Semiology in pedodontics: Reminder of carious pathology and its complications

Semiology in pedodontics: Reminder of carious pathology and its complications

The WHO considers caries disease to be the third leading global morbidity scourge. The majority of dental procedures are devoted to caries treatment, even though most practitioners have little understanding of the mechanisms that initiate caries, how to identify at-risk patients, and what treatment plan to implement to prevent its progression. Too often, only the consequences of caries disease are treated, not the disease itself. Dentistry must move towards early diagnosis of at-risk populations, the development of preventive measures, and better management of these populations.

2. Definition :

The term caries is often used to refer to both the disease and the cavitation. It currently seems preferable to use the terms “carious disease” to refer to the pathology and “carious lesion” to refer to its consequences.

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Tooth decay, one of the most widespread chronic diseases in the world, is an infectious and transmissible pathology. Individuals are exposed to it throughout their lives. This multifactorial disease is the result of interactions between the oral ecosystem and calcified dental tissues. It consists of a demineralization process leading to the progressive destruction of the hard tissues of the tooth. This loss of dental structure is the symptom of the pathology. The lesions begin with minimal mineral loss at the microscopic level and can progress to total destruction of the tooth.

3. Etiology and pathogenesis of caries:

In reality, carious lesion progression is a dynamic process alternating between periods of progression and periods of arrest or even regression. The progression of a carious lesion can stop at any stage depending on the oral environment. These changes in progression are reflected by differences in surface condition: an active, non-cavitated enamel lesion is rough and dull, while an inactive enamel lesion is smooth and shiny. This difference in surface texture is a good indicator of caries severity.

Cariogenic bacteria that colonize dental surfaces ferment the sugars provided by food, which allow their survival. The metabolic wastes released are acids, particularly lactic acid. These lead to a drop in local pH: this is the demineralization phase. Salivary buffer systems allow a rise in pH and a

Reprecipitation of previously dissolved crystals: this is the remineralization phase. The evolution of the caries process depends on the balance between pathological factors and physiological defense parameters. Indeed, the demineralization process begins when the pH of the bacterial plaque is no longer buffered by saliva, i.e. below 5.5. Caries thus progresses when the demineralization phenomenon is greater than that of remineralization.

The four factors that influence its progression are described: host-substrate-bacteria-time.

Streptococci mutans (SM) are considered to be the main bacteria initiating dental caries. Their number, regardless of ethnic group, is a key indicator of caries risk. Thus, children with a high level of SM have a higher caries risk. However, recent studies show that the SM/caries relationship is not so absolute. A high proportion of SM can be present on the surface of a tooth without caries developing and, conversely, caries can occur without the presence of SM. Thus, other acidogenic bacteria such as lactobacilli and low pH non-SM can be

responsible for the initiation of a carious lesion.

1. Acquisition of flora

Although some studies have shown the presence of SM in newborns, at birth the newborn’s oral cavity is generally sterile. It will be progressively colonized by microorganisms inoculated most often via saliva and coming from various sources (food, drink, objects, etc.). The acquisition of oral streptococci and Gram-negative bacteria occurs mainly through contact with the parental flora (vertical contamination).

The proliferation of oral flora occurs in conjunction with the increase in dental surfaces. Thus, the establishment of temporary dentition creates a new habitat allowing bacterial colonization. This period, between the nineteenth and thirtieth month, is called the “window of infection.” Early colonization is correlated with the age at which the first caries appear.

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2. Types of bacteria

The acquired exogenous pellicle is an acellular film composed of proteins covering the dental surface. It primarily provides protection against demineralization, but allows bacteria in the oral cavity to adhere to the tooth. Successive colonizations lead to the formation of an increasingly complex biofilm, commonly called dental plaque. The first bacteria to colonize the dental surface, called non-SM, are Streptococcus sanguinis , oralis and mitis , representing 95% of the streptococcal population, or 56% of the bacteria in the biofilm. Mutans streptococci , for their part, represent only 2% of the initial streptococcal population. Subsequently, this primary biofilm, the dominant streptococci, changes and becomes the dominant actinomycetes. When a precarious leukoma, a primary enamel lesion (white enamel lesion), appears, the SM rate becomes higher but the biofilm is still predominantly composed of non-SM and actinomycetes. In cavitary lesions reaching the dentin, SM then represent 30% of the bacterial biofilm, indicating that this bacterium is directly responsible for the activity of carious lesions. Non-SM bacteria are the most adhesive to proteins and sugars, and produce polysaccharides, thus initiating biofilm formation. When this biofilm is subjected to prolonged exposure to sugars, the acidogenicity of non-SM bacteria and actinomycetes increases, transforming the biofilm to bacteria with higher acidogenic potential, SM and lactobacilli. Later, after the formation of a cavity, lactobacilli are responsible for the progression of the lesion. This bacterial adhesion is a virulence factor. Cariogenic bacteria metabolize dietary carbohydrates. This metabolism produces acids, including lactic acid, propionic acid, and formic acid, which cause the pH to drop. Below the threshold of 5.5, the

mineral phase of the tooth is likely to demineralize.

Sucrose is the most frequently involved carbohydrate. However, bacteria can utilize all fermentable sugars, including starch when cooked. The amount of fermentable carbohydrate ingested is not of great importance because a minimal amount is immediately ^utilized .

3. Host Response

Different general and local factors specific to each individual influence the development of caries. Among the general factors, enamel quality and saliva are the two important parameters. Saliva participates in cleaning dental surfaces and remineralization thanks to calcium and phosphate ions. The quality of salivary flow is an important parameter in assessing caries risk: if it is reduced, the caries risk increases. Saliva is mainly composed of water (99.5%). However, among the remaining 5%, we find inorganic and organic compounds such as salivary proteins (histatins, mucins, statherins). These proteins have antibacterial, antiviral and antifungal actions.

Modulations in the immune response alter each individual’s susceptibility to caries. It has been shown that certain alleles of the HLA (major histocompatibility complex) system allow for a greater effectiveness of the immune response.

4. Substrate and time

Bacteria metabolize all sugars. The most common culprit is sucrose. The amount of sugar ingested is not the most important factor; a small amount is enough to produce a cariogenic acidic pH. However, the frequency of exposure is very important. Repeated sugar intake within a short period of time prevents saliva from exercising its buffering capacity.

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4. Dentino-pulp complex of temporary teeth
5. From a morphological point of view:

Due to their morphological and physiological characteristics, temporary teeth are particularly sensitive to dental caries and its complications.

From a morphological point of view:

• the thickness of the hard tissues (enamel, dentin) is low, making the pulp volume proportionally large;
• the large diameter of the dentin tubules promotes bacterial penetration;
• The pulp horns are long and tapered, therefore close to the enamel surface. Pulp involvement due to carious or traumatic attacks is therefore frequent and rapid. In addition, the risk of pulpal breach during excision of the carious lesion is high;
• the pulp floor has numerous pulpoperiodontal canals communicating with the interarticular space, rapidly promoting damage to the furcation;
• The root canal anatomy is complex, the numerous accessory canals make it impossible to completely remove infected pulp parenchyma and necrotic debris, which is the cause of endodontic treatment failures. Root perforations during instrumentation are also possible;
• Divergent roots, the thinness of their apex and asymmetric physiological root resorption make the determination of the working length random and increase the difficulty of canal shaping and obturation.

2. From a physiological point of view:

The pulp tissue of temporary teeth is similar to that of permanent teeth. It is a young, highly vascularized connective tissue with high enzymatic and odontoblastic activity. This helps explain its hyperplastic reactions (Torneck, 1985);

• The innervation is not as dense as in permanent teeth, which explains why temporary teeth appear less sensitive than them (Rapp et of., 1968). This axiom may also be due to physiological resorption, which would result in nerve degeneration. However, there is no evidence that temporary teeth are less sensitive than permanent teeth, and any pulp treatment requires the use of anesthesia.
• the pathophysiology of the temporary tooth appears to evolve according to the different stages

, but this opinion is controversial.

Figure 1 : Pathophysiology of the temporary tooth (according to Fortier and Demars-Fremault, 1987)

5. The dentino-pulp complex of immature permanent teeth:

• The permanent tooth is considered immature when its root is still developing and apical closure is not complete. The apposition of secondary dentin in the pulp chamber and along the root is a continuous physiological process. Its low thickness when the tooth is immature confronts the practitioner with a large pulp volume which explains the very sensitive behavior of the young tooth to aggression (Smith, 2002).
• The very rapid progression of caries in immature permanent teeth is explained by the histomorphological characteristics of the young dental organ. At the time of eruption in the oral cavity, the tooth is said to be immature. Amelogenesis is complete, but the surface and subsurface layers of the post-eruptive enamel are porous and irregular, and therefore highly sensitive to chemical-bacterial aggressions in the oral environment. Enamel maturation is completed over the years by incorporation, on the surface, of mineral substances contained in the diet and saliva. This post-eruptive maturation will occur gradually, giving the dental surface resistance to the carious process. If a first molar erupts in a mouth with numerous caries, it will immediately be confronted with a cariogenic bacterial environment.

6. Semiology:
7. The risk of caries in children ( RCI):
   1. Determination of individual caries risk according to age
8. Before tooth eruption : The presence of salivary Streptococcus mutans (SM) increases the RCI. Contamination is inherent to vertical transmission from the environment. The main vectors are the pacifier or spoon which passes directly from the mouth of the adult to that of the child. In addition, the multiplication of sugary drinks intake increases their concentration (Powell, 1998; Harris et al., 2004; Warren et al., 2009) and therefore the RCI.
9. In temporary dentition : The main sign of high RCI is the presence of cavities, particularly in the temporary incisors. Sometimes, their number is replaced by the value of the caof (missing, decayed or filled tooth surfaces), item c, decayed temporary tooth surfaces, being the most important. In addition, the presence of plaque visible to the naked eye and a high level of SM or salivary lactobacilli should be noted. When interviewing parents, consumption of sugary drinks between your main meals, repeated at least 3 times a day, constitutes another sign of high RCI. Finally, brushing, if it is not daily, further increases this risk. On the other hand, the type of children’s toothpaste, fluoride-based or not, does not influence this risk. The presence of just one of these items is enough to define the subject as having high RCI. However, it was shown that in the absence of poor oral hygiene habits and repeated consumption of sugary drinks during the day, the other items did not increase the RCI subject to caries treatment.
10. In mixed dentition and young adults :

It is recommended to assess individual caries risk (ICR) at the first consultation and to reassess it periodically as it can vary over time. It is recommended to distinguish only two categories of ICR: high and low, based on the results of the interview, clinical examination and radiological assessment. Recommendations and prescriptions are made according to age and ICR

2. Primary caries, secondary caries

The term primary caries is used to define a cavity present on a tooth surface free of any restoration.

Among secondary caries, we differentiate the residual lesion located under a restoration from the recurrent lesion adjacent to the edges of the latter.

Secondary caries results from one or more causes:

• incomplete removal of infected tissues during first-line treatment;
• failure to comply with prophylactic measures (plaque control, fluorides);
• deficiency of marginal adaptation of restoration;

3. Active caries and arrested caries

Carious lesions can be differentiated according to their activity, which has a key impact on their management, although sometimes the clinical distinction between active or stopped caries is not always easy.

An active carious lesion is progressive and progresses rapidly towards the pulp. It is mainly located on the proximal surfaces of molars, canines and incisors.

It is not very extensive on the surface but spreads in depth. It very quickly leads to pulp necrosis and is not accompanied by the formation of reactional dentin.

On clinical examination, this lesion appears brownish and easily excavated. There is also dentin sensitivity. However, the tooth is asymptomatic until the marginal ridges collapse, at which point septum syndrome appears.

When the lesion has been present for a long time and shows no progression, it is considered inactive or arrested . It is located preferentially on the occlusal surfaces of molars, and on the vestibular and proximal surfaces of incisors and canines. It is very extensive on the surface but, in general, it does not reach the pulp. Clinical examination reveals the presence of a hard, smooth, shiny reaction dentine of variable color: yellow, brown or black. There is no dentin sensitivity.

The line between active and arrested caries is thin. Depending on the ecological balance of the biofilm covering the area and the oral environment, different stages can exist.

4. Initial caries:

The term initial caries indicates that the lesion is detected at a very early stage. Its diagnosis is made with or without the use of optical aids. The tooth is observed before and after careful drying in order to specify the severity of the enamel damage. The first signs of carious lesion detectable by the eye are called “white spot”, “precarious leukoma” or “initial lesion”. Its clinical appearance appears as an opaque white change in the enamel and a rough surface. Probing must be delicate. Indeed, if the probe is a tactile aid necessary to remove the plaque

, it is necessary to avoid any damage that would create cavitation.

5. Early childhood caries:

• Caries in young children or infants differ in certain characteristics

Previously, the definition mainly considered their etiology and the emphasis was placed on poor eating habits. Thus, the term “baby bottle tooth decay or syndrome”

seems far too reductive to us today. The term “early childhood caries”

» (ECC) (early carie childhood) introduces a broader definition and a better

understanding: the cause is not only due to poor eating habits. ECC is defined by the presence of more than one decayed, missing (due to caries) or filled tooth in a child 71 months or younger. Between 3 and 5 years, it is characterized by the

presence of one or more decayed, extracted or treated maxillary temporary incisors.

• These cavities are associated with frequent consumption of carbohydrate-containing beverages, particularly bottle feeding at bedtime, or prolonged breastfeeding (between 1 and 2 years) with very long feeding times. Liquids taken in while the child sleeps stagnate around the maxillary incisors and can cause rapid and severe destruction of dental structures ^.
• The lesions are characterized by the appearance of opaque white demineralized areas on the smooth surfaces of the maxillary incisors. At this stage, the lesions are reversible, but in the absence of changes in the oral environment, the carious lesions extend deep and superficially in the anterior sector and reach the occlusal and then proximal surfaces of the temporary molars.

6. Hidden caries

Hidden caries is the term used to define a lesion that has reached the dentin, which is difficult to detect on clinical examination, but is large enough and demineralized enough to be detected on radiographic examination. The enamel made resistant by the incorporation of fluorides is not broken,

However, microbial invasion has occurred through microcracks reaching the underlying dentin. Nevertheless, prophylactic cleaning and careful drying of the area must be performed.

allow this type of caries to be detected during clinical examination

7. Cavities induced by radiation or sugar medications

Radiation induces a decrease in saliva flow. Sugary medications taken in the evening after brushing teeth (e.g., homeopathic granules) promote sugar retention in the oral cavity. Both of these factors increase the risk of carious lesions.

8. Cavities during orthodontic treatment

For Fortier and Demars-Fremault, their appearance is most often linked to a lack of brushing.

From an aggravating factor in orthodontic treatment, it has become a risk factor in its own right.

9. Location:

The location of carious lesions also varies depending on the child’s age:

• at 20 months, cavities are located on smooth surfaces (early childhood caries)
• At 3 years of age, they are observed in the pits and fissures of temporary molars.
• around 4 or 5 years of age, the proximal surfaces of the temporary molars (twin cavities) are more frequently affected.

7. Special features of temporary teeth and immature permanent teeth
8. Temporary tooth

The temporary tooth has thinner layers of enamel and dentin than the permanent tooth. The pulp chamber is proportionally wider and the pulp horns are closer to the tooth surface. The carious lesion therefore reaches the pulp much more quickly, leading to frequent pulp treatments and ^{complications} .

The thinner pulp floor has numerous pulpoperiodontal canals communicating with the interradicular space. This explains the rapid involvement and bone loss of the interradicular area in cases of pulp necrosis. Complex root canal anatomy is the main cause of failure of endodontic treatments of primary teeth. The numerous accessory canals make it impossible to completely remove the pulp parenchyma and necrotic and infected debris.

Root canal shaping is particularly delicate due to the pronounced curvature of the roots and their thinness in the apical area. The apical foramina can be multiple and occupy different positions, evolving according to root resorption.

The contact between the primary molars is made by ellipsoid surfaces. It is then common for the distal surfaces of the first primary molars and the mesial surfaces of the second primary molars to be affected at the same time. These carious lesions are called “twin caries”.

Certain sites are preferentially affected by caries depending on the type of temporary tooth:

• on the maxillary and mandibular temporary incisors, the mesial surfaces are most often affected;
• on the canines, these are the vestibular faces;
• on the first mandibular molars, the occlusal, proximal and vestibular surfaces;
• on the maxillary first molars, occlusal and proximal surfaces

2. Immature permanent tooth
3. Morpho-histological characteristics:

The very rapid progression of caries in permanent teeth is explained by the histomorphological characteristics of the young dental organ. At the time of eruption in the oral cavity, the tooth is said to be “immature”. Amelogenesis is complete, but the surface and subsurface layers of the post-eruptive enamel are porous and irregular, and therefore highly susceptible to

chemobacterial attacks on the oral environment.

Maturation is completed over the years by the incorporation, on the surface, of mineral substances contained in food and saliva.

This post-eruptive maturation occurs gradually, giving the dental surface resistance to the carious process.

In addition, the dentin tubules are wide and therefore very permeable, also contributing to the rapid spread of caries.

If a first molar erupts in a mouth with many cavities, it is immediately confronted with a cariogenic bacterial environment.

4. Special case of the first permanent molar:

The first permanent molar is the first permanent tooth to erupt around the age of 6. It comes in behind the primary molars and does not push out any primary teeth. This explains why its arrival can go unnoticed.

Its eruption is slow: between 5 and 32 months. Self-cleaning of the occlusal surfaces is impossible and its position in the back of the oral cavity makes it difficult for young children to brush, as the occlusal surfaces are located below the occlusal plane of the temporary molars.

The irregular occlusal morphology of the grooves, especially in young teeth before attrition, promotes plaque retention and thus increases the risk of caries.

Location

The location of caries in young teeth is generally symmetrical. The susceptibility in decreasing order is: the first molar, the second molar, the premolars, the maxillary incisors and canines, and finally the mandibular incisors and canines.

8. Complications

Complications can be local, affecting the tooth or the underlying germ, or general, which can affect general and/or craniofacial development.

1. Local

Before any therapeutic decision is made, a correct diagnosis of the pulp condition based on clinical and radiographic examinations is necessary. Pulp sensitivity tests are performed, although they are unreliable in young children.

Figure 2: Diagnosis of pulp condition

1. Septum syndrome:

This is a complication of caries affecting the proximal surfaces of the molars. The child complains of spontaneous pain, punctuated by meals, which is linked to food compaction due to the collapse of the marginal ridges, thus creating a defective contact point. The interdental gingival papilla is irritated by the compression of food residues. It is edematous, inflamed and sometimes there is destruction of the marginal bone. Septum syndrome can be the starting point of periodontitis. In this case, the pulp of the affected teeth may be vital or show signs of reversible or irreversible inflammation. Treatment consists of restoring interproximal contacts and performing the appropriate pulp treatment if necessary.

2. Reversible pulp inflammation of temporary teeth:

This is a chronic inflammation due to deep decay. The inflammation remains confined to the cameral chamber. The treatment of choice is pulpotomy. If the pulp hemorrhage is uncontrollable, it is irreversible inflammation.

3. Irreversible pulp inflammation of temporary teeth:

Spontaneous, acute pain that wakes the patient at night is the pathognomonic sign of a pulp with irreversible inflammation. It is relatively fleeting in primary teeth. Treatment is pulpectomy if the primary tooth is in stage I or II, or extraction if root resorption is greater than half the root.

4. Pulp necrosis of temporary teeth without periodontal complications

This is the most common pathology of an untreated decayed temporary tooth. Most often painless, it can affect all or part of the root pulp, and be responsible for a mixed pathology combining signs of pulp inflammation and signs of necrosis.

If there are no associated signs of periodontium and the tooth does not show resorption, a pulpectomy should be performed followed by a watertight coronal restoration.

5. Pulp necrosis of temporary teeth with periodontal complications:

This is the most complex and serious complication due to its possible repercussions on the general condition and the underlying germ of the permanent tooth.

The acute form is most often observed in mature primary teeth (stage II). The clinical signs are the same as for permanent teeth. Radiographic examination allows assessment of the extent of bone destruction in the interradicular and periapical areas. The chronic form is more common when the primary tooth is in stage III.

Redness, swelling, an abscess or a fistula may be observed on the gum.

The presence of a depression felt on palpation of the vestibule is a sign of resorption of the alveolar bone which indicates the extraction of the tooth concerned.

In the case of an associated periodontal lesion of endodontic origin (fistula, abscess, external resorption, periapical or inter-radicular radiolucency) or the presence of internal resorptions, the extraction of the tooth is carried out.

6. Furcation involvement

Due to the thinness of the pulp chamber floor and the multitude of pulpoperiodontal canals, there is very frequent involvement of the inter-radicular zone, which is progressively destroyed. In the advanced stage, the appearance of a parula is the clinical sign.

7. Cellulite:

Sometimes, pulp necrosis can be complicated by cellulitis. Second temporary molars are more frequently involved than first molars. Fever, asthenia and the existence of

lymphadenopathy. Systemic antibiotic treatment is necessary before any local treatment. The emergency therapeutic procedure consists of opening the pulp chamber and placing the offending tooth under occlusion. When the clinical signs have disappeared, the offending tooth is extracted.

2. Complications involving the underlying tooth germ

Pulp pathologies, if left untreated, can affect the underlying germ and cause:

• of dyschromia;

• hypoplasias;
• from a stoppage in the development of the permanent tooth;
• of a follicular cyst which can cause the permanent tooth germ to be pushed out;
• of pericoronitis which may be responsible for the early exfoliation of the germ ^.

1. Complications in immature permanent teeth

Caries, when it affects immature permanent teeth, must be diagnosed and treated as quickly as possible to preserve pulp vitality and thus allow the physiological formation of the tooth’s roots. Immature permanent teeth are characterized by incomplete root formation and an open apex. When the root has reached its final length, the apex remains open for approximately 2 years. This highly vascularized area has very significant cellular potential.

Complications of carious lesions can be pulpal (chronic or acute inflammation) and periodontal (chronic or acute apical periodontitis). Their progression is more rapid in young permanent teeth, due to the immaturity of the tissues.

In cases of reversible pulp inflammation, preserving tooth vitality is the primary objective. Treatment consists of removing the carious lesion followed by capping the pulp tissue with a biomaterial.

In cases of acute pulp inflammation or necrosis, endodontic treatment that allows root closure (apexification) is performed. Recently, a better alternative to

Apexification treatment has been described. Preservation of the potential of pulp and mesenchymal stem cells of the dental papilla allows revascularization of the canal and completion of the root.

9. Conclusion :

In children, carious disease must be identified as soon as it appears in order to apply preventive measures to limit the progression of the carious lesion.

The different clinical forms must be recognized and appropriate therapies for each clinical situation must be known to limit the complications of the latter.

Semiology in pedodontics: Reminder of carious pathology and its complications

  Untreated cavities can cause painful abscesses.
Untreated cavities can cause painful abscesses.
Dental veneers camouflage imperfections such as stains or spaces.
Misaligned teeth can cause digestive problems.
Dental implants restore chewing function and smile aesthetics.
Fluoride mouthwashes strengthen enamel and prevent cavities.
Decayed baby teeth can affect the health of permanent teeth.
A soft-bristled toothbrush protects enamel and sensitive gums.
 

Semiology in pedodontics: Reminder of carious pathology and its complications