Pathologies of temporary teeth

Pathologies of temporary teeth

1. Non-carious and non-traumatic pathologies:

 1-1. Eruption anomalies

1.1.1. Early eruption

One or two incisors may be present at birth. 

                           1.1. 2. Delayed eruption

 We will only speak of “delayed eruption” if there is a delay of more than 12 months compared to the normal date of development.

1-2. Teething accidents: There are 3 types: local, regional, general

• Local accidents : gingivo-dental pruritus. If there is suppuration, it is pericoronitis which is painful.  
• Regional accidents : nasal hydrorrhea, jugal erythrosis, tearing, hypersalivation are due to trigemino-sympathetic irritation.  
• General accidents: Accidents are of the following type:
  •  hyperthermia for 3 days; 
  •  dental bronchitis; 
  •  various digestive disorders.

1-3. Anomalies of numbers and morphology  :

• number anomaly:
• Total anodontia: is due to a hereditary factor, preventing the formation of dental germs

• Hypodontia : . Oligodontia
• This is the partial absence of groups of teeth. 

          Hyperdontia :  Supernumerary teeth are often observed in the middle,  

1.4/anomaly of shape and structure  :

1.4.1. Volume anomalies:

macrodontia exp IC)  

Microdontia It is common in Down syndrome.

1.4.2. Conformation anomalies:

Coronal root laceration: characterized by non-alignment of the root in relation to the axis of the crown. 

• Gemination: is the attempt of a germ to subdivide.

1.5. Position anomalies:

• 1. malpositions and migrations: are very rare in primary teeth; 

1.6. color anomalies or dyschromia:

• These dyschromias will be of genetic or acquired origin.
  A/ Dyschromias of genetic origin
  
  
  * Neonatal jaundice. 
• B/ Acquired dyschromia:     B-1) Pathological dyschromia: These result from dental caries, treatments, pulp loss or pulp necrosis. B-2) Traumatic dyschromia (also pathological)
  
  
  
     

Pathologies of temporary teeth

•     B -3 Drug-induced dyschromia:
  * tetracyclines administered to pregnant women (from the 4th month of gestation) and to young children up to the age of 8 years cause unsightly and indelible discolorations.

Pathologies of temporary teeth

• * Fluorosis : The enamel is dull, dull, opaque, with irregular whitish spots on the surface. The outermost layer of enamel is hypermineralized. 

1-7. Structural anomalies:

• Beltrami’s infantile melanodontia.
• Amelogenesis imperfecta.
• Cap de pont dysplasia.
• Dentinogenesis imperfecta.
• Hereditary brown hypoplasia.

We distinguish those that reach the enamel and others the dentin.

1.7.1. At the enamel level: enamel structural anomalies may have an acquired or hereditary origin.

• Acquired
  •  Partial enamel hypoplasia: very common, temporary teeth are less often affected than permanent teeth.
•  Fluorosis: The enamel is dull with chalky spots. The teeth may be whitish and, depending on the level of fluoride absorbed, their color can vary from yellow to dark brown. 

• Hereditary
  • Beltrami Romieu’s infantile melanodontia
• Alteration of the enamel of the temporary tooth which is seen in children from twelve months.
• This is a dysplasia (anomaly of the formation) of the enamel which is hereditary. It results in the disappearance of the enamel (it dissolves or detaches in patches). From then on, the teeth are no longer protected and begin a process of destruction. The first teeth affected (sometimes the only ones) are the upper incisors.
• Small patches of enamel come off. They gradually turn black, then break down, leaving only snags.
• Amelogenesis imperfecta : This is a hereditary disease. It affects all teeth. It can present several clinical forms.
  •  Hereditary enamel hypoplasia : this corresponds to a disorder of the adamantine matrix during amelogenesis. 
  •  Hypomineralization of enamel : the enamel is soft, crumbly. There is a disturbance of mineralization. 
  •  Rickets : it can leave significant damage to the enamel. 
  •  Cleft lip and palate : very often, the enamel of children who have them is affected by structural anomalies.

1.7.2. At the dentin level

• Dentinogenesis imperfecta or Cap de Pont dysplasia: this is a hereditary disease. Both sets of teeth are affected. The teeth are orange barley sugar colored, translucent, opalescent. These teeth are devoid of enamel, of which only very thin islands remain. There is excessively rapid wear of all the crowns. The radiological image is that of a “bell clapper”: the crown appears globular due to corono-radicular stricture, the root is slender due to dentin hypoplasia. 

2. Carious pathologies of temporary teeth:

1. Special features of temporary teeth with regard to caries: 

In children, if the etiology of caries is essentially due, as in adults, to interactions between cariogenic bacteria, a diet rich in carbohydrates and the host’s susceptibility, other factors further increase the caries risk. Indeed, in young children the salivary concentration of defense factors is lower, and salivary flow is also lower. In parallel with this decrease in salivary flow, there is also a decrease in the oral clearance of dietary sugars. On the other hand, temporary teeth have morphological and physiological characteristics that will influence the clinical signs of caries disease.

• These characteristics are represented, for temporary teeth, by:
  •  a thinner layer of enamel and dentin. Very thin enamel has a lower degree of mineralization than that of the permanent tooth, which is why its demineralization will be rapid as will pulp damage; 
  • a large pulp chamber explaining the rapidity of pulp damage during pathologies and even therapeutic treatments 
  • the existence of pulpo-periodontal canals connecting the thin pulp floor of the molars with the inter-radicular zone
• a dentino-pulp complex characterized by a greater width of the dentinal tubules, greater vascularization of the pulp, a low thickness of the dentin and a variable pulp physiology depending on the physiological stage of the temporary tooth. 
• This pulp is also less sensitive to painful stimuli, probably due to a lower density of nerve fibers.

2. Clinical manifestations:

• The most frequently affected teeth are the molars and maxillary incisors, while the canines and mandibular teeth, with the exception of the molars, are very often free of caries. 
• Before 5 years of age, the most common location is the occlusal surface of the molars. Mandibular molars are more affected than maxillary molars, and maxillary and mandibular second molars have a greater susceptibility to caries. During this period, there are not yet proximal contacts, and the proximal surfaces of the molars are generally not carious.
• In contrast, during growth, proximal contacts are established and The frequency of caries on the proximal surfaces of temporary molars is greater when there is caries on the occlusal surface. The distal surface of the second temporary molar becomes more susceptible to caries from the eruption of the first permanent molar. 

Pathologies of temporary teeth

• Pit and fissure caries observed in molars are mainly due to the difficulty in properly cleaning these areas of high plaque retention. The initial damage often results in discoloration of the bottom of the grooves.
• The clinical manifestations of caries in primary teeth are represented by:
  •  progressive caries; 
  •  the caries stopped; 
  •  poly caries or complex forms.

3. Clinical form of caries according to the evolution:

• It is particularly important in temporary dentition to make a differential diagnosis between the 2 common forms, progressive caries and arrested caries, it will be based on 6 criteria which will be both clinical and radiological:
• The location of the caries.
• The extent of the loss of substance.
• Staining of hard tissues.
• Texture of fabrics.
• Presence or absence of reactive dentin.
• Sensitivity.

1. progressive caries:

• progressive caries, rapidly progressing towards the pulp complex, located mainly on the proximal surfaces of the molars, canines and incisors. quickly leads to pulp necrosis and is not accompanied by the formation of reactive dentine. Probe examination shows, once the enamel has disappeared, the presence of softened dentine; EXP distal caries of the 1st ^molar and mesial caries of the 2nd ^temporary molar. It develops without any symptoms, this double lesion only becomes painful when one of the marginal ridges collapses, by compression of the interdental papilla with food compaction
• the child complains of sharp pain, worse after meals “septum syndrome” which, if exteriorized, may suggest pulp damage.
• In the majority of cases, the progression is towards necrosis, 

2. stopped caries , located at the level of the occlusal surfaces of the molars and on the vestibular and proximal surfaces of the incisors and canines. Unlike the previous lesion, the clinical examination reveals the presence of a reactional dentine , hard, smooth, shiny, of variable color yellow, brown or black. These teeth are characterized by an absence of sensitivity to different stimuli: cold, hot, probe examination
3. poly caries or complex forms  : 

• Baby bottle tooth decay or baby bottle syndrome; This type of pathology is generally observed in children over 12 months old. This term describes rampant caries whose etiology is complex. These caries are due to:
  •  excessive and repeated consumption of carbohydrates before bedtime or at nap time (pacifier with a teat dipped in honey, sucking on a candy or a piece of chocolate), significant consumption of pediatric medicated syrups; 
  •  infection with mutans streptococci; and/or continued bottle feeding. The bottle contains sweetened milk or sweetened water or fruit juice.
• This pathology is characterized by an initial attack on the vestibular and palatine surfaces of the upper incisors, leading to very rapid destruction of the crown and accompanied by exposure, most often painless, of the dentine. The other teeth are also affected by the same process. 
• This process occurs in three stages:
  •  colonization by mutans streptococci. 
  •  an intense multiplication and accumulation of these streptococci as a result of the excessive and frequent consumption of cariogenic substrates; 
  •  rapid demineralization and cavitation of enamel, which results clinically in rampant caries.

Four clinical stages can be described:

Stage 1 : initial damage. This is a stage where the lesions are reversible and are observed between 10 and 20 months on the maxillary anterior teeth. The enamel is characterized by a zone of white, opaque demineralization located at the cervical level of the tooth, more rarely on the proximal faces. 

Stage 2 : Dentin involvement. It is observed at the age of 16-24 months and is characterized by more pronounced carious lesions in the maxillary anterior teeth affecting the dentin, which takes on a yellow-brown color. These lesions, at this stage, worry parents and children begin to complain of greater sensitivity to cold. The maxillary first temporary molars present initial lesions in the cervical and proximal areas.

Stage 3 : deep involvement. It is observed between 20 and 36 months and is characterized by significant and deep lesions of the maxillary anterior teeth accompanied by pulp irritation. The child complains of pain caused by chewing, drinking and brushing as well as spontaneous pain at night and lasting several minutes. The maxillary first molars are in stage 2 and stage 1 can be diagnosed on the mandibular first molars as well as on the maxillary canines.

Stage 4 : 

traumatic injury. It is diagnosed at the age of 30-48 months and is characterized by a fracture of the crown of the maxillary anterior teeth due to enamel-dentin destruction. These teeth are necrotic in most cases. The maxillary first molars are in stage 3 and are the cause of pulp pain. The maxillary second molars and canines may be in stage 2 as well as the mandibular first molars.

• This type of lesion must be differentiated from Beltrami’s infantile melanodontia which is also observed in temporary teeth. It is characterized by:
  •  by the appearance of brownish spots on the vestibular surface of the maxillary incisors which will extend in depth, gradually destroying the dental crown; 
  •  and by a black coloration of the dentin stumps.
• These lesions affect all temporary teeth (with the exception of the mandibular incisors).

4. Complications of caries:

Local and locoregional complications of caries in deciduous teeth are mainly represented by:

1. septum syndrome: is a particular form affecting the interdental septum. A local irritation, in the form of a bad interdental point.

Subjective signs: during questioning, the child complains of sharp pain, generally exacerbated by meals, localizable, classic analgesics allow it to recede

        Clinical signs: The teeth are affected by proximal caries, the preferential location of this lesion is at the level of the 2nd ^molar , the carious involvement may be of low thickness and will be of a progressive type.

• The interdental papilla is inflamed and congested.
  • The application of clinical tests, thermal or percussion tests, does not provide any significant information.

Differential diagnosis: must be made:

•  Pulp inflammation caused by progressive proximal caries.
•  the parulic lesion indicates bone damage related to pulp necrosis; this lesion is generally located at a distance from the epithelial attachment opposite the tooth concerned. 

Radiological signs:  confirm 

• proximal carious cavitations.
• Possible slight ligament thickening.
• Whether or not the alveolar and bone areas are intact, septum syndrome will always be suspected at the level of proximal caries, whatever the pulp pathology.

2. Furcation involvement  :

The furcation is an area of ​​very frequent infectious complications, with the permanent tooth in the process of forming.

Furcation pathology constitutes a real difficulty in choosing a therapy; it remains one of the major reasons for extraction of temporary molars.

Clinical examination: the clinical examination allows us to observe a gingival abscess close to the epithelial attachment, this periodontal pathology can be independent of a pulp pathology, this is the most frequent case of diagnostic error, this will highlight:

• The state of the pulp, vitality or necrosis.
• The presence of septal syndrome.
• Periodontal status compared to the physiological stage of resorption.
• Radiological diagnosis

It is easy there is complete disappearance of the architecture of the inter-radicular bone.

3. Complications involving the underlying germ:

Pulp pathologies can, if left untreated, cause pericoronitis, hypoplasia, dyschromia or even a stoppage of development of the replacement tooth. These pathologies can also cause a follicular cyst. 

3. Pulp pathologies:  Pulpopathies:

The pain associated with pulpitis is very short-lived in the temporary tooth and responds to the usual painkillers, so the child almost never comes to see a doctor for this condition. 

Acute, throbbing pain is frequently an expression of septal syndrome. 

The clinical signs: are those of carious lesions. 

 Radiological examinations : confirm pulp proximity and highlight the absence of peri-dental or inter-dental bone involvement. 

1. Clinical forms and classification:

• The typical pain of pulpitis described in adults is not encountered in children, who experience symptoms such as discomfort or pain when chewing.
• Kunzel proposes the following clinical classification

     1- serous pulpitis ; deep cavity, closed pulp chamber and transient pain caused by “pressure and sugar”; the child can indicate the causative tooth 

    2- purulent pulpitis : deep cavity with softened dentin up to the pulp chamber, spontaneous pain; localized or radiating, significant at night; opening the pulp chamber relieves the patient 

    3- chronic ulcerative pulpitis : communication of the caries cavity to the pulp chamber; exploration with a probe reveals pain and pain when chewing

    4- chronic granulomatous pulpitis : significant destruction of the crown with hyperplastic proliferations of the pulpal connective tissue of various dimensions or a single pulpal polyp which can fill the pulp chamber with poor symptoms and pain when chewing 

4. Pulp necrosis:

• This is the most common pathology of an untreated decayed temporary tooth . This necrosis, most often painless, follows pulp damage. On multi-rooted teeth it can affect all or part of the radicular pulp and thus be responsible for a mixed pathology combining signs of necrosis and signs of pulp inflammation.  

5. Periapical pathologies: Apical periodontitis: Two clinical forms are commonly observed:
   1. the acute form: 

Clinical signs  : are important, there is a history of spontaneous , pulsatile , sharp pain which, unlike septum syndrome or pulpitis, can recur. Adenopathy is common and the general condition is altered , hyperemia , asthenia , palpation can highlight dental mobility. 

Radiological signs  this periodontitis is observed most frequently at the level of the temporary molars at stage II , 

For a therapeutic decision, the conservation of the temporary tooth by treatment and root canal filling should be chosen if the following criteria are met: 

• The child is in good general condition.
• Clean oral cavity.
• Long-lasting coronary reconstruction possible.

2. Chronic form: 

 More frequent at the level of the temporary tooth at stage III, the tooth represents at this period a largely open entity, authorizing numerous pulpo-periodontal exchanges. 

Subjective signs  : are comparable to those of septum syndrome 

Clinical signs: Coronary destruction is often significant. 

Congested and hyperplastic interdental papillae 

The parulid, if present, is distant from the epithelial attachment. 

Clinical tests are worthless, tooth mobility is not constant. 

Vestibular palpation allows us to suspect the disappearance of the alveolar bone. 

Pathologies of temporary teeth

• Radiological signs  : allow the diagnosis to be established, the absence of radio opacity of the inter-radicular and inter-dental alveolar bone indicates the extent of the lesion. 

Pathologies of temporary teeth

6. Traumatic pathologies: Trauma .

1. The cracks.
2. Simple fractures .
3. Complex fractures.
4. Coronal root fractures
5. Root fractures.
6. Lateral intrusion/dislocation.
7. Concussion/subluxation
8. Expulsion

4. Conclusion:

• the child must undergo check-ups with a pediatric dentist in order to intercept any pathology and avoid complications, however the care of young children poses difficulties in cooperation and often in  therapeutic decisions , this is why the practitioner must have the appropriate skills in equipment and expertise .
• Child care remains a difficult exercise because it requires much more than simple knowledge of dental physiology and pathology and restorative techniques; 
• The practitioner must be able to demonstrate psychology and patience
• The advent of new techniques and materials has expanded our therapeutic possibilities
• Adhesive dentistry is playing an increasingly important role in these restorative techniques.

Pathologies of temporary teeth

  Sensitive teeth react to hot, cold or sweet.
Sensitive teeth react to hot, cold or sweet.
Ceramic crowns perfectly imitate the appearance of natural teeth.
Regular dental care reduces the risk of serious problems.
Impacted teeth can cause pain and require intervention.
Antiseptic mouthwashes help reduce plaque.
Fractured teeth can be repaired with modern techniques.
A balanced diet promotes healthy teeth and gums.
 

Pathologies of temporary teeth