Dental Caries.pdf details notes about teeth

Intestinal obstruction anatomy, physiology ,etjiolgy,pathogenesis,clinical features,diagnosis,treatment

1. Dental Carries
Name: JayaramanMohanraj
ArumugamKarthickumar
Course: 3
Group: 46

2. Dental Caries
Dental caries is a common chronic infectious resulting from tooth-adherent
cariogenic bacteria, primarily Streptococcus Mutans, which metabolize
sugars to produce acid, demineralizing the tooth structure over time. This
activity describes the evaluation and management of dental caries and
highlights the role of the interprofessionalteam in evaluating and treating
patients with dental caries.

3. Etiology
Dental caries is a term that refers to both the disease and the resulting lesion. The caries process
occurs in the biofilm, which is permanently active with every pH fluctuation , and the lesion
manifests in the dental hard tissues.
Dental caries occurs when the biofilm microbiota that normally resides in the oral cavity in
homeostasis change to an acidogenic, aciduric, and cariogenic population due to the frequent
consumption of sugars. The result of this shift can be clinically invisible or lead to a net mineral loss
within the tooth’s hard structures, resulting in a visible carious lesion. caries, the process, can exist
without caries, the visible lesion.

4. Etiology

5. Therefore, dental caries is considered a dietary-microbial disease that
requires a cariogenic biofilm and regular exposure to fermentable
carbohydrates (glucose, fructose, maltose, and sucrose) from the diet.
Behavioral, psychological, and social factors also play a significant role in
the disease process. Fluoride’s capacity to prevent caries is a well-known
fact, and insufficient fluoride exposure should also be considered
contributing factor in the disease process.

6. Epidemiology
Dental caries is a major healthcare problem as it is the most prevalent
disease worldwide. Almost 100% of adults are affected by dental caries. The
disease concentrates in groups with low socioeconomic status, and despite
being easily preventable, its prevalence did not significantly decrease over
the last thirty years.

7. Carious lesions have a higher percentage and incidence of certain bacterial species: Streptococcus mutans, Streptococcus
sobrinus, and Lactobacilli, isolated from advanced caries. The specific plaque hypothesis was based on this finding,
believing that only specific bacteria caused the disease. Indeed, Streptococcus mutans, in particular, are strongly linked to
caries, but caries can develop in sites where Streptococcus mutansare absent. This observation gave rise to the
nonspecific plaque hypothesis, where caries is believed to result from the net metabolic activity of the microbiota of the
biofilm. Although the etiologyof dental caries is not completely specific, we cannot ignore that a limited type of bacteria
is consistently found in higher numbers from the affected areas. The currently accepted concept is the ecological plaque
hypothesis.
The ecological plaque hypothesis believes that dental caries is not caused by a specific type of microorganism acting alone
but is the result of a shift in the microbiota of the dental biofilm towards more cariogenic species. Oral acidic conditions
from regular sugar consumption select the bacteria that empathize more with this environment and eliminate the benign
species that do not tolerate such conditions.

8. Demineralization and remineralization
Fermentable carbohydrates are metabolized by the biofilm bacteria that produce organic
acids, primarily lactic acid. These end products of bacterial metabolism accumulate in the fluid
phase of the biofilm, causing a pH drop and demineralization of the surface layer of the tooth.
The enamel porosity increases, the spaces between the crystals widen, and the surface softens,
which provides an opportunity for the acids to get deeper into the tooth structure and
demineralize the subsurface.
At this point, the reaction products of the demineralization –calcium and phosphate –
accumulate in the enamel surface and can protect it from further mineral loss. Also, available
fluoride can help to protect from surface demineralization.

9. •Sugars are swallowed and cleared by saliva that can return the biofilm pH to neutrality thanks to its
buffer capacity; calcium, phosphate, and fluoride now remineralize the tooth’s surface.
•If the acidic conditions perpetuate, the pH drops will continue reaching a point when the rate of
mineral loss in the subsurface is higher than the surface, resulting in a subsurface lesion. When there
is sufficient mineral loss, a white spot becomes clinically visible.
•A white spot can be arrested or reversed if behavioral changes and preventive measures are
implemented (ICDAS 1 and 2). If caries progresses further, microcavities are formed in the enamel
due to the increased surface porosity, clinically corresponding to an ICDAS code 3. The surface
lesion will collapse with time, leaving a macroscopic hole (ICDAS 5 or 6). Despite the severity of the
lesion at this point, it can still be arrested, but the cavity will remain.

10. Tissues
Carious tissue consists of four different zones histologically, among which three zones are visible
clinically. The outer layer consists of the necrotic zone and contaminated zone containing microbial
biofilm, which can be appreciated clinically as soft mineralized tissue of the tooth.
This necrotic zone has a very high microbial load. The next zone is the zone of demineralization
characterized by very few microorganisms, minimal nutrients, and an anaerobic atmosphere. This zone
can be correlated clinically as leathery dentine. Finally, the innermost zone near the pulp is the
translucent zone of a firm, softer dentine. Demineralization and the absence of microorganisms
characterize this zone because microbial flora cannot penetrate till this depth.

11. Tissues of
Dental Caries

12. Clinical Signs
The first clinical sign of the disease is a white spot, which is the expression of the enamel
subsurface demineralization – the surface enamel is more mineralized. If the acid challenge
continues, the previously smooth enamel surface becomes rough. Eventually, enamel
microcavitations and cavitations may occur – the average time that the carious lesions remain
radiographically in the enamel was suggested to be three to four years , but lesions are highly
variable, and they have the potential to regress.
As the caries process progresses, the dentin also experiences mineral loss and bacterial invasion,
which in return produces secondary dentin to protect the pulp.

13. •Active or Inactive?
•We can determine if a carious lesion is active or inactive according to several
factors:
•Location: is the lesion in a plaque stagnation area? Is it located along the gingival
margin?
•Aspect: is it white or brown? Is it matte or shiny?
•Texture: is it rough or smooth?
•Integrity: is it cavitated or non-cavitated?
•Gingival bleeding on probing: is the gingiva bleeding on probing?

14. •A carious lesion is considered active when it shows more of these
characteristics: it is whitish, matte, has a rough texture (when
carefully touched with the tip of a blunt probe), has plaque
stagnation, is cavitated, and if there is gingival bleeding.
•By contrast, a carious lesion is presumed inactive if it has the
opposite characteristics: brownish, shiny, smooth, non-cavitated, it is
not associated with plaque and away from the gingival margin, and
there is no gingival bleeding on probing.

15. •Root Caries
•A root caries also starts as a subsurface demineralization like an enamel caries;
however, root caries becomes softer at an earlier stage.These lesions tend to look
extensive, but they rarely exceed 0.5 to 1 mm deep. A root caries provides time to
implement plaque control measurements to arrest them thanks to the slow rate of
microbial penetration and tissue degradation they experience.
•Recurrent Caries
•A recurrent or secondary caries is a new caries that forms at the restoration’s
margin. A microleakage of the restoration causes it; however, this leakage does not
result in an active demineralization under the filling.

16. Treatment And Management
Treatment/ management: management of dental caries should be aimed at
1.detecting initial lesions,
2.determining caries activity,
3.performing a caries risk assessment,
4.preventing new carious lesions,
5. preserving dental tissue,
6.maintaining teeth for as long as possible.

17. Existing caries should be initially managed by non-invasive procedures (e.g.,
remineralization, biofilm removal, sealing) instead of removing dental tissue.
Cavitated lesions should be arrested or controlled following a minimally invasive
approach, e.g., repairing a defective restoration instead of replacing it.
Non-invasive Procedures
We do not need to place a filling in a lesion that can be accessed by easy cleaning
measures that will disturb the biofilm, such as fluoride-containing toothpaste.

18. White spot lesions, including initial occlusal lesions.
When on a bitewing x-ray, approximal lesions are limited to the enamel or are just into dentin. (It is
improbable that these lesions are cavitated in modern populations).
Cavitated and non-cavitated root surface lesions that can be reached by cleaning implements.
If a recurrent lesion adjacent to a restoration is cleansable, it does not require restoration.
In 2016 The International Caries Consensus Collaboration presented recommendations for carious tissue
removal and cavitated lesions management. They based the decision-making process on whether the lesion can
be reached by cleaning implements – cleansable lesion – or not – non-cleansable lesion; if surface cavitation is
present, the lesion should be considered non-cleansable and active.

19. The resulting consensus was as follows:
“Noncleansable cavitated dentine caries cannot be managed by biofilm removal, remineralization, or sealing alone.
However, in the primary dentition, these lesions might be transformable into cleansable lesions and managed via
nonrestorative cavity control.”
“Certain occlusal lesions might appear clinically non-cavitated but radiographically extend significantly into
dentine. If such lesions cannot be arrested through biofilm control alone, fissure sealing can be carried out; however,
the integrity of the sealant needs to be monitored, and there is a possibility, until more evidence has emerged, that a
“trampoline” effect may lead to failure of the sealant and a restoration will be required.”
Furthermore, Kidd et al. Recommend performing invasive treatments in cavitated occlusal lesions (ICDAS codes 3 or
higher) visible in dentin on a bitewing x-ray and cavitated approximal lesions that are clearly in dentin on a
bitewing x-ray.

20. Tooth Decay
Tooth decay, also known as cavities or caries, is the breakdown of teeth due to acids
produced by bacteria. The cavities may be a number of different colors from yellow to
black.
 Symptoms may include pain and difficulty with eating. Complications may include
inflammation of the tissue around the tooth, tooth loss and infection or abscess
formation.

21. Causes of
Dental Caries

22. Cause
The cause of cavities is acid from bacteria dissolving the hard tissues of the teeth (enamel, dentin and
cementum).
The acid is produced by the bacteria when they break down food debris or sugar on the tooth surface.
Simple sugars in food are these bacteria’s primary energy source and thus a diet high in simple sugar is a risk
factor. If mineral breakdown is greater than build up from sources such as saliva, caries results.Risk factors
include conditions that result in less saliva such as: diabetes mellitus, Sjögren syndrome and some
medications.

23. Medications that decrease saliva production include antihistamines and antidepressants.
Dental caries are also associated with poverty, poor cleaning of the mouth, and receding gums resulting in
exposure of the roots of the teeth.
Worldwide, approximately 3.6 billion people (48% of the population) have dental caries in their
permanent teeth as of 2016. The World Health Organization estimates that nearly all adults have dental
caries at some point in time.
In baby teeth it affects about 620 million people or 9% of the population.
They have become more common in both children and adults in recent years. The disease is most
common in the developed world due to greater simple sugar consumption and less common in the
developing world. Caries is Latin for “rottenness”.

24. •Parotid gland, are likely to lead to dry mouth and thus to widespread tooth decay. Examples include Sjögren
syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and
antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also
occlude the flow of saliva to an extreme degree. This is known as meth mouth. Tetrahydrocannabinol (THC),
the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known in
colloquial terms as “cotton mouth”. Moreover, 63% of the most commonly prescribed medications in the
United States list dry mouth as a known side-effect.Radiation therapy of the head and neck may also damage
the cells in salivary glands, somewhat increasing the likelihood of caries formation.
•Susceptibility to caries can be related to altered metabolism in the tooth, in particular to fluid flow in the
dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet “significantly suppresses the rate
of fluid motion” in dentin.

25. •The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco
contain high sugar content, increasing susceptibility to caries. Tobacco use is a significant risk factor for
periodontal disease, which can cause the gingiva to recede. As the gingiva loses attachment to the teeth due
to gingival recession, the root surface becomes more visible in the mouth. If this occurs, root caries is a
concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel.
Currently, there is not enough evidence to support a causal relationship between smoking and coronal
caries, but evidence does suggest a relationship between smoking and root-surface caries. Exposure of
children to secondhand tobacco smoke is associated with tooth decay.
•Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge
and ionic radius similar to bivalent calcium, such as cadmium, mimic the calcium ion and therefore
exposure to them may promote tooth decay.

26. • Poverty is also a significant social determinant for oral health.Dental caries have been linked
with lower socio-economic status and can be considered a disease of poverty.
• Forms are available for risk assessment for caries when treating dental cases; this system using
the evidence-based Caries Management by Risk Assessment (CAMBRA). It is still unknown if the
identification of high-risk individuals can lead to more effective long-term patient management
that prevents caries initiation and arrests or reverses the progression of lesions.
• Saliva also contains iodine and EGF. EGF results effective in cellular proliferation,
differentiation and survival.Salivary EGF, which seems also regulated by dietary inorganic iodine,
plays an important physiological role in the maintenance of oral (and gastro-oesophageal) tissue
integrity, and, on the other hand, iodine is effective in prevention of dental caries and oral health.

27. Symptoms
Person experiencing caries may not be aware of the diseaseThe earliest sign of a new carious lesion is the
appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of
enamel. This is referred to as a white spot lesion, an incipient carious lesion or a “micro-cavity”.
As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation
(“cavity”). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure
cannot be regenerated. A lesion that appears dark brown and shiny suggests dental caries were once present
but the demineralization process has stopped, leaving a stain. Active decay is lighter in color and dull in
appearance.

28. As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color
and become soft to the touch. Once the decay passes through the enamel, the dentinal tubules, which have passages to the
nerve of the tooth, become exposed, resulting in pain that can be transient, temporarily worsening with exposure to heat,
cold, or sweet foods and drinks.
A tooth weakened by extensive internal decay can sometimes suddenly fracture under normal chewing forces. When the
decay has progressed enough to allow the bacteria to overwhelm the pulp tissue in the center of the tooth, a toothache can
result and the pain will become more constant. Death of the pulp tissue and infection are common consequences. The tooth
will no longer be sensitive to hot or cold but can be very tender to pressure.
Dental caries can also cause bad breath and foul tastes.
 In highly progressed cases, an infection can spread from the tooth to the surrounding soft tissues. Complications such as
cavernous sinus thrombosis and Ludwig angina can be life-threatening.

29. Prevention
Below 8 years of age to prevent swallowing of toothpaste. After brushing with fluoride toothpaste, rinsing should be avoided
and the excess spat out. Many dental professionals include application of topical fluoride solutions as part of routine visits
and recommend the use of xylitol and amorphous calcium phosphate products. Silver diamine fluoride may work better than
fluoride varnish to prevent cavities. Systemic fluoride is found as lozenges, tablets, drops and water fluoridation. These are
ingested orally to provide fluoride systemically. Water fluoridation has been shown to be beneficial to prevent tooth decay,
especially in low social economical areas, where other forms of fluoride is not available. However, a Cochrane systematic
review found no evidence to suggest that taking fluoride systemically daily in pregnant women was effective in preventing
dental decay in their offspring.

30. •While some products containing chlorhexidine have been shown to limit the progression of existing tooth decay;
there is currently no evidence suggesting that chlorhexidine gels and varnishes can prevent dental caries or reduce
the population of Streptococcus mutans in the mouth.
•An oral health assessment carried out before a child reaches the age of one may help with management of caries.
The oral health assessment should include checking the child’s history, a clinical examination, checking the risk of
caries in the child including the state of their occlusion and assessing how well equipped the child’s parent or
carer is to help the child prevent caries. To further increase a child’s cooperation in caries management, good
communication by the dentist and the rest of the staff of a dental practice should be used. This communication
can be improved by calling the child by their name, using eye contact and including them in any conversation
about their treatment.

31. •Prevention of dental caries includes regular cleaning of the teeth, a diet low in sugar, and small
amounts of fluoride.
•Brushing one’s teeth twice per day and flossing between the teeth once a day is recommended.
Fluoride may be acquired from water, salt or toothpaste among other sources.
•Treating a mother’s dental caries may decrease the risk in her children by decreasing the number
of certain bacteria she may spread to them.
•Screening can result in earlier detection. Depending on the extent of destruction, various
treatments can be used to restore the tooth to proper function or the tooth may be removed.
There is no known method to grow back large amounts of tooth.The availability of treatment is
often poor in the developing world. Paracetamol (acetaminophen) or ibuprofen may be taken for
pain.

32. Thank You