Terminology and epidemiological data of carious lesions
Introduction
Dental caries is a multifactorial, transmissible, chronic infectious disease characterized by localized destruction of dental tissues by acids produced by bacterial fermentation of dietary carbohydrates (Fejerskow 2004 and Selwitz 2007).
The associated infectious and multifactorial qualifiers express the predominance of the bacterial factor (no bacteria, no caries) and the existence of risk factors necessary for the stimulation of cariogenic bacterial activity.
I/Definition
In 1970, the WHO defined caries as an acquired disease, characterized by an alteration of the hard tissues of the tooth, leading to the formation of a cavity.
The lesion follows a progressively rapid course, and if it is allowed to evolve, it will become complicated.
infection of the pulp; of the alveolo-dental ligament; of the bone tissue; of the peri-maxillary tissue; of the lymph nodes and even at a distance at the level of the various systems of the organism.
We are therefore talking about carious disease.
II- oral ecosystem and dental plaque:
For a long time it was thought that the carious process consisted only of demineralization of enamel crystals, followed by degradation of the dentin, all leading to the formation of a cavity.
According to the current concept, the emphasis is on the demineralization-remineralization cycle of chemical reactions occurring at the level of the tooth structure.
The carious process is seen as the result of a prolonged imbalance in the oral cavity, which would cause the factors favoring the demineralization of enamel and dentin to prevail over those that facilitate the remineralization and repair of these tissues.
III- Multifactorial etiologies
High levels of acid concentrations and frequent contact lead to demineralization of the tooth surface.
Natural protective factors and repair mechanisms can be strengthened in the majority of patients, which allows the problem to be controlled to some extent.
The balance between health and disease is delicate and involves acid from bacteria-laden plaque competing with the protective factors produced by normal saliva flow and good oral hygiene.
1* Bacterial flora and plaque
Normally, different bacterial strains live in the oral cavity and some can colonize the tooth surface, forming dental plaque.
Bacterial plaque induces the fermentation of carbohydrates from food and beverages leading to the production of acid ions on the tooth surface. Acids also come from gastric reflux… juices and syrups
Some carbohydrates, once present in the mouth, are found in solution in saliva and become usable by the microorganisms in plaque which metabolize them, thus causing an immediate drop in pH of 2 to 4 points on the surface of the tooth.
2* analysis of dental factors.
a- morphological factors : promote a predisposition to caries.
the shape of the teeth
The size of the teeth
The shape of the arches
The shapes and depths of the furrows
Non-coverage of enamel at cervical level.
These factors are genetically determined; we can talk about the risk of caries attack based on morphological predispositions.
b- tooth resistance factors:
The harder the enamel, the less likely it is to decay. The more calcium is released, the more acid-sensitive the enamel is.
The more decayed it is
3* analysis of infectious factors: caries is a polymicrobial disease, it is an attack on the hard tissues of the tooth caused by bacteria.
Which bacteria are incriminated?
Most of the microorganisms in dental plaque are capable of breaking down sugars into acids; they are cariopathogenic bacteria, most often streptococcus.
These polysaccharides contribute to the formation of plaque and allow the adhesion of bacteria (real glue).
4* general diseases and dental caries:
There is a relationship between dental caries and general diseases to the extent that these diseases affect the teeth, the individual’s immunology, their resistance, their oral hygiene.
5* Oral hygiene and tooth decay. The relationship between the two is beyond doubt.
V/ terminology
The term “caries” refers indistinctly to the disease and the lesion, but we will more readily speak of carious disease or carious lesion depending on whether we wish to emphasize the pathological process or its after-effects.
From an anatomical point of view:
Coronal caries : a caries starting with enamel
Root caries : triggered in the exposed cementum and dentin areas of the root.
Depending on the site:
pit and groove caries located on occlusal surfaces and other crevices
smooth surface caries : those affecting the proximal surfaces and cervical regions of the clinical crown.
“Primary” caries : this is a lesion that started at a site free of restoration.
“Secondary” caries and “recurrent” caries will indicate a lesion adjacent to a restoration that started at the marginal level.
Depending on the activity:
so- called “active” caries , i.e. lesions in progression (more or less slowly or quickly)
“inactive” or “arrested” caries, i.e. those which no longer progress due to favorable changes in the environmental balance in favor of remineralization.
At any time, an active lesion can become inactive and vice versa.
Depending on severity or stage of development:
Initial caries : This is a lesion diagnosed at a very early or early stage.
The terms “early” caries, “moderate” caries and “advanced” caries are acceptable in clinical practice to indicate respectively enamel (included enamel-dentin junction), medium dentin and deep dentin involvement.
The term “established ” caries indicates that the dentin is involved and that surgical intervention and restoration are necessary.
Figurative terms may be used to describe a more specific clinical form:
“creeping caries” and “hidden caries”
Rampant caries are multiple, active caries that spread in sheets across tooth surfaces and occur in the same patient.
Hidden caries: the designation particularly highlights the inadequacies and difficulties in diagnosing occlusal lesions.
VI/ Protective dietary factors
Certain foods provide protective factors against demineralization.
Plaque is less likely to adhere to the tooth surface in the presence of fatty materials.
Dairy products, especially cheese, but perhaps also nuts, fall into this category.
Other foods can act as buffers in their own right. Foods that require vigorous chewing can be considered protective, because chewing significantly increases saliva flow, and therefore buffering capacity.
Saliva
Saliva plays a major role in protecting teeth against acid attack. The most convincing clinical illustration is represented by the rapid and considerable damage caused to the dental structure by the sudden loss of saliva (xerostomia).
Protective factors of saliva
• Ca2+ ions
• Film
• Buffering power of bicarbonates
• Salivary flow
• Fluoride ion content
The quality and quantity of saliva secreted varies throughout the day and declines during sleep. Unstimulated saliva contains little bicarbonate buffer with fewer Ca2+ ions
Reflex stimulation of salivary flow by chewing (e.g., chewing gum) or by the presence of acidic foods (such as citric acid) can increase flow by a factor of more than ten.
Following an acid attack, saliva is the main source of natural protection and repair.
Reduction of salivary flow below 0.7 ml/min may increase caries risk.
Fluorides
They react directly on contact with enamel and dentin and produce several effects:
• Form fluoroapatite which is less soluble than
Hydroxyapatite
• Inhibit demineralization
• Improve remineralization
• Inhibit bacterial metabolism
• Reduce the permeability of dental structure
• Inhibit plaque formation
Fluorine plays a key role in the demineralization—remineralization process. In an acidic environment, fluoride ions react strongly with free Ca2+ and PO42- ions to form fluoroapatite crystals Ca10(PO4)6(OH.F)12,
Daily consumption of fluoridated water throughout life increases resistance to caries for all age groups, from childhood to old age.
Topical applications of fluoride may also help inhibit the development of dental caries in individuals at high risk of caries.
Fluoride ions will not only prevent the development of initial lesions, but also stabilize existing lesions. This means that they can:
Contribute to the remineralization of early enamel caries
Partially remineralize carious dentin and thereby slow down or stop the carious process in the cavitary lesion
Remineralize root surface lesions so that restoration is not necessary
VII/ Epidemiology
Dental caries remains a public health problem worldwide and in all industrialized countries since, according to data collected in 2004 by the WHO, it affected 60 to 90% of school children and the vast majority of adults (Petersen et al; 2005).
In our country, from 1994 to 2000, the assessments carried out using the support of the school health program show that dental caries is the most common pathology in schools, with a prevalence of 37 to 40%.
Epidemiological indices of cariology
Dental epidemiological indices measure the severity of the specific condition at a given time by quantifying, according to a graduated scale, clinical observations.
In other words, they express, by precise numerical ratings, a given qualitative state.
The CAOD index
Developed by Klein and Palmer in 1930 and used by the WHO since 2003, it represents the sum of decayed, missing, filled teeth (or DMFT for decayed missing filled teeth).
It constitutes the reference indicator for measuring the incidence of caries in a subject and consequently in a targeted cohort of subjects or any population. Its value is: 0 ≤ CAOD ≤ 32
Comparative evolution of dental caries (DMFT index) in 12-year-old children, according to WHO, 2003
One of the limitations of epidemiological surveys in cariology was highlighted by Pitts (2004). This author warns practitioners against the abuse of the expression “free from caries”.
Indeed, conventional examination without X-rays or diagnostic aids, as practiced during screening campaigns, inevitably underestimates the real caries state and minimizes the need for prevention. One expression of this “delay in diagnosis” is the development of “hidden caries”
Each practitioner must develop his practice and adapt it to the real needs of patients. Epidemiology provides valuable information in this regard:
Future generations will have fewer cavities to treat with restorative dentistry and fewer teeth to replace than current generations, but they will need to be monitored throughout their lives,
Caries disease will mainly affect the temporary and permanent molars;
The lesions will be mainly located within the pits and grooves of the occlusal surfaces, and, to a lesser extent, on the smooth surfaces,
The speed of progression of lesions, which slows with age and depending on preventive behavior (Petersen and Yamamoto 2005), will be more conducive to micro-invasive surgical interventions;
The establishment of specific monitoring of the elderly will be essential to prevent the appearance and development of root caries.
Conclusion
The appearance and development of a carious lesion is characterized by the simultaneous presence of several factors:
Endogenous causes: the internal environment intervenes in the initiation of caries through the salivary pathway ; normally saliva protects the teeth against cariogenic agents ; caries begins if the defense by saliva becomes insufficient because an endogenous cause has set in.
Exogenous causes: acting directly on the surface of the tooth where the decay begins
Terminology and epidemiological data of carious lesions
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