface
without
the
formation
of
dysfunctional mineral deposits on the tooth surface, it also serves as a lubricant for the tooth surfaces by that it protecting from various physical forces.
29 HISTATINS Histatins are a group of histidine rich proteins is a smallest protein in salivary fluid having molecule weight of about 3404 KD.
It has
antimicrobial effect as well as ability to affect mineralization several types of histanins 1,2,3,5. The major forms of oral cavity are 1,3,5 → it has ability to binds with hydroxyapatite, from there It prevents precipitation of calcium sulfate from super saturated saliva and inhibit crystal growth and there by enhancing the stability of hydroxyapatite present on the tooth surface. PROLINE RICH PROTEINS Molecular weight of proline rich proteins is 10 to 30 KD. It has ability to bind with hydroxyapatite of enamel thereby preventing precipitation of calcium phosphate thereby protecting enamel surface and preventing demineralization. Two types of proline rich proteins: 1. Acidic it binds with hydroxyapatite 2. Basic it binds with bacteria. The activity of oral bacteria bound to proline rich proteins and their role in caries development remains an important issue, it secreted from major salivary gland. E.g., Parotid. CYSTATINS Protease inhibitors with an average mass of about 15 KD it inhibit the harmful actions of proteases on the soft tissue of the oral cavity. Same action as proline rich proteins.
30 MUCINS They are large molecular weight glycoprotein composed mostly of carbohydrates and product of acinar cells from sub mandibular, sublingual and minor salivary gland the major salivary mucins are MG1, MG2. MG1 – 1000 KD MG2 – 120 KD It is protecting to tooth surface from chemical and physical attack including acid challenge. It has a primary role of contributing to the enamel pellicle. The ability to cause aggregation has been reported to be directly related to promotion of caries resistance. SALIVA AS BUFFERING FLUID Saliva has a significant buffering activity and its buffering activity varies from patient to patient. A major determinant of salivary pH is its buffering capacity.
Bicarbonate is the major buffer in saliva and its
concentration in saliva increases as salivary flow rate increases. The greater the acidity the more likely the demineralization of tooth decays. A reduction in salivary flow leads to a corresponding reduction in buffer capacity with important implications on dental plaque, pH, and caries susceptibility. Other buffers include in saliva are. UREA It is metabolized by plaqueurease and resulting in release of ammonia and an increase the plaque pH some urea originate from gingival crevices however, human parotid saliva contains up to 9mg / dl under stimulated conditions.
31 SUMMARY Saliva has three important functions. 1. Buffering ability. 2. A cleansing affect 3. Antibacterial action Fluoride is another important constituent in saliva.
The ability of
saliva to deliver fluoride to the tooth surface constantly. Concentration of fluoride in saliva is 0.03ppm action of fluoride is prevent the conversion of 2- phosphoglycerate to phosphoenol pyruvate, by inhibiting the enzyme enolase, thus prevent the production of acids from bacteria. It binds with hydroxyapatite from fluoro-apetite it is very resistant to acid this preventing caries. DISEASE OF SALIVARY GLAND Xerostomia: Defined as perception of oral dryness is often due to reduction in salivary flow rate, of major and minor salivary gland: CAUSES 1.
Radiation -Damage for acinar units.
2.
Sjogren’s Syndrome - Inflammation of the glands with lymphocyte infiltration - Especially in acinar cells.
32
DRUGS 1. Anticholinergic H1 Blockers 2. Antimuscuranic 3. Anti tricyclic depressant 4. α-Adrenergic, β-Adrenergic leads to dental caries . CARIES PROCESS Dental caries is a result of microbial process where the mineral constituents
of
the
tooth
principally
calcium,
phosphate
are
demineralized by organic acids produced by bacteria this acids are generated from dietary fermentable carbohydrates such as mono saccharides (Glucose and fructose) and disaccharide (Sucrose & Maltose) production of acids by plaque microorganisms.
The demineralization
phase starts with the formation of organic acids by plaque bacteria after exposure to fermentable carbohydrates.
Plaque microorganisms can
generate a wide range of organic acids.
Homo Fermentive Bacteria : Such as various streptococci and lactobacilli produce mostly lactic acid as their end product.
Hetero Fermentive Bacteria : Produce mixture of organic acids such as acetic, propinoic, butyric, formic and succsinic acid among all these acids lactic acid is considered to be the main acid involved in caries formation. Glucose ↓ Glucose – 6 – Phosphate ↓ 2 – Phosphate Glycerate ↓ Enolase Phaspho Enal pyruvate ↓ Pyruvate ↓
33 Lactic Acid (H+) Acid producing by plaque bacteria diffuses from the cells into the plaque with result in increased in H+ (Hydrogen Ion) concentration of plaque fluid. The plaque fluid is extra-cellular fluid that surrounds the bacteria and transports bacteria products to the enamel surfaces.
This is proved by Stephen
In his experiments used antimony touch electrodes
He observed typical curve result when plaque pH is plotted against time.
Resting Condition pH is 7, under fasting conditions pH of plaque can be in the alkaline range as high as pH 7.8.
After exposure to
fermentable carbohydrates (sugars) the pH drops rapidly than gradually returns to its resting value over a 30 to 60 minute period.
A pH depression from 7 to 4 represents a 1000 fold increase in hydrogen ion concentration and provided tremendous driving force for bacterial acids to diffuse in to the tooth.
This curve is called “Stephen Curve”.
This low resting pH is caused by acid production from intra cellular polysaccharides.
Diffusion of acids in to the tooth the next phase of the caries process is the diffusion of acids generated by the dental bio-film on to in to the tooth. As the pH of plaque drops hydroxy ion concentration build up in plaque fluid. Producing concentration gradient that causes acid to penetrate into the enamel. Enamel can be considering as porous solid in which water in the inter crystalline spaces serves as a channel for acids to diffuse and attack the crystals the effective pore size of sound enamel
34 has been estimated to range from 1.4 to 2.4 nm 2 and to represent 0.1% to 0.8% by volume. Acid diffusion in to enamel can take place at the micro structural level through the inter crystalline spaces and inter prismatic spaces and possibly through developmental defects like enamel cracks. ENAMEL DEMINERALIZATION AND REMINERALIZATION DEMINERALIZATION The
mineral
component
of
enamel,
dentin
cementum
is
hydroxyapatite Ca10(PO4)6(OH)2 . In neutral environment hydroxyapatite is equilibrium with local aqueous environment, which is saturated with Ca++ PO43- Ions. Hydroxyapatite is reactive to hydrogen ions at pH 5.5 (or) below H + reacts with phosphates in the aqueous environment. And it convert PO 43→HPO42- by addition of H+ and H+1 is buffered at the same time and than hydroxyapatite crystals dissolve, this termed demineralization. Ca10(PO4)6(OH)2+H+
Ca2+ + HPO42- + OH
REMINERALIZATION Demineralization process can be reversed if the pH is neutral there are sufficient Ca2+, PO43-. In the immediate environment this ions unite again and rebuilding of partially dissolved apatite crystals and it is termed remineralization.