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Dental caries
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dental caries

dental caries

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  • 1.  1883- W.D. Miller found bacterial involvement in the development of caries.  1891- G.V. Black put forth the concept of Extension for Prevention.  1907- Mckaley in Colorado springs noticed decreased incidence of caries in patients with mottled enamel.  1917- GV Black laid down the basic tenets for the design of cavities prescribed for restoring carious lesion.
  • 2.  1945- sorbitol was recommended as a substitute for sucrose due to its reduced fermentation .  1945- air abrasion was 1st described by Dr. Robert Black.  1951- S.S White Company- Air dent air abrasion unit.  1966- Markley modification of the cavity designs laid by Black to more conservative preparation .  1969 : invention of glass ionomer cements (reported in 1971 by Wilson & Kent).
  • 3.  1974- Brudevold influence of fluoride.  1977- Simonsen introduced preventive resin restoration.  Mid 1980s- ART was pioneered in Zimbabwe and Tanzania.  1980- tunnel restoration was reintroduced by Hunt & Knight.  1997- new classification of caries by G.J. Mount and Hume.
  • 4.  The history of understanding caries in human has passed through two distinct era.  The first , which is lasted until the twentieth century and may still ongoing today, is the observational era.  The second, which is developed and revolutionized our understanding of the causes and treatment ,is scientific era.  Still caries management is in gray year, in terms of restoration and preventive dentistry. Al Ismail et al, Dental caries in the second millennium, journal of dental education 2001;65:953-959.
  • 5.  DEFINITION Dental caries is a microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substances of the tooth. SHAFER  Dental caries is the disease produced by metabolic end products of certain micro organisms that results in dissolution of inorganic components of enamel ,dentin and cementum and degradation of their organic structure . G NETTLEMAN
  • 6.  Dental caries is defined as a localized post eruptive, pathological process of external origin, involving softening of hard tooth tissues, and proceeding into the formation of cavity. WHO  It is an infectious microbial disease of the teeth that results in localized dissolution and destruction of the calcified tissues. ROBERTSON
  • 7.  It is the most prevalent chronic disease affecting the human race. Once it occurs, its manifestations persist throughout life even though the lesion is treated.  There are practically no geographic areas in the world whose inhabitants do not exhibit some evidence of dental caries.  It affects persons of both sexes in all races, all social- economic straits and every age group.  It usually begins soon after the teeth erupt in the oral cavity. Persons who never develop carious lesions are designated “caries free”. No satisfactory explanation of their cario resistance has been found.  Hundreds of dental research investigators for more than a century have studied various aspects of dental caries problems. Despite this extensive investigation, Many aspects of etiology are still under observation and efforts at preventions have been partially successful .
  • 8. A detail of a tooth (to the right = enamel). It is 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
  • 9. 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.
  • 10. 1.Based on anatomical site 2.Based on progression 3.Based on virginity of lesion 4.Based on extend of caries 5.Based on tissue involvement 6.Based on pathway of caries spread 7. Based on number of tooth surface involved 8. Based on chronology 9 .Based on whether caries is completely removed or not during treatment 10.Based on tooth surface to be restored 11.Black’s classification and Finn's modification 12.WHO system 13.G.J Mount classification
  • 12.  Highest prevalence of all caries bacteria rapidly colonize the pits and fissures of the newly erupted teeth.  These early colonizers form a “bacterial plug” that remains in the site for long time ,perhaps even the life of the tooth .  Type & nature of the organisms prevalent in the oral cavity determine the type of organisms colonizing the pit & fissure.
  • 13. • Numerous gram positive cocci, especially dominated by s.sanguis are found in the newly erupted teeth. • The appearance of s.mutans in pits and fissures is usually followed by caries 6 to 24 months later. • Sealing of pits and fissures just after tooth eruption may be the most important event in their resistance to caries. • Shape, morphological variation and depth of pit and fissures contributes to their high susceptibility to caries. • Caries expand as it penetrates in to the enamel.
  • 14. NANGO (1960):Based on the alphabetical description of shape– 4 types  I & U type: self cleansing and somewhat caries resistant.  V type: narrow slit like opening with a larger base as it extend towards DEJ .Caries susceptible; also have a number of different branches.  K type: also very susceptible to caries.
  • 15.  Entry site may appear much smaller than actual lesion, making clinical diagnosis difficult.  Carious lesion of pits and fissures develop from attack on their walls.  In cross section, the gross appearance of pit and fissure lesion is inverted V with a narrow entrance and a progressively wider area of involvement closer to the DEJ.
  • 16.  Less favorable site for plaque attachment, usually attaches on the smooth surface that are near the gingiva or are under proximal contact.  In very young patients the gingival papilla completely fills the interproximal space under a proximal contact and is termed as col. Also crevicular spaces in them are less favorable habitats for s.mutans.  Consequently proximal caries is less lightly to develop where this favorable soft tissue architecture exists.
  • 17.  The proximal surfaces are particularly susceptible to caries due to extra shelter provided to resident plaque owing to the proximal contact area immediately occlusal to plaque.  Lesion have a broad area of origin and a conical, or pointed extension towards DEJ.  V shape with apex directed towards DEJ.  After caries penetrate the DEJ softening of dentin spread rapidly and pulpally.
  • 19.  Linear enamel caries ( odontoclasia ) is seen to occur in the region of the neonatal line of the maxillary anterior teeth.  The line, which represent a metabolic defect such as hypocalcemia or trauma of birth, may predispose to caries, leading to gross destruction of the labial surface of the teeth.  Morphological aspects of this type of caries are atypical and results in gross destruction of the labial surfaces incisor teeth.
  • 20.  The proximal root surface, particularly near the cervical line, often is unaffected by the action of hygiene procedures, such as flossing, because it may have concave anatomic surface contours (fluting) and occasional roughness at the termination of the enamel.  These conditions, when coupled with exposure to the oral environment (as a result of gingival recession), favor the formation of mature, caries-producing plaque and proximal root-surface caries.  Root-surface caries is more common in older patients.
  • 21.  Caries originating on the root is alarming because 1. it has a comparatively rapid progression 2. it is often asymptomatic 3. it is closer to the pulp 4, it is more difficult to restore  The root surface readily allows plaque formation in the absence of good oral hygiene.  The cementum covering the root surface is extremely thin and provides little resistance to caries attack.  Root caries lesions have less well-defined margins, tend to be U-shaped in cross sections, and progress more rapidly because of the lack of protection from and enamel covering.
  • 22. Acute caries Chronic caries Arrested caries
  • 23.  Acute caries is a rapid process involving a large number of teeth.  These lesions are lighter colored than the other types, being light brown or grey, and their caseous consistency makes the excavation difficult.  Pulp exposures and sensitive teeth are often observed in patients with acute caries.  It has been suggested that saliva does not easily penetrate the small opening to the carious lesion, so there are little opportunity for buffering or neutralization.
  • 24. • These lesions are usually of long-standing involvement, affect a fewer number of teeth, and are smaller than acute caries. • Pain is not a common feature because of protection afforded to the pulp by secondary dentin • The decalcified dentin is dark brown and leathery. • Pulp prognosis is hopeful in that the deepest of lesions usually requires only prophylactic capping and protective bases. • The lesions range in depth and include those that have just penetrated the enamel.
  • 25.  Caries which becomes stationary or static and does not show any tendency for further progression.  Both deciduous and permanent affected.  With the shift in the oral conditions, even advanced lesions may become arrested .  Arrested caries involving dentin shows a marked brown pigmentation and induration of the lesion [the so called ‘eburnation of dentin’]  Sclerosis of dentinal tubules and secondary dentin formation commonly occur.
  • 26.  Exclusively seen in caries of occlusal surface with large open cavity in which there is lack of food retention.  Also on the proximal surfaces of tooth in cases in which the adjacent approximating tooth has been extracted.
  • 27. Initial caries/Primary caries Secondary caries/Recurrent caries
  • 28.  A primary caries is one in which the lesion constitutes the initial attack on the tooth surface.  The designation of primary is based on the initial location of the lesion on the surface rather than the extent of damage.
  • 29. • This type of caries is observed around the edges and under restorations. • The common locations of secondary caries are the rough or overhanging margin and fracture place in all locations of the mouth. • It may be result of poor adaptation of a restoration, which allows for a marginal leakage, or it may be due to inadequate extension of the restoration. • In addition caries may remain if there has not been complete excavation of the original lesion, which later may appear as a residual or recurrent caries.
  • 30.  Recurrent carious lesion are mostly located on the gingival margins of classII and classV restorations.  Overhangs, are predisposing factors for plaque accumulation and development of recurrent caries.  The development of recurrent caries is unrelated to micro leakage. Ivar A. Mjor et al ,Clinical diagnosis of recurrent caries,Journal of American Dental Association 2005;136:1426-1433.
  • 31.  Incomplete removal of caries is beneficial specially in case of deep carious lesion in terms of risk of pulpal exposure, post-operative pulpal symptoms, overall failure, and caries progression.  Risk of failure is similar in complete or incomplete excavation. F.Schwendicke et al, Incomplete caries removal, Journal Of Dental Research 2013;92:306-314.
  • 32. Incipient caries Occult caries Cavitation
  • 33.  The early caries lesion, best seen on the smooth surface of teeth, is visible as a ‘white spot’.  Histological the lesion has an apparently intact surface layer overlying subsurface demineralization.  Significantly may such lesion can undergo remineralization and thus not an indication for restorative treatment
  • 34.  These white spot lesion may be confused initially with white developmental defects of enamel formation, which can be differentiated by their position [ away from the gingival margin], their shape [unrelated to plaque accumulation] and their symmetry [they usually affect the contra lateral tooth].  Also on wetting the caries lesion disappear while the developmental defect persist.
  • 35.  It is believed that bite wing and OPG radiographs along with noninvasive adjuncts like fiber optic transillumination (FOTI),laser luminescence, electrical resistance method (ERM) are used for diagnosis these occlusal lesions.  These lesion are not associated with microorganisms different to those found in other carious lesion.  These carious lesion seem to increase with increasing age.  Occult carious lesion are usually seen with low caries rate which is suggestive of increase fluid exposure.
  • 36.  It is believed that increased fluid exposure encourages remineralization and slow down progress of the caries in the pit and fissure enamel while the cavitations continues in dentine, and the lesions become masked by a relatively intact enamel surface.  These hidden lesions are called as fluoride bombs or fluoride syndrome.  Recently it is seen that occult caries may have its origin as pre- eruptive defects which are detectable only with the use of radiographs.
  • 37.  Once it reaches the dentinoenamel junction, the caries process has the potential to spread to the pulp along the dentinal tubules and also spread in lateral direction.  Thus some amount of sensitivity may be associated with this type of lesion.  This may be generally accompanied by cavitation.
  • 38. 1. Initial caries 2. Superficial caries 3. Moderate caries 4. Deep caries 5. Deep complicated caries
  • 39. Dental caries can be divided into 4 or 5 stages  Initial caries: Demineralization without structural defect. This stage can be reversed by fluoridation and enhanced mouth hygiene.  Superficial caries (Caries superficialis):Enamel caries, wedge-shaped structural defect. Caries has affected the enamel layer, but has not yet penetrated the dentin.
  • 40. 3. Moderate caries (Caries media): Dentin caries. Extensive structural defect. Caries has penetrated up to the dentin and spreads two-dimensionally beneath the enamel defect where the dentin offers little resistance. 4. Deep caries (Caries profunda): Deep structural defect. Caries has penetrated up to the dentin layers of the tooth close to the pulp. 5. Deep complicated caries (Caries profunda complicata) :Caries has led to the opening of the pulp cavity (pulpa aperta or open pulp).
  • 42. caries involving only one tooth surface caries involving two surfaces of tooth caries that involves more than two surfaces of a tooth SIMPLE CARIES COMPOUND CARIES COMPLEX CARIES
  • 43. Early childhood caries Adolescent caries Adult caries
  • 44.  Early childhood caries(ECC) would include, two variants: Nursing caries and rampant caries.  The difference primarily exist in involvement of the teeth [ mandibular incisors ] in the carious process in rampant caries as opposed to nursing caries. ECC
  • 45. Type I(MILD )  Involves molars and incisors  Seen in 2-5 years  Causecariogenic semisolid food +lack of oral hygiene Type II (MODERATE)  Unaffected mandibular incisors  Soon after first tooth erupts  Causeinappropriate feeding +lack of oral hygiene Type III(SEVERE)  All teeth including mandibular incisors  Causemultitude of factors
  • 46.  Emma O’ Keefe confirmed that factors occurring during the first year of life affect ECC. Also found that maternal factors influence bacterial acquisition, whereas colonisation was mediated by oral health behaviour and practices and feeding habits. Emma O’Keefe, Early childhood caries,Evidence based dentistry 2013;14:40-41
  • 47.  SYNONYMS Nursing caries, Nursing bottle mouth, Nursing bottle syndrome, Bottle-Propping caries, comforter caries, Baby Bottle mouth, Nursing Mouth Decay, Baby bottle tooth decay, tooth cleaning neglect.  NEW NAME Maternally derived streptococcus mutant disease (MDSMD)
  • 48. Seen in infant and toddler  Affects primary dentition Mandibular incisors are not involved ETIOLOGY Improper bottle feeding Pacifier dipped in honey/other sweeteners
  • 49. Seen in all ages, including adolescence. Affects primary and Permanent dentition. Mandibular incisors are also affected. ETIOLOGY MULTIFACTORIAL  Frequent snacks  Sticky refined CHO  Decreased salivary flow Genetic background
  • 50.  This type of caries is a variant of rampant caries where the teeth generally considered immune to decay are involved.  The caries is also described to be of a rapidly burrowing type, with a small enamel opening.  The presence of a large pulp chamber adds to the woes, causing early pulp involvement.
  • 51.  With the recession of the gingiva and sometimes decreased salivary function due to atrophy, at the age of 55-60 years, the third peak of caries is observed.  Root caries and cervical caries are more commonly found in this group.  Sometime they are also associated with a partial denture clasp.
  • 52. RESIDUAL CARIES  Residual caries is that which is not removed during a restorative procedure, either by accident, neglect or intention.  Sometimes a small amount of acutely carious dentin close to the pulp is covered with a specific capping material to stimulate dentin deposition, isolating caries from pulp.  The carious dentin can be removed at a later time.
  • 53.  Most widespread clinical utilization O for occlusal surfaces M for mesial surfaces D for distal surfaces F for facial surfaces B for buccal surfaces L for lingual surface Various combinations are also possible, such as MOD –for mesio- occluso-distal surfaces.
  • 54. Class 1 lesions: •Lesions that begin in the structural defects of teeth such as pits, fissures and defective grooves. Locations include Occlusal surface of molars and premolars. Occlusal two thirds of buccal and lingual surfaces of molars and premolars. Lingual surfaces of anterior tooth.
  • 55. Class 2 lesions:  They are found on the proximal surfaces of the bicuspids and molars.
  • 56. Class 3 lesions:  Lesions found on the proximal surfaces of anterior teeth that do not involve or necessitate the removal of the incisal angle.
  • 57. Class 4 lesions:  Lesions found on the proximal surfaces of anterior teeth that involve the incisal angle.
  • 58. Class 5 lesions:  Lesions that are found at the gingival third of the facial and lingual surfaces of anterior and posterior teeth.
  • 59. Class 6 (Simon’s modification):  Lesions involving cuspal tips and incisal edges of teeth.
  • 60.  Class1 : cavities involving the pits and fissure of molar teeth and the buccal and lingual pits of all teeth.  Class 2: cavities involving proximal surface of molar teeth molar teeth will access established from the occlusal surface.  Class 3: cavities involving proximal surfaces of anterior teeth which may or may not involve a labial or a lingual extension.
  • 61.  Class 4: a restoration of the proximal surface of an anterior tooth which involves the restoration of an incisal angle.  Class 5: cavities present on the cervical third of all teeth, including proximal surface where the marginal ridge is not included in the cavity preparation.
  • 62. In this classification the shape and depth of the caries lesion scored on a four point scale D1. clinically detectable enamel lesions with intact (non cavitated) surfaces. D2. Clinically detectable cavities limited to enamel. D3. Clinically detectable cavities in dentin. D4. Lesions extending into the pulp.
  • 63. •This new system defines the extent and complexity of a cavity and at the same time encourages a conservative approach to the preservation of natural tooth structure. •This system is designed to utilize the healing capacity of enamel and dentine.
  • 64. Pits, fissures and enamel defects on occlusal surfaces of posterior teeth or other smooth surfaces. Proximal enamel immediately below areas in contact with adjacent teeth. The cervical one third of the crown or following gingival recession, the exposed root. Site 1 Site 2 Site 3
  • 65. Size1:Minimal involvement of dentin just beyond treatment by remineralization alone. Size2: Moderate involvement of dentin. Following cavity preparation, remaining enamel is sound, well supported by dentin and not likely to fail under normal occlusal load. The remaining tooth structure is sufficiently strong to support the restoration.
  • 66. Size 3: The cavity is enlarged beyond moderate. The remaining tooth structure is weakened to the extent that cusps or incisal edges are split, or are likely to fail or left exposed to occlusal or incisal load. the cavity needs to be further enlarged so that the restoration can be designed to provide support and protection to the remaining tooth structure. Size4: Extensive caries with bulk loss of tooth structure has already occurred.
  • 67. SITE SIZE Minimal 1 Moderate 2 Enlarged 3 Extensive 4 Pit and fissure 1 1.1 1.2 1.3 1.4 Contact area 2 2.1 2.2 2.3 2.4 Cervical 3 3.1 3.2 3.3 3.4
  • 68. •Radiography is frequently associated with xerostomia due to decreased salivary secretion, an increase in viscosity and low PH. •This and other causes of decreased salivary secretion may lead to a rampant form of caries, including the significance of saliva in preventing caries.
  • 69.  Three types of defects due to irradiation 1. Lesion usually encircling the neck of teeth amputation of crowns may occur . 2. Begins as brown to black discoloration of tooth .Occlusal surface and incisal edges wear away. 3. Spot depression which spreads from any surface .
  • 70.  Caries causes damage by demineralization and dissolution of tooth structure
  • 71. sucrose +cariogenic plaque nutrients to Organic acids lowering of ph(if below 5.5) dissolution of tooth mineral In caries active individual ph remains below 5.5 for 20-50 mins following single exposure to sucrose.
  • 72. WORMS – According to the ancient Sumerian text, toothache was caused by a worm that drank the blood of the teeth and fed on the roots of the jaws. This legend of the worm was discovered on one of many clay tablets excavated near Niffer, Ur, and other cities within the Euphrates valley of the lower Mesopotamian area and estimated to date from about 5000 BC. Oracle bones from the shang dynasty, dating before 1000 BC, bear the Chinese character for caries. The idea that caries is caused by a worm was almost universal at one time, as evidenced by the writing of Homer and popular lore of China, India, Finland, and Scotland .
  • 73. GUY DE CAHULIAC (1300- 1368)-The greatest surgeon of middle ages believed that worms caused dental decay .As a cure he advocated fumigation with seeds of leek, onion and hyoscyamus. The Chinese and Egyptians used fumigation in earlier times, and fumigation devices continued to be used in England as early as the nineteenth century. HUMORS – The ancient Greeks considered that a persons physical and mental constitution was determined by the relative proportions of the four elemental fluids of the body - blood, phlegm, black bile, and yellow bile which corresponds to the four humors –sanguine, phlegmatic, melancholic and choleric .All diseases, including caries could be explained by an imbalance of those humors.
  • 74.  The vital theory regarded dental caries as originating within the tooth itself, analogous to bone gangrene.  This theory proposed at the end of eighteenth century, remained dominant until the middle of the nineteenth century .  A clinically well known type of caries is characterized by extensive penetrations into the dentin, and even into the pulp, but with a barely detectable catch or a fissure.
  • 75.  Parmly (1819) rebelled against the vital theory and proposed that an unidentified “chemical” agent was responsible for caries .He stated that caries began on the enamel surface in locations where the food putrefied and acquired sufficient dissolving power to produce the disease chemically.  Support for the chemical theory came from Robertson (1835) and Regnart (1938) who actually carried out experiments with different dilutions of organic acids (such as sulphuric and nitric) and found that they corroded enamel and dentin.
  • 76.  1843 erdl described filamentous parasites in the “ surface membrane” of teeth.  Shortly thereafter Ficinus ,a Dresden physician observed filamentous microorganisms ,which he called denticulate in material taken from carious activities .He implied that these bacteria caused decomposition of the enamel and then the dentin .  Neither erdl nor ficinus explained how these organisms destroyed tooth structure.
  • 77.  This theory is a blend of the above two theories, because it states that caries is caused by acids produced by microorganisms of the mouth. it has been customary to credit this theory to W. D miller (1890), whose writings and experiments helped to establish this concept on a firm basis. The work of W. D Miller (1853-1907) at the university of Berlin has a most profound effect on the understanding of caries etiology and subsequent caries research.
  • 78. In a series of experiments Miller demonstrated the following facts,  Acid was present within the deeper carious lesions, as shown by reaction on litmus paper.  Different kinds of foods (bread, sugar, but not meat) mixed with saliva and incubated at 37 ⁰C could decalcify the entire crown of a tooth .  Several types of mouth bacteria (at least 30 species where isolated) could produce enough acid to cause dental caries.  Lactic acid was an identifiable product in carbohydrate –saliva incubation mixtures .  Different microorganisms (filamentous ,long and short bacilli ,and micrococci ) invade carious dentin .  Miller concluded that no single species of microorganism caused caries but rather that the process was mediated by an oral microorganism capable of producing acid and digesting protein .
  • 79. According to this theory , the organic component is most vulnerable and is attacked by hydrolytic enzymes of microorganisms ,this precedes the loss of the inorganic phase .  Gottlieb (1944) maintained that the initial action was due to proteolytic enzymes attacking the lamellae ,rod sheaths ,tufts and walls of the dentinal tubules. o He suggested that a coccus, probably staphylococcus aureus ,was involved because of the yellow pigmentation that he considered path gnomonic of dental caries .  Frisbie (1944) also described caries as a proteolytic process involving depolymerization and liquefaction of the organic matrix of enamel. The less soluble inorganic salts could then be freed from their “organic bond” favoring their solution, by acidogenic bacteria that secondarily penetrate along widening paths of ingress .
  • 80.  Pincus (1949) contended that proteolytic organisms first attacked the protein elements ,such as the dental cuticle and then destroyed the prism sheaths. The loosened prisms would then fall out mechanically.  He also suggested that sulfatases of gram-negative bacilli hydrolyzed “mucoitin sulfate” of enamel or chondrotin sulphate of dentin and produced sulfuric acid . The released sulfuric acid could combine with the calcium of the mineral phase .  It should be noted that the composition of the organic components of enamel does not resemble that of connective tissue and an abundance of sulphated polysaccharides has not been demonstrated. The pincus’ theory remains ,therefore ,without experimental support.
  • 81. According to this theory, decalcification is mediated by a variety of complexing agents ,such as acid anions ,amines ,amino acids ,peptides polyphosphates ,and carbohydrate derivatives .oral karatinolytic bacteria are thought to be involved in the process. Differences in the keratin content of the enamel in children with high caries and low caries experience are considered important . It should be noted that only a small fraction of the protein of enamel bears any resemblance to the keratin of hair.  Schatz and Martin challenged the chemo-parasitic theory advocated the proteolysis – chelation theory and stated that acid may prevent tooth decay by interfering with growth and activity of protolytic bacteria .
  • 82.  Dental caries is a multifactorial disease in which there is interplay of three principle factors – the HOST ( primarily the saliva and teeth ) , the MICROFLORA , and the SUBSTRATE , or diet . In addition a fourth factor TIME must be considered in the etiology of caries .  For caries to occur , conditions within each of these factors must be favorable . In other words caries requires a susceptible host, a cariogenic oral flora , and a suitable substrate .
  • 84.  Micro flora: Acidogenic bacteria that colonize the tooth surface.  Host: quantity and quality of saliva, the quality of the tooth, etc.  Diet: intake of fermentable carbohydrates, especially sucrose, but also starch.  Time: Total exposure time to inorganic acids produced by the bacteria of the dental plaque.
  • 85.  Bacteria metabolize sugars and produces acid.  pH decreases and enamel demineralised.  Bacterial colonization and acid production increases without oral hygiene.  Demineralisation vs. Remineralisation.
  • 87.  Saliva refers to the mixture of secretions in the oral cavity . The mixture consists of fluids derived from the major salivary glands ( Parotid , submandibular , sublingual ) from the minor glands of the oral mucosa and traces from the gingival exudates .  There is no doubt that saliva significantly influences the caries process as evidenced by animal experiments in which the salivary glands are surgically extirpated . It is only fair to point out that removal of salivary glands is a drastic procedure affecting, in addition to saliva other factors which in themselves influence caries development. These factors include 1) Difference in food and water consumption 2) Longer eating time 3) Greater food retention 4) Possible alterations in the bacterial flora of the mouth . 5)Maturation of the enamel .
  • 88. Tooth morphology and arch form  A susceptible host is one of the factors required for caries to occur . Tooth morphology has long been recognized as an important determinant . For example attempts to induce caries in dogs have been unsuccessful mainly because of the wide spacing and the conical shape of the teeth .  On the basis of clinical observation it is known that the pit and fissure areas of the posterior teeth are highly susceptible to caries . Food debris and microorganisms readily impact in the fissures .  Certain surfaces of the tooth are more prone to decay whereas other surfaces rarely show decay . For eg. In mandibular first molar the likelihood of decay in descending order is occlusal , buccal , mesial , distal and lingual , whereas in maxillary first molars the order is occlusal , mesial , palatal , buccal and distal. .
  • 89. An intraoral variation exists in susceptibility to caries between different tooth types . The more susceptible permanent teeth are the mandibular first molars closely followed by the maxillary first molars and the mandibular and maxillary second molars . The second premolars , the maxillary incisors and the first premolars are the next in sequence , whereas the mandibular incisors and canines are the least likely to develop lesions . Irregularities in arch form , crowding , and overlapping of the teeth also favor the development of carious lesions .
  • 90.  There is good evidence to indicate that enamel surface is more caries resistant than the sub surface .  A pumping mechanism has been proposed whereby matter is transported from the inner enamel to the surface zone and from the surface zone to the saliva .  There is net movement of inorganic mineral phase from the inner enamel to the oral cavity. The surface enamel appears unaltered simply because it is continuously being regenerated by precipitation of solid phases .  However , when “white spots” have been examined by scanning electron microscopy , the initial stage of such active carious lesions has been characterized by openings in the outer enamel surfaces through eroded focal holes .
  • 91.  Accordingly , the concept of a relatively ineffective surface layer , described in transverse sections examined by micro radiography or light microscopy , needs revision in view of the surface defects, which represents signs of focal demineralization .  By transmission electron microscopy , the enamel surface is seen to be dented by irregular destruction of appetite crystals . Small micro defects starting at the enamel surface and reaching the deeper enamel layers have been observed .
  • 92.  Changes of the enamel such as decrease in density and permeability and an increase in nitrogen and fluoride content, occurs with age .  These alterations are part of the post eruptive “maturation” process whereby teeth become more resistant to caries with time .  The concentration of fluorides of the surface layer of enamel increases as the fluoride concentration of the drinking water increases, and such enamel is less soluble in acids. Furthermore , the higher the fluoride concentration of the water supply , the lower the prevalence of caries .
  • 93.  Microorganisms implicated in the etiology of dental caries must be acidogenic as well as acidouric to initiate carious lesions.  In enamel the microorganisms must be able to colonize the tooth surface and survive in competition with less harmful species ,forming bio films –the so called Dental Plaque .  As early as 1960 ,Fitzgerald and keys showed that certain microorganisms isolated from human dental plaque when inoculated in germ-free rodents on a high –sucrose diet ,resulted in the spread of rampant caries. Therefore dental caries should be regarded as an infectious transmissible disease .
  • 94. Three cariogenic bacteria  Mutans streptococci(MS)  S.mutans, s.sobrinus, s.sanguinis, s.salivariaus, s.milleri  Lactobacilli  L.acidophilus, L.casei  Actinomyces  While not the first colonize the tooth, studies have shown S.mutans to be the main culprit in dental caries
  • 95.  There is abundant support for the so –called specific plaque hypothesis ,introduced by Loesche(1982,1986) ,which proposes that some specific species of the plaque flora be regarded as major pathogens in the etiology of dental caries . Included in the major pathogens are those bacteria associated with caries in humans and also able to induce carious lesions in experimental animals .The most important are the mutans streptococci, there are seven species, of which two s.mutans and s.sobrinus ,are closely associated with caries in humans .  The second genus closely associated with caries is lactobacillus ,commonly isolated from carious dentin .  Also associated with the etiology of dental caries ,but considered to be less cariogenic than s.mutants ,s. sobrinus .and lactobacillus, are actinomyces odontologica, actinomyces naeslundii, and some other species of mutant streptococci.
  • 96.  Dental caries is a bacterially based disease. When it progresses, acid produced by bacterial action on dietary fermentable carbohydrates diffuses into the tooth and dissolves the carbonated hydroxyapatite mineral—a process called demineralization.  Pathological factors including acidogenic bacteria (mutans streptococci and lacto- bacilli), salivary dysfunction, and dietary carbohydrates are related to caries progression.  Protective factors—which include salivary calcium, phosphate and proteins, salivary flow, fluoride in saliva, and antibacterial components or agents— can balance, prevent or reverse dental caries.
  • 97.  Caries progression or reversal is determined by the balance between protective and pathological factors.  Fluoride, the key agent in battling caries, works primarily via topical mechanisms: inhibition of demineralization, enhancement of remineralisation and inhibition of bacterial enzymes.  Fluoride in drinking water and in fluoride-containing products reduces caries via these topical mechanisms.  Antibacterial therapy must be used to combat a high bacterial challenge.For practical caries management and prevention or reversal of dental caries, the sum of the preventive factors must outweigh the pathological factors. John D.B. Featherstone, science and practice of caries prevention, JADA 2000;131:887-898
  • 98.  In 1924 Clarke isolated a streptococcus that predominated in many human carious lesions and that he named streptococcus mutans because of its varying morphology. Clarke noted that s.mutans adhered closely to tooth surfaces in artificially induced caries .For the next 40 years, s.mutans was virtually ignored , until the 1960s when it was “ rediscovered” and its prevalence in plaque confirmed .  Characteristics of this group of streptococci have been described .They are non motile , catalase-negative, gram –positive cocci in short or medium chains . On mitis-salivarius agar they grow as highly convex to pulvinate (cushion –shaped)colonies. These colonies are opaque ;the surface resembles frosted glass.  These s.mutans variants also posses caries –inducing properties ,and when re-isolated from infected animals they may resume the original rough colonial form.
  • 99. Streptococcus in chains
  • 100.  When cultured with sucrose they form polysaccharides that are insoluble or can be precipitated with one part ethanol .This property of forming insoluble extra cellular polysaccharides from sucrose is regarded as an important characteristic contributing to the caries –inducing properties of s.mutans.  Mutants of s.mutans ,which lack the ability to synthesize insoluble glucans or to stick to glass surfaces, do not cause smooth surface caries.  Streptococcus mutans exhibits several important properties ; 1) it synthesizes insoluble polysaccharides from sucrose 2) it is a homo fermentative lactic acid former . 3) it colonizes on tooth surfaces 4) it is more aciduric than other Streptococci  cariogenic strains of S.mutans contain lysogenic bacteriophage ,which has not been isolated from non cariogenic strains . Non cariogenic mutants of S.mutans are unable to adhere to glass and have decreased ability to form insoluble polysaccharide .If this mutants are infected with lysogenic phages , they are transformed , acquiring the ability to adhere and form abundant insoluble polysaccharide .
  • 101.  s.mutans isolates can be grouped into three “chemotypes” based on differences in the composition of the cell wall. Atleast seven sero types of S.mutans have been found . Compared to s.sanguis ,s mutans is more aciduric and can reproduce in a culture medium at a pH as low as 4.3.  S.mutans forms a homogenous group , based on physiological ,ecological ,and morphological characteristics ,and has been recognized as a distant species by the National Communicable Disease Center .However ,analysis of the guanosine and cytosine content and hybridization studies on the homologies of the DNA isolated from strains of s.mutans revealed significant differences . These cariogenic organisms ,though phenotypically similar ,are genetically heterogeneous ,and were therefore divided into five genotypes or “genospecies”.
  • 102.  However, because their nucleic acid base content and sequence are too disparate ,these “mutans –like” organisms have been divided into separate species , namely s.mutans, streptococcus rattus ,streptococcus sobrinus ,streptococcus ferus of the “mutans –group”.  s.mutans, s.rattus ,and s.cricetus have been accepted and appear on the Approved Lists of Bacterial Names.  S.mutans and S.sobrinus are most commonly found in human plaque . S.cricetus and s rattus are less common in humans ,and s.ferus only occurs in rats .
  • 103.  Lactobacilli are gram positive ,non spore –forming rods that generally grow best under micro aerophilic conditions. Isolation and enumeration of oral lactobacilli have been facilitated by use of selective agar medium which suppresses the growth of other oral organisms by its low pH (5.4) .  Lactobacilli are found mostly as transients in the mouth of infants . Lactobacilli represents about 1% of the oral flora. L.casei and L.fermentum are the most common oral species. T he population of oral lactobacilli is influenced by dietary habits. A favorite habitat of lactobacilli is in the dentin of deep carious lesions.
  • 105. Lactobacilli and its role in caries.  Lactobacilli, or organisms resembling lactobacilli have been reported in the oral cavity ever since Miller enunciated the chemo parasitic theory. In 1925, Bunting and his collaborators claimed that bacillus Acidophilus was the specific etiological factor responsible for the initiation of caries. Subsequent investigators have isolated other types of lactobacilli besides L. acidophilus in saliva, plaque, and carious lesions.  Small anaerobic lactobacilli (L minutus) have been isolated consistently from pockets of patients with chronic periodontitis. The genus lactobacillus includes many species with a broad range of guanosine + cytosine content. The following are the most commonly encountered in the mouth.
  • 106. The following are the most commonly encountered in the mouth. Homofermentative Heterofermentative L. casei L. fermentum L. acidophilus Actobacillus brevis Lactobacillus plantarum Lactobacillus buchneri Lactobacillus salivarius Lactobacillus cellobiosus  In isolates of lactobacilli from human carious dentin, the homofermentative out numbered the heterofermentative variety. It was argued that lactobacilli are both acidogenic and aciduric and could, therefore, multiply in the low pH of plaque and carious lesions. Using selective culture media , counts of lactobacilli in the saliva could be correlated with the prevalence of dental caries. Furthermore the growth site of lactobacilli was reported to correspond to the sites of clinically diagnostic carious lesions. • When such lesions were restored, most of the growth sites of the lactobacilli were removed.
  • 107.  Acceptance of the doctrine that lactobacilli were the etiological agents of dental caries was not universal, however as more information on the microbial composition of dental plaque became available it was found that lactobacilli constitute only a minor fraction (1/10000) of the plaque flora  Amount of acid that can be formed by the relatively small number of lactobacilli present in plaque is almost insignificant in comparison with that produced by other acidogenic oral micro organisms. In humans lactobacilli can be isolated from the saliva, tooth surfaces, dorsum of the tongue, vestibular mucosa, and hard palate.  L.acidophilus is most frequently isolated from saliva. Lactobacilli have a relatively low affinity for the tooth surface. The establishment of oral lactobacilli coincides with the development of carious lesions. L casei is the predominating lactobacillus in dental plaque and carious dentin. Fitzgerald interprets such data to mean that lactobacilli are more a consequence than a cause of caries initiation.
  • 108. ECOLOGICAL SHIFT Reminerlization Deminerlization
  • 109.  Actinomyces is a gram –positive ,nonmotile ,non-spore- forming organisms occurring as rods and filaments that vary considering in length . Filaments are usually long and slender and are branching .  The species that have been found in the oral cavity are: Facultative anaerobic Anaerobic A. naeslundii A .israelii A. viscosus Actinomyces meyeri A. odontolyticus
  • 110.  All species of Actinomyces ferment glucose ,producing mostly lactic acid ,lesser amounts of acidic 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 caries, fissure caries ,and periodontal destruction when inoculated into gnotobiotic rats .  A viscosus has been separated into two ,and A naeslundii into four ,serological types.
  • 111.  Actinomyes is a good plaque former ,capable of adhering to wires and forming tenacious deposits on the teeth.  It is the most common group of microorganisms isolated from the sub gingival micro flora and from plaque of human root surfaces caries.  It is found in the supragingival plaque of all children and comprises about 50 % of all cells present.  A naeslundii predominates in the tongue ,salivary flora ,and in the plaque of young children ,while plaque from teenagers and adults has a higher proportions of A viscosus.
  • 112.  Ingestion of food may affect oral-dental health care by both systemic and local mechanisms .  Nutritional effects are mediated systemically ; dietary effects are mediated locally in the oral cavity .  The systemic effects results from the absorption and circulation of nutrients to all cells and tissues and may be mediated through influences on development of teeth , the quality and quantity of salivary secretions , improved host resistance and improved function .  Dietary constituents exert their local effects by influencing the metabolism of oral flora and by modifying salivary fluids and indirectly the qualitative aspects of salivary secretion .
  • 113.  Dental caries is a interaction between diet, cariogenic flora and tooth of the host.  Significant, also , is the fact that the tooth is relatively passive in the caries process. The environmental challenge to teeth from products of bacterial substrate reactions is often the most important variable in the caries process. Thus , even teeth that are well formed and mineralized cannot withstand a strong environmental challenge from the chemical by-products of a highly cariogenic flora and a high concentration of the substrate in the oral cavity .  Also diets and eating patterns change with age, making it difficult to assess nutrition influences on dental tissue .
  • 114. Vitamin D  Metabolism of Vitamin D : Vit. D along with Parathyroid hormones and calcitonin play primary roles in regulating the concentration of calcium and inorganic phosphate in the plasma and extracellular fluids ,by regulating the movement of these ions in and out of cell and in controlling mineralization of bones and teeth .  Enamel Hypoplasia : Enamel Hypoplasia is the most common abnormality of development and mineralization of human teeth . The lesion is characterized by a quantitive defect in enamel tissue resulting from a undetermined metabolic injury to the formative cells - Ameloblasts .  Recent evidences have suggested that the etiology of enamel hypoplasia is highly specific and linked with disorders of calcium and phosphate haemostasis .Enamel hypoplasia was found in conditions characterized bu hypocalcaemia but not in those characterized by hypophosphotemia . ( Nikiforuk and Fraser , 1981 ) .
  • 115.  Clinically enamel hypoplasia is seen as a roughened surface with discreet pitting or circumferential band like irregularities which post eruptively acquire a yellow brown stain.  Enamel hypoplasia is clinically significant not only because of its disfiguring and the restorative treatment cause ,but because it may effect caries susceptibility.  Mellanby (1936) reported that there is a strong co-relation between hypoplasia in the teeth of British school children and caries susceptibility . Similarly , various other studies by Allen , 1941 ; Bibby , 1943 ; Carr , 1953 have reported similar conclusions .
  • 116.  The only member of the vitamin B complex which has been associated with caries is pyridoxine ( Vitamin B6) . The vitamin has been stated to reduces caries in rats . But the effect was not confirmed on monkeys . ( Cole et al , 1980 )  These experiments do not suggest that deficiency of pyridoxine is responsible for caries but that large unphysiological doses , in which pyridoxine is being used as a drug rather than as a vitamin reduces caries by modifying the oral flora .
  • 117.  Deficiency of essential fatty acids in man is rare and evaluation of the role of these nutrients on caries rates is not available .  Fat consumed post eruptively in diets of animals , has been co-related with caries reduction . ( Williams et al , 1982 )
  • 118.  where Kwashiorkor is prevalent .  Low intake of cariogenic food .  Shaw, 1970 and Navia, 1979 showed that protein deficiency induced in rats caused:  -smaller teeth , -a delay in eruption , - and a greater susceptibility to caries .  These may be due to reduced salivary flow and therefore reduced total buffering capacity , reduced remineralization and anti-bacterial activity.
  • 119.  Intolerance to disaccharide or monosaccharide occurs because of a deficiency of a specific enzyme involved in the metabolism of sugar. A condition known as hereditary fructose intolerance provides direct link between sugar ingestion and dental caries. Hereditary fructose intolerance  In 1959 Froesch described an inborn error of fructose metabolism transmitted by an autosomal recessive gene .  Episodes of pallor, nausea vomiting ,coma and convulsions following ingestion of fruit containing fructose or cane sugar.  Tolerance test shows marked hypoglycemia(8mg/100ml, a sharp increase in blood fructose concentration ,and drop in serum phosphorus levels.
  • 120.  Persons with Hereditary fructose intolerance show a strikingly reduced dental caries experience when compared to a controlled population of the same age. (Marthelar,1967)
  • 121. Constituents : Polysaccharides and Sugars • The four carbohydrates starch, sucrose , fructose and glucose comprise the greatest proportion of foods consumed by man. • The main polysaccharide(starch) is not highly cariogenic in animals or man at least in some circumstances.
  • 122.  Excessive and frequent use of highly fermentable mono-and disaccharides is correlated with high caries rate.  While Glucose , Fructose , Lactose and Mannose have been shown to be cariogenic in animal experiments, they are usually minor constituents of human foods as they are present only in dried fruits , honey and milk .  Sucrose is by far the commonest dietary sugar consumed and is considered ARCH CRIMINAL OF ORAL CAVITY.
  • 123. Physical Properties of Foods and Cariogenicity Some important physical properties that determine food texture are: 1) Mechanical properties : hardness , cohesiveness , viscosity , adhesiveness . 2) Geometric properties: particle size and shape. 3) others : moisture and fat contents . • From a dental stand point the physical properties of food may have significance by affecting food retention , food clearance , solubility and oral hygiene . • Adhesive properties of foods have been measured and correlated with their retention in the mouth after ingestion . .
  • 124.  The high fibrous , cellulose content of plant foods exert a mechanical cleansing action on teeth  The physical texture and chemical composition of food is known to effect salivary flow rates .Saliva that is rapidly flowing is more alkaline than the resting saliva and more super saturated with calcium and phosphate and thus may be more caries inhibitory.  Physical properties of food , particularly those that improve the cleansing action and reduce the retention of food within the oral cavity and increase saliva flow , are to be encouraged in everyday diets . However , clinical evidence that consumption of these food items will significantly reduce caries , is lacking.
  • 125.  saliva incubated with refined foods caused a greater dissolution of tooth enamel than when incubated with unrefined foods .  Mixtures that included bran , wheat germ , unrefined treacle and cane juice contained protective factors .  The protective substance identified was Phytate – a polyphosphate, which when applied to tooth enamel reduces its solubility and has caries inhibiting effects. (Jenkins,1966)
  • 126.  Some dietary items are highly acidic and affect the pH in plaque and saliva .  Natural foods such as lemons , apples , fruit juices and carbonated beverages , are sufficiently acidic as to cause demineralization of enamel that is in prolonged contact with them .
  • 127.  Prime culprit of Dental decay and Periodontal diseases .  Plaque – a soft adherent collection of salivary products and bacterial colonies on the teeth .  It accumulates on the surface of the teeth continuously throughout the life span.  Eliminating this disease producing material is by continuously removing it by tooth brush and dental flossing.
  • 128.  Unrestricted plaque growth produces local environmental conditions that may promote the accumulation of pathogenic bacterial species .  High frequency sucrose exposure is the single most important factor in producing a cariogenic plaque .
  • 129.  The factors that control the presence of individual species in plaque are termed ecological determinants. - Host resistance - extent and nature of shelter for bacteria - host diet - oral hygiene - status of the dentition - and composition of the oral flora . These various factors can be viewed as links in a chain of reactions eventually leading to caries.
  • 130.  Plaque growth begins approximately six hours after the thorough cleaning of the teeth.  The first phase of plaque development is the deposition of adherent products from the saliva.  Composed of mucin, which forms the thin adherent layer on the teeth called the pellicle .  Once the pellicle has been formed on the clean tooth surface, bacteria that inhabit the oral cavity attach themselves to the pellicle. After attachment ,the bacteria multiplies to form large masses of bacterial colonies.
  • 131.  These begin to occur approximately eighteen hours after thorough cleaning of the teeth and continue until the plaque is fully mature at the end of three weeks.  Mature plaque consists primarily of bacteria of various types. Some bacteria produce harmful chemical substances and others produce substances that are needed by neighboring bacteria to survive.  Still other organisms produce adherent substances that are interspersed with the bacteria and hold the plaque intact on the surface.
  • 132.  Supra gingival plaque consists of a different combination of bacteria than Sub gingival plaque.  The bacteria in supra gingival plaque is capable of producing acids that can erode the surface of the tooth and also thrive in an acidic environment.  The sub gingival plaque consists of bacteria that do not grow well in the presence of acid. It does not produce acids, but rather other chemical compounds that penetrate the soft gingival tissue and cause it to become inflamed.  Therefore, supra gingival plaque, because of its acidic nature, is responsible for dental caries. Sub gingival plaque because of its capacity to produce substances that are toxic to soft tissues, is responsible for periodontal diseases.
  • 133.  Streptococcus mutans is one of the first organisms to attach to the pellicle and multiply.  The streptococci are capable of producing both polysaccharides and acids from carbohydrates.  These polysaccharides help attach the streptococci to the pellicle.  The acid they produce is capable of demineralizing the enamel layer of the tooth.
  • 134.  Other organisms in dental plaque produce various substances that help the bacteria mass attach to the pellicle.  The plaque because of its thickness and density prevents acid produced within it from being diluted by saliva or neutralized by chemicals contained in the saliva.  Therefore the acid rather concentrated adjacent to the tooth surface can break down the enamel more quickly.  Once the caries process is initiated, another organism, lactobacillus, can become retained in the decayed area. Since the lesion is acidic, these organisms thrive and like those of streptococcus mutans, they convert sugar to acid, which in turn attacks tooth structure.
  • 135. ENAMEL CARIES The small lesion had has been divided into zones based upon its histological appearance when longitudinal ground sections are examined with light microscope. It is subdivided into 4 zones  Translucent zone at the inner advancing front of the lesion.  Dark zone lies superficial to the translucent zone.  The Body of the lesion is the third zone and lies between the dark zone and the apparently undamaged enamel surface..  Unaffected zone is the fourth zone and is superficial to the lesion .
  • 136. Early smooth surface caries ,ground section visualized by polarized light after Imbibition with quinoline The dark zone shows positive birefringence (golden brown) and surrounded by peripheral translucent zone (left), In white. The Body of the lesion has become positively birefringent while the surface zone appears to be unaffected as shown negative (blue –green) birefringence (middle) .In the dry specimen the surface zone still shows some negative bifrengerence indicating that it has lost not more than approx 1% of its mineral content, in contrast to the 25% mineral loss more deeply (right).
  • 137.  The deepest zone and represents the advancing front of the enamel lesion.  Has a structure less appearance when perfused with quinoline solution and examined with polarized light .  Pores or voids form along the enamel prism (rod) boundaries, presumably because of the ease of hydrogen ion penetration during the carious process.  When these boundary area voids are fitted with quinoline solution, (same R.I as enamel) the features of the area disappear.  The pore column of translucent enamel caries is 1%, 10 times greater than normal enamel.
  • 138.  The next deepest zone is dark zone because it does not transmit polarized light. The light blockage is caused by the presence of many tiny pores too small to absorb quinoline.  These smaller air or vapor filled pores make the region opaque.  The total pore volume is 2% to 4% .  There is some speculation that the dark zone is not really a stage in the sequence of the breakdown of enamel, rather the may be formed by deposition of ions into an area previously only containing large pores.
  • 139.  Experimental remineralization has demonstrated increase in the size of the dark zone at the expense of the body of the lesion. There is also a loss of crystalline structure in the dark zone, Suggesting of a process of demineralization and remineralization.  The size of the dark zone is probably an indicator of the amount reminerlization that has recently accoured .
  • 140.  The body of the lesion is the largest portion of the incipient lesion. It has pore volume , varying from 5% at the periphery to 25% at the center.  The striae of Retzius are well marked in the body of the lesion indicating preferential mineral dissolution along the areas of relatively higher porosity.  The first penetration of caries enters the enamel surface via the striae of Retzius. The inter prismatic areas and these cross- striations provide access to the rod (prism) cores, which are then preferentially attacked.  Bacteria may be present in this zone if the pore size is large enough to permit their entry.
  • 141. Early smooth surface caries ; ground section shows the body of the lesion, containing Enhanced striae of retzius ,enclosed between the dark and peripheral translucent zones and the intact surface. Enamel zones
  • 142.  It is relatively unaffected by the caries attack.  It has lower pore volume than the body of the lesion (less than 5%) and a radiopacity comparable to unaffected adjacent enamel.  It has been hypothesized that hyper mineralization and increased fluoride content of the superficial enamel are responsible for the relative immunity of the enamel surface. However removal of the hyper mineralized surface by polishing fails to prevent the reformation of a typical well mineralized surface over the carious lesion. Thus, the intact surface over incipient caries is a phenomena of the caries demineralization process rather than any characteristics of the superficial enamel.
  • 143.  As the enamel lesion progresses conical shaped defects in the surface zone can be seen by SEM. These are the first sites where bacteria can enter into a carious lesion.  Arresting the caries process at this stage results in a hard surface that may at time be rough though cleanable.
  • 144. Caries advancement in dentin proceeds through three changes: 1) Weak organic acids demineralize the dentin. 2) Organic material of the dentin ,collagen degenerates and dissolves. 3) The loss of structural integrity is followed by invasion of bacteria.
  • 145. Deepest area is normal dentin which has tubules with odontoblastic process that are smooth and no crystals in the lumens.  The inter tubular dentin has normal cross banded collagen and normal dense apatite crystals.  No bacteria in the tubules.  Stimulation of dentin (eg :by osmotic gradient, a bur, a dragging instrument or air blow) produces a sharp pain.
  • 146.  Zone of demineralization of the inter tubular dentin and initial formation of very fine crystals in the tubule lumen at the advancing front.  Odontoblastic process damage is evident.  No bacteria are found in this zone.  Stimulation of dentin produces pain.  Dentin is capable of remineralization.
  • 147.  This dentin is softer than normal dentin and shows further loss of mineral from the inter tubular dentin and many large crystals in the lumen of the tubules.  Stimulation produces pain.  Intact collagen can serve as a template for the remineralization of the inter tubular dentin and thus this region is capable of self repair , provided the pulp remains vital.
  • 148.  Zone of bacterial invasion and is marked by widening and distortion of the dentinal tubules which are filled with bacteria.  There is very little mineral present and the collagen is irreversibly denatured.  Dentin in this zone will not self repair .This zone cannot be remineralized and must be removed before restoration. Tubules filled with bacteria
  • 149.  Outer most decomposed dentin that is teeming with bacteria.  No recognizable structure to the dentin and collagen ,and minerals are absent.  Removal of infected dentin is essential to sound, successful restorative procedure as well as prevention of spreading of infections.
  • 150. INFECTED DENTIN AFFECTED DENTIN 1) Softened demineralized Softened demineralized dentin teaming with bacteria dentin not yet invaded by bacteria 2) Collagen is irreversibly Collagen cross linking denatured remains 3) Cannot be remineralized Acts as a template for remineralization 4)Soft necrotic tissue followed Softer than normal dentin by dry leathery dentin. Flakes discolored but does away with instrument. not flake easily 5)Dyes – 1% Acid red in propylene glycol .Stains only irreversible denatured collagen. Does not stain
  • 151. Infected dentin Affected dentin Zone of Bacterial invasion Zone of Demineralisation Zone ofDentinal sclerosis Zone of Fatty degeneration Retreating Odontoblastic process zZone of Decomposed dentin one
  • 153.  Aims of prevention (Sturdevant): 1. Limiting pathogen growth & metabolism 2. Increasing resistance of tooth surface to demineralization 3. Caries control methods which include operative procedures.
  • 154.  There are three levels of prevention of dental caries. 1. Primary prevention – is defined as “actions taken prior to the onset of the disease, which removes the possibility that the disease will ever occur.” 2. Secondary prevention - is defined as “actions which halt the progress of a disease at its incipient stage and prevents complications.”
  • 155. . Tertiary prevention- is defined as “ all measures available to reduce or limit impairments & disabilities, minimizing suffering caused by existing departures from good health & to promote the patients adjustments to the irremediable condition.” Essentials of Preventive and Community dentistry. Soben Peter.
  • 156. levels of prevention Primary prevention Secondary prevention Tertiary prevention Preventive services Health promotion Specific protection Early diagnosis and prompt treatment Disability limitation Rehabilitation Services provided by the individual Diet planning, demand for preventive services, periodic visit to dental office Appropriate use of fluoride, ingestion of fluoridated water, use of fluoridated dentifrices Self examination and referral, utilization of dental services Utilization of dental services Utilization of dental services Services provided by community Dental health education programs, promotion of lobby efforts Comm. or school water fluoridation, school fluoride mouth rinse program, school fluoride tablet program, school sealant program Periodic screening and referral, provision of dental services provision of dental services provision of dental services Services provided by the dental profession Patient education, plaque control program, diet counseling, recall, reinforcement, Topical application of fluoride, supplements/ rinse preparation, pit Complete exam, prompt treatment of incipient lesions, preventive resin restoration, pulp Complex restorative dentistry Removable and fixed prosthodontic minor tooth movement, implants
  • 157.  By improving oral hygiene  By diet modification  By use of salivary stimulants  Fluoride application  Pit and fissure sealants  Antibiotic  laser
  • 158. KEY’S TRIANGLE Xylitol Plaque Tooth Sugar CARIES Saliva Fluoride Multiple Factors Sealant Antiseptics
  • 159.  Plaque free tooth surfaces do not decay.  Oral hygiene procedures -Tooth brushing -Flossing -Professional prophylaxis  Daily personal oral hygiene recommended for good hygiene and for control of gingival diseases
  • 160. Total length: 6.0-7.5 inches Length of brushing plane: 1-1.25 inches Width of brushing plane: 5/16-3/8 inch Filament height: 7/16 inch Filament diameter Soft: .007 inch Medium: .012 inch Hard: .014 inch
  • 161.  Any brush which allows pt. to comfortably access all tooth surfaces is acceptable although a medium brush with small head is recommended.  Powered brush – physically handicapped.  Brush at least twice daily with toothpaste for effective plaque removal.  Toothbrush to be replaced every 3 months or when bristles become permanently bent.
  • 162.  Oral-b triumph™  Oral-b professional care™ 8000 series  Oral-b sonic complete  Oral-b advancepower™ 900 series
  • 163.  Roll – modified stillman technique  Vibrator-stillman,charters, or bass method(sucular).  Circular – the fones technique  Vertical – the leonard technique  Horizontal – the scrub technique
  • 164. Position of brush on tooth surface
  • 165.  Method - bristles are directed apically at 45 ⁰ to long axis of tooth, gentle force applied into sulcus.  Use gentle but firm vibratory strokes without removing bristle ends from sulcus. At least 20 vibrations.  The tips of the bristles should be forced to enter the gingival sulcus and the embrasures as far as possible.  Apply the brush to the next group teeth.  The entire stroke is repeated at each position around the maxillary and mandibular arches, both facially and lingually.
  • 166.  Approximal surfaces and malaligned teeth or these are additional cleaning required (1)dental floss or tape (2)wooden sticks (3)interdental brushes (4)single tufted brushes
  • 167.  Nylon, yarn or teflon; waxed or unwaxed  Waxed preffered in young where interdental papilla fills interdental spaces. Technique  About 15-18 inches taken.  Wrap the two ends of the floss around the middle fingers of both hands.  Thumb and index finger used to control the floss.  Both thumbs are manipulated to floss maxilla.  Both forefingers are manipulated to floss mandible.
  • 168. Length of dental floss
  • 169. Wrap the two ends of the floss around the middle fingers of both hands
  • 170. Floss-ready to use
  • 171.  Gently guide the floss past the contact point using back and forth motion.  Avoid “snapping”.
  • 172.  Wrap the floss around proximal surface of one tooth and slip it under marginal gingiva 'sawing' motion taken to remove plaque
  • 173.  Rotate the floss on the fingers to use a fresh, unsoiled section of floss as needed.
  • 174.  Patients with gingival recession which causes interdental spaces to open up.  Placed such that base of triangle rests on gingiva.  Pick is repeatedly moved in and out of the gingiva.
  • 175. Dental woden sticks
  • 176.  Cone shaped brushes with nylon bristles.  Used when there are wide interdental spaces and also for cleaning around bridges.  Brush selected should be slightly larger than the gingival embrasures.
  • 177. Interdental brushes
  • 178.  Useful aids in malaligned teeth.  Highly effective in the lingual surface of mandibular premolars, where tongue impedes toothbrush.  May provide access to furcation areas and isolated areas of deep recession.
  • 179. Unitufed brushes
  • 180. TYPE I embrasure TYPE II embrasure TYPE III embrasure
  • 181.  It is removal of a shallow, enamel developmental fissure or pit to create a smooth ,saucer–shaped surface that is self cleansing or easily cleaned. Indications- Fissure depth less than ¼ to 1/3 the thickness of the enamel. Procedure Developmental faults are removed with the side of a flame shaped diamond stone, leaving a smooth surface.
  • 182.  Usually available as paste form.  Can be used in conjunction with tooth brushing.  Aid in cleaning and polishing tooth surfaces.  Not necessary to effectively remove dental plaque.  Some dentifrices contain abrasives that help remove stain and polishing agents that restore tooth luster.
  • 183. Dentrifices
  • 184.  Some have a compound added to reduce calculus formation and fluoride can be added to prevent dental caries.  Free fluorides should be available in the paste not to the ingredients in the abrasive system.  They can also contain desensitizing agents that are beneficial to patients with tooth sensitivity such as exposed dentin surfaces.
  • 185.  Helpful in identifying areas of plaque retention.  Tablet or solution form. A red dye (erythrosin) is most commonly used.  A two-tone dye has the advantage of differentiating mature dental plaque (stains blue) from newly formed bacterial plaque (stains red).  Used after toothbrushing to improve plaque control measures.
  • 186. Disclosing agent
  • 187. Professional tooth cleaning measures  Selective removal of plaque by the dentist using mechanically driven instruments like contra-angled handpiece with bristle brush and fluoride prophylaxis paste.
  • 188. 1) Substances which alter the surface of tooth structure a. Fluoride. b. Iodides. c. Bis-biguanides. d. Silver nitrate. e. Zinc chloride and potassium ferrocyanide. 2) Substances which interfere with carbohydrate degradation through enzymatic reaction/alterations a. Vitamin K. b. Sarcoside.
  • 189.  3) Substance which interfere with bacterial growth and metabolism a. Urea and ammonium compounds b. Chlorophyll c. Nitrofurans d. Caries vaccine
  • 190. Chlorhexidine  Highly effective against plaque microorganisms causing gingivitis and periodontal disease.  Prevents bacterial adhesion on tooth surface.  0.12% mouth rinse at bedtime for 2 weeks  1% gel or 40% varnish professionally applied .Once a week for several weeks reduces caries incidence in high risk patients.  It helps in remineralization of incipient caries.
  • 191. 'Vaccine' is an immunobiological substance designed to produce specific protection against the given disease. It stimulates the production of protective antibody and other immune mechanisms. HISTORY o First developed by Williams 1944 using a lactobacillus vaccine. o Bowen in 1976 demonstrated monkeys immunized by whole live cells of S.mutans developed lesser caries. o Underwood and Miller published in 1881 bacteria are involved in the pathogenesis of dental caries was clearly expressed in a paper .
  • 192. The subcellular component which are currently being seriously proposed as vaccines are (a) Glucosyltransferases (GTF) (b) Wall associated proteins. (c) Adhesins. (d) Glucan- binding protein.
  • 193. Pellicle glycoprotein PBP* (Adapted from Slots & Taubman, 1992) s.mutans Glucan binding protein *PBP: Pellicle Binding Protein Initial Attachment
  • 194. + Sucrose Glucose Fructose GTF-I* GTF-S* (Adapted from Slots & Taubman, 1992) *GTF: Glucosyltransferase I: Insoluble form or GTF-B and GTF-C S: Soluble form or GTF-D GTF Binding Glucans Glucans
  • 195. S,mutan (Adapted from Slots & Taubman, 1992) Pellicle Glycoprotein Glucan Binding Protein Glucans Aggregation
  • 196. (Adapted from Slots & Taubman, 1992) S. mutans
  • 197. Two purified proteins from the surface of S. mutans serotype c are currently being suggested for use as dental caries vaccines- 1. Antigen I/II or B described by Lehner and his colleagues, 2. Antigen A - a small molecular weight cell wall protein
  • 198.  Group of the extracellular enzymes involved in synthesis of polymer (glucans) from sucrose.  Genes responsible for glucan synthesis in S. mutans are gtfB, gtfC, and gtfD  Inactivation of the gtfD gene has also resulted in a mutant gene with lower cariogenicity on smooth surfaces  Passive administration of antibody to GTF in diet can also protect rats from experimental dental caries.  Thus, presence of antibody to glucosyltransferase in oral cavity prior to infection can significantly influence the disease outcome, presumably by interference with one or more of the functional activities of the enzyme
  • 199.  Adhesins are the receptors which allow S.mutans to bind with pellicle.  Adhesins from two principal human pathogens, Streptococcus mutans and Streptococcus sobrinus have been purified.  Numerous immunization approaches have shown that active immunization (with intact antigen) or passive immunization can protect subjects from dental caries
  • 200.  The ability of mutans streptococci to bind to glucan is presumed to be mediated, at least in part, by cell wall- associated proteins (GBP).  Protection can be achieved by either subcutaneous injection of GbP in the salivary gland region or by mucosal application by the intranasal route.  Saliva samples from young children often contain IgA antibody to GbP, indicating that initial infection with S. mutans can lead to natural induction of immunity to this protein.
  • 201.  Recombinant Vaccines/Attenuated Expression Vectors- Attenuated mutant Vectors such as Salmonella, which contain plasmids expressing recombinant peptides, can target the vaccine to appropriate inductive lymphoid tissue for mucosal responses.  Conjugate Vaccines - other vaccine approach which may intercept more than one aspect of mutans streptococcal molecular pathogenesis is chemical conjugation of functionally associated protein/peptide components with bacterial polysaccharides.
  • 202. -Added to the value of including multiple targets within the vaccine is that conjugation of protein with polysaccharide enhances the immunogenicity polysaccharide entity. -Subcutaneous injection with conjugate-induced systemic IgM and IgG antibody responses to both peptide and polysaccharide, which could be boosted upon subsequent injection.
  • 203. o Heart cross-reactive antigens (HCRA )have been identified in S. mutans , which when injected in animals may damage to the heart. Streptococcus mutans antibodies, possibly reacts with, the myosin component of the heart tissues . o The precise timing and number of injections which might ultimately be required in children has not yet been determined. o Apart from logistic consideration of availability of patients and coordination with other vaccine programmers, fundamental details of the level and longevity of immune responses in humans are not yet known.
  • 204.  Unlike traditional vaccines, which are injected directly into the bloodstream, the nasal spray vaccine works by way of the mucosal immune system—an antibody-producing “factory” that resides in the body’s mucosal surfaces, such as the lining of the respiratory, digestive, and urogenital tracts.
  • 205. Shivkumar et al,dental caries vaccine,Indian Journal of Dental Resident 2009;20:99-106
  • 206.  Dietary sucrose has two important detrimental effects on plaque. 1 – frequent ingestion provide stronger potential for S.Mutans colonization . 2 – Mature plaque exposed to sucrose rapidly metabolizes into organic acids lowering pH.  Diet modification recommended for pt. With active caries and those with high caries risk.
  • 207. Points considered at the examination Measures to reduce caries risk and/or to stop ongoing caries activity Frequency of meals Number of meals+ snacks should be kept on a low level. Elimination of sugars and consistency of food Sugars should be eliminated as fast as possible. Foods needing active chewing lead to an increased salivation, which is desirable. Fermentable carbohydrates Polysaccharides, disaccharides and monosaccharides, but the capacity differs between different products. Protective and favorable elements in diet Fluorides ,calcium, phosphates, fats and proteins Sugar substitutes Use of sugar substitutes results in a lower acid formation.
  • 208. ADEQUACY OF DIET Determine the number of servings of food in each of the basic five food groups and compare this with the recommended number of servings.
  • 209.  MILK- contain lactose ....Least cariogenic  CHEESE- casein phosphatase give anticariogenic property  Fibrous foods  TEA - green and black tea  Artificial sweeteners(xylitol)  Prevent S.Mutans from binding to sucrose  Increase concentration of amino acids and ammonia neutralizing plaque acids  Bacteriostatic, as they are nonfermentable  Increase salivary flow, enhance remineralization
  • 210.  When the salivary glands are capable of secreting, chewing gum stimulates salivary flow.  A chewing gum containing xylitol or chlorhexidine ( or both) may be particularly useful.  Patients with dry mouths in whom the salivary glands are irreparably damaged and cannot secrete , are not helped by chewing but may benefit from an artificial saliva spray containing calcium, phosphate ,and fluoride ions
  • 211. o Finnish name for Xylitol is "koivusokeri", or birch sugar. o Imfeld classified the caries preventive features of xylitol into ‘passive’ and ‘active’ properties o ‘Passive’ properties - surround its non fermentability by oral microorganisms, and thus its substitution in the diet is effectively sugar restriction. o ‘Active’ properties- include disturbance of bacterial metabolism, growth or adhesion, or a role in facilitating remineralization of lesions. o Regular use of chewing gum has been shown to be a means of promoting remineralization, due to the accompanying enhancement of salivary flow and buffer capacity. British Dental Journal 2003;194( 8):429-436
  • 212. Xylitol action
  • 213.  Have anticariogenic activity as shown in laboratory, animal and human in situ experiments [Reynolds et al., 1999, 2003., Shen et al., 2000]  CPP stabilizes amorphous calcium phosphate and also localizes it at the tooth surface thus leading to increased rate of remineralization than with ACP alone.
  • 214.  Promotes remineralization of enamel subsurface lesions with hydroxyapatite [Reynolds, 1997]  Improves crystallinity and lowers microstrain than normal tooth enamel.  18.8 mg of CPP-ACP complex significantly remineralizes 2 times better than control sugar- free gums (Shen et al 2001) Remineralation
  • 215.  Topical crème with bio – available calcium and phosphate.  A water based, sugar free crème containing CPP – ACP
  • 216.  Saliva has important role in caries prevention.  Xerostomia patient increased caries risk is seen.  Gums, paraffin waxes, or salivary substitutes can be prescribed as adjuncts  Malic acid, pilocarpine etc is effective in the treatment  Sugar free chewing gum, ascorbic acid also helps in salivary flow.
  • 217.  Fluoride therapy is the delivery of fluoride to the teeth topically or systemically in order to prevent tooth decay. Mechanism of action  Precipates fluorapatite into tooth structure from the calcium and phosphate ions present in saliva. Fluorapatite makes enamel more resistant to caries attack.  Helps in mineralization of hypo mineralized areas that are often present in a newly erupted tooth.
  • 218.  Fluoride ingested during tooth development makes teeth slightly smaller with shallow fissures and decreased cusp heights. Effects of fluoride  Increases resistance of enamel to caries.  Increases rate of post operative maturation.  Enhance remineralization of incipient caries.  Interferes with bacterial enzymatic process and prevents bacterial adhesion.  Modifies tooth morphology when ingested during tooth development.
  • 219. Systemic  Fluoridated community water  School water fluoridation  Salt fluoridation  Milk fluoridation  Fluoride tablets and drops Topical  Professionally applied Self applied solution  Prophylactic dentrifices pastes  Mouth rinses  Varnishes and gels
  • 220. Fluoridated community water  Children with developing permanenent teeth.  Optimum level – 1 ppm public water supply must be available. School water fluoridation  Optimum level 4.5 – 5.5 ppm.  Fluoride tablets and drops.  Contain sodium fluoride or calcium fluoride.  Amount required varies according to age, weight and dietary pattern of child.
  • 221. AGE FLUORIDE CONTENT IN DRINKING WATER (PPM) 0-0.3 0.3-0.6 > 0.6 0.25-2 YRS 0.25 0 0 2-3 YRS 0.5 0.25 0 3-13 YRS 1.0 0.5 0
  • 222. Salt fluoridation › 200-350 mg Fl/kg of salt Milk fluoridation 43% reduction in DMFS with 200 ml milk/day (7 ppm) for 5 yrs
  • 223. › Tablets: 0.125, 0.25, 0.5 mg › Oral rinse: 5 ml = 1mg › Drops: 1 drop = 0.1 mg
  • 224. (1)Professionally applied topical fluorides Prophylactic pastes containing fluoride  -In high risk caries patients  -Clean and supply fluoride in one step  -Contain Zr silicate abrasive Fluoride solutions  -Naf(2%) & Snf2(8%) solution Fluoride gels  - Acidulated phosphate fluoride gel (apf) Fluoride varnishes  - Provide high uptake of fluoride into enamel  - Most cost effective fluoride delivery
  • 225. GEL
  • 226.  Clinician applies a thin layer onto teeth.  Application time is several minutes.  Patient avoids eating for several hours and avoids brushing till next morning.  Varnish sets on contacting moisture.  Only tooth brushing needed before applying. Disadvantage – temporary tooth color change AGENTS USED – Naf in organic lacquer. Difluorosilane in polyurethane lacquer and chloroform.
  • 227. [A] fluoride dentifrices  Sodium fluoride, stannous fluoride and sodium monofluorophosphate.  Usually contain 1000 ppm of fluoride.  Cleared from mouth by spitting rather than rinsing and used twice a day. [B] fluoride mouth rinses  Sodium fluoride and acidulated phosphate fluoride.  Additive effect when used along with topical or systemic application.
  • 228. Age Type of dentifrice used <4yrs Fluoridated dentifrice not recommended. 4-6yrs Brushing twice with non-fluoridated and once with fluoridated dentifrice. 6-10yrs Brushing once with non-fluoridated and twice with fluoridated dentifrice. >10yrs Brushing thrice a day with fluoridated dentifrice.
  • 229. 1 – high dose/low frequency  Used best in weekly rinsing programs in schools 2 – low dose/high frequency  Used best by individual patients at home  High caries risk/caries active pt. Should rinse daily.  Optimal application time in the evening.  10 ml used for 1 min after which eating or drinking should be delayed for 1 hour.
  • 230.  Fluorides are less effective in preventing pit and fissure caries  Sealants have 4 important preventive effects: #Mechanically fills pits and fissures with an acid resistant resin. #Deny cariogenic organisms their habitat. #Render pit and fissure easier to clean. #Arrest incipient carious lesion.
  • 231. Placement of sealant
  • 232. “Sealants have been shown to be effective to have long-term retention to cause regression of active lesions, and to be superior to amalgam restoration in terms of time requirements” Indications  High risk for caries patients.  Recently erupted molars with deep, retentive pits and fissures.  Teeth with signs of incipient occlusal caries.  Adult patients with suspicious fissures. Types 1.Glass ionomer sealants (type iii) 2.Resin sealants
  • 233.  'Laser' is an acronym for 'light amplification by the stimulation emission of radiation'. Its theoretical basis was postulated by Albert Einstein.  First tooth exposed to laser light was in 1960.  Laser light in dentistry is a unique, non-ionizing form of electromagnetic radiation that can be employed as a controlled source of tissue stimulation, cutting or ablation, depending on specific parameters of wavelength, power and target tissue.
  • 234.  Laser treatment particularly in combination with topical fluoride application (NaF, APF), increase resistance against caries, desensitization of hypersensitive dentine (Er:YAG) and improve marginal seal under composite resin (Nd:YAG).  C02-laser = Caries inhibition up to 82.7%  Er:YAG-laser = Reduction in surface lesion depth (root surfaces 39%, primary enamel surfaces 56%)  Nd:YAG-laser (with Duraphat) = Caries inhibition (pits and fissures 43%, smooth surfaces 80%).
  • 235. Defintion of caries activity (Messer, Aus Dent J, 2000)  “the rate at which dentition is destroyed by caries, represented by the sum of the new carious lesions and enlarged lesions per unit time”
  • 236. › To determine the need and extent of preventive measures › Indicator of patient cooperation › Aid in timing of recalls › Determine success of therapeutic measures › Motivate and monitor the effect of education programs. › To identify high risk groups/individuals › Aid in determination of prognosis › Precautionary signal to orthodontist › Guide to insertion of expensive restorations
  • 237.  Lactobacillus colony count test  Snyder test  Reductase test  Buffer capacity test  Fosdick calcium dissolution test  Dewar test  S.mutans level in saliva test-screening tests  Cariostat test  Caries risk test
  • 238.  Microbial tests › Mutans streptococci- strip mutans, dentocult SM, cariescreen SM › Lactobacilli- dentocult LB  Salivary tests › Salivary buffering capacity – dentobuff system › Salivary flow rate- proflow, oricult  Normal flow rate : 0.25 -0.35 ml/min  Stimulated flow rate: 1-3 ml/min
  • 239.  Hadley - 1933  number of bacteria in saliva by counting the number of colonies appearing on Tomato Peptone Agar or Rogosa Agar  METHOD › Saliva collected › 1:10 & 1:100 dilution made › Spread on agar plate › Incubated for 3-4 days at 37 C
  • 240. CFU/ML CARIES ACTIVITY 0-1000 Little or none 1000-5000 Slight 5000-10,000 Moderate > 10,000 Marked  No. of colonies
  • 241.  Measures the rapidity of acid formation when saliva inoculated in glucose agar  METHOD: › saliva sample is collected. › Media contains  peptone 20 gms  Dextrose 20 gms  Sodium chloride 5 gms  Agar 16 gms  Bromocresol green 0.02 gms
  • 242. CARIES ACTIVITY COLOR CHANGE FROM BLUE/GREEN TO YELLOW High 24 hrs Medium 48 hrs Slight 72 hrs Immune no change>72 hrs Caries activity
  • 243.  Modification of snyder test  Uses less agar i.e 5ml per tube  Saliva is directly drooled into tubes  Incubated for 4 days at 37deg C  Color change is noted from bluish green to yellow
  • 244.  Measures the activity of the salivary enzyme reductase  Sample is mixed with an indicator ie diazoresorcinol  Changes in color measured after 30 secs & 15 mins
  • 245. COLOUR TIME SCORE CARIES ACTIVITY Blue 15 min 1 Non conducive Orchid 15 min 2 Slightly conducive Red 15 min 3 moderate conducive Red Immediately 4 Highly conducive Pink or white Immediately 5 Extremely conducive
  • 246.  5 ml of saliva measured into a beaker.  pH of saliva adjusted to 7.0 by addition of lactic acid  Level of lactic acid is re-recorded  Lactic acid is then added to sample until a pH of 6.0 is reached  The number of ml of lactic acid needed to reduce the pH from 7 to 6 is a measure of buffer capacity  DENTOBUFF STRIP SYSTEM
  • 247. final pH value Buffer capacity blue 6.0 or more high green 4.5 - 5.5 medium yellow 4.0 or less low
  • 248. more than 0.25 normal 0.1 - 0.25 low less than 0.1 very low
  • 249. 25 ml of gum stimulated saliva is collected Placed in an 8 inch test tube with 0.1 gm of powdered human enamel Tube shaken for 4 hrs, then again analyzed for calcium content The amount of enamel dissolution increases as the caries activity increases DEWARS TEST- pH is measured
  • 250.  Plaque/toothpick method  Saliva/ tongue blade method  S. mutans adherence method  S. mutans dip-slide methods  S. mutans replicate technique
  • 251. Plaque samples placed in ringers solution Samples are shaken until homogenized Plaque suspensions streaked across a mitis salivarius agar plate containing sulphadimetine
  • 252. Aerobic incubation at 37 C for 72 hrs, the cultures are examined under microscope GRADE COLONIES/10 FIELDS 1 None 2 < 8 3 ≥ 8
  • 253. Saliva/plaque samples obtained using tongue blades Inoculated on Mitis salivaris agar for 48 hrs at 37 C Counts of more than 100 CFU are prop to greater than 106 colonies per ml of saliva by conventional methods Advantages STRIP MUTANS TEST-Jensen & Bratthall (1989)
  • 254. Chair side method STRIP MUTANS TEST
  • 255. Saliva inoculated in MS broth for 24 hrs at 37 C  After growth, the supernatant removed  Cells adhering to the glass examined macroscopically SCORE NO OF COLONIES - No growth expressed + Few deposits from 1-10 ++ Scattered deposits of smaller size +++ Numerous minute deposits & more than 20 large deposits (indicates > 105 CFU/ml)
  • 256.  Procedure A: DENTOCULT SM › Saliva on agar coated slide › Bacitracin disks on the slide, incubate for 48 hrs › Colony density (small blue colonies) compared with model chart:  0-negligible  1-< 105  2- 105 to 106  3- >106
  • 257. Procedure B: CARIESCREEN SM › Bacitracin tablet in buffered diluent in which saliva is placed › Dip-slide coated with MS agar placed in vial › Incubate for 48 hrs at 37 C › Use reference colony density chart that shows equivalent of  10,000, 50,000, 100,000, 250,000, 500,000, 1,000,000
  • 258.  To localize S. mutans on tooth surfaces  Imprint of tooth surface taken with impression matrix  Incubated at 37 C overnight  Observe directly for growth on the matrix at specific sites  e.g.- occlusal/root surfaces
  • 259. Recently advocated - new, quick, effective test CRT has 2 components: ›CRT BACTERIA two-in-one dip-in-slide test which identifies counts of Mutans & Lactobacilli Stimulated saliva is applied to dip-in-slide Incubated for 48 hrs at 37 deg C
  • 260. CRT BUFFER •Available in strip form, which changes color to indicate whether the patient has a high, medium or low buffering capacity. •This occurs within 5 mins.
  • 261. I. Hand cutting instruments:- The cutting instruments are used to cut hard and soft tissues of the mouth. Excavators are used for removal of caries and refinement of the internal parts of the cavity, chisels are used primarily for cutting enamel. Excavators :- The four subdivisions of excavators are ordinary hatchet , Hoes, angle formers and spoon excavators. Chisels :- Chisels are intended primarily for cutting enamel . They are grouped as :- straight, slightly curved, biangle enamel hatchet gingival marginal trimmer.
  • 262. Majority of the caries removal procedures on enamel and dentin is accomplished by using rotary instruments. Five factors are potentially responsible for the discomfort and pain that is associated with cavity preparation.  sensitivity of vital dentin  pressure on tooth  bone conducted noise and vibration  high pitched noise of air turbine handpiece  Development of high temperature at cutting surface
  • 263.  R.D. Black originally developed air abrasion in 1945.  He preliminary investigation into other alternative pseudo mechanical method for removal of caries. It involved bombarding the tooth surface with high velocity particles, conventionally aluminum oxide was carried in a stream of air.  Depending on the natural of the abrasive used this technique has the ability of abrading efficiently both sound dentin and enamel.
  • 264.  In this method there is no rise in temperature.  This is a relatively pain free procedure.  Polycarbonate resin or aluminum hydroxyl appetite mixtures might be more selective in carious dentin removal leaving healthier sound tissues virtually unscratched.
  • 266.  A recent development from the original ultrasonic is the use of high frequency sonic air scalars with a modified abrasive tips a technique known as Sono Abrasion.  The tips described an elliptical motion with a transverse distance between 0.08- 0.15mm and a longitudinal movement of between 0.055- 0.135mm.  They are diamond coated on one side using 40 micro meter grit diamond an are cooled using water irrigant at a flow rate of between 20 –30 ml/min.
  • 267.  currently there are three different instrumental tips.  A length ways halved torpedo shaped 9.5 mm long and 1.3 wide.  A small hemisphere 1.5mm in diameter  A small hemisphere 2.2 mm in diameter.  If the applied pressure air is too great, the cutting efficiency is reduced due to damping and oscillation.
  • 268.  Air polishing is a process by which water soluble particles of sodium bicarbonate to which tri calcium phosphate, is added to improve the flow characteristics, are applied onto a tooth surface using air pressure.  It has been suggested that air polishing would be used for the removal of carious dentine at the end of cavity preparation.
  • 269.  In 1976 Goldman & Kronman reported on the possibility of removing caries material chemically using N- Mono glycine and N- Mono Chloro Aminobutryt.  Caries dentin softened by this is readily removed by lightly abrading its surface with an applicator tip.
  • 270.  Carisolv consists of two carboxy methyl cellulose base gels . A red gel containing 0.1 M .Amino Acids Nacl, NaoH and erythrosine . second containing sodium hypo chlorite.  The two are thoroughly mixed in equal parts at room temperature before use and applied using hand instruments on to the exposed carious dentine ,left for 60 seconds prior to gently but firmly abrading away the softened dentine to leave a hard caries –free cavity.
  • 271.  Since the development of the first ruby laser by MAIMAN in 1960 researchers postulated that it could be applied to cutting both hard and soft tissues in the mouth.  The efficacy of lasers will depend on numerous factors including the wavelength characteristics, pulse energy, repetition rate.
  • 272.  Lasers that are currently been investigated for more selective hard tissue abrasion include  Er. YAG & ND. YAG  Carbon dioxide lasers  Excimers lasers: › Argon Freon › Xenon : Chlorine  Holmium lasers  Dye Enhanced laser ablasion British Dental Journal 2000; 188: 476–482
  • 273. Featherstone John D.B,The science and practice of caries prevention,JADA 2000;131:887-899
  • 274. The clinical management of dental caries has been primarily directed at the treatment of the consequences of the diseases process by placing restoration and not at curing the disease. The widespread use of fluorides has dramatically reduced the prevalence of dental caries and the rate of progression of the carious lesion. These changes permit dentist to adopt to more conservative management strategies directed at prevention and cure of dental caries.
  • 275. Thank you