Pathology of temporary teeth

Pathology of temporary teeth

Tooth decay is considered by the WHO to be the third leading global morbidity scourge. It is a chronic, infectious, and transmissible disease.

The appearance of these lesions in the temporary dentition and the speed of their development depend on several factors, the main ones being the histological and physiological characteristics of the tissues concerned, the quantity and frequency of carbohydrates in the diet, the presence of bacterial plaque linked to oral hygiene, and the quantity and quality of saliva.

Etiology and pathogenesis of caries:

Dental caries is a multifactorial disease of bacterial origin. It occurs when pathogenic oral flora produces acids resulting from the breakdown of carbohydrates. These organic acids, following a drop in plaque pH, diffuse through the enamel and dissolve its mineral elements. If the demineralization process thus initiated does not stop, it leads to cavitation: this is clinically observable dental caries.

Causal factors of caries disease

Diagnosis of the pulp condition

Diagnosis of the pulp condition is decisive for the choice of appropriate treatment and therefore, for a good prognosis, it is based on:

The clinical examination.
The history of symptomatology
The answer to the different test.

The major difficulty in making a diagnosis is that very young children often have great difficulty expressing what they feel due to a lack of vocabulary.

The pain expressed by the child helps the practitioner in interpreting signs of vitality or necrosis. The radiographic examination makes it possible to assess the physiological stage, to visualize the root morphology and the proximity of the underlying germ and, finally, to objectify internal resorptions or periapical or furcation damage.

The pulp conditions of temporary teeth are:

⇒ The pulp is healthy after traumatic or accidental exposure during cavity preparation. It can be kept alive if treated correctly;

⇒ The pulp exposed by a carious lesion always presents partial or total chronic inflammation or necrosis;

⇒ Partial or total pulp necrosis can be the result of untreated caries, or traumatic pulp exposure.

⇒ Pulp necrosis may develop after dislocation trauma when pulp circulation has been interrupted.

Carious pathology of the temporary tooth
1. Active caries and arrested caries

⇒ The active carious lesion : is progressive and progresses rapidly towards the pulp:

Essential seat: proximal surfaces of molars, canines and incisors.
Not very widespread 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: it appears brownish and easily excavated with dentin sensitivity, but the tooth remains asymptomatic until the marginal ridges collapse, at which point septum syndrome appears.

⇒ The inactive or stopped carious lesion :

Present for a long time and shows no progression
Preferred seat: occlusal surfaces of molars, vestibular and proximal surfaces of incisors and canines.
It is very widespread on the surface but, in general, it does not reach the pulp.
Clinical examination reveals the presence of hard, smooth, shiny reaction dentin 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.

Rampant caries: are multiple, active carious lesions occurring in the same patient and spreading in a sheet. They are often located on smooth surfaces. They have different terminologies depending on their etiology.

Early Caries in Young Children ( ECC )
- ECC is defined as the presence of more than one decayed, missing (due to caries), or filled tooth in a child 71 months of age or younger.
- They are associated with frequent consumption of carbohydrates, which is done by different means (sweetened baby bottles, chocolate milk, sugary medication, etc.) and particularly with

bedtime, or prolonged breastfeeding (between 1 and 2 years) with very long feeding times. Frequently very poor, or even non-existent, oral hygiene.

Four clinical stages can be described:

⇒ Stage 1: The initial lesion of the enamel

Initial damage, lesions are reversible
Observed between 10 and 20 months on the maxillary anterior teeth.
It is characterized by a white, opaque area of demineralization located at the cervical level of the tooth, more rarely on the proximal surfaces.
Diagnosis requires careful drying of the tooth using the air/water syringe.
The child did not complain of any pain or sensitivity.

⇒ Stage 2:

Dentin damage.
Observed at the age of 16-24 months.
It is characterized by more pronounced carious lesions in the maxillary anterior teeth affecting the dentine, which takes on a yellow-brown color.
Children begin to complain of increased sensitivity to cold.
The maxillary first temporary molars present initial lesions in the cervical and proximal areas.

⇒ Stage 3:

Deep injury.
Observed between 20 and 36 months.
It 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 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 the maxillary canines.

⇒ Stage 4: (progressive polycaries)

Traumatic injury.
It is diagnosed at the age of 30-48 months.
It 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 first maxillary molars are at stage 3 and are causing pulp pain.
The maxillary second molars and canines may be in stage 2 as may the mandibular first molars.

Complications of carious pathology of the temporary tooth: they can be local, affecting the underlying tooth or germ, or general, which can affect general and/or craniofacial development.
1. Local:

⇒ Septum syndrome:

Common in children, this pathology is a complication of caries affecting the proximal surfaces of the first and second temporary molars (twin caries). It is associated with the collapse of the marginal ridges.
Spontaneous pain, punctuated by meals, which is linked to food compaction due to the collapse of the marginal ridges, thus creating a defective point of contact.
The interdental gingival papilla is irritated by the compression of food residue.
It is edematous, inflammatory and sometimes there is destruction of the marginal bone.
Septal 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 appropriate pulp treatment if necessary.

⇒ Reversible pulp inflammation:

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

⇒ Irreversible pulp inflammation:

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

⇒ Pulp necrosis without periodontal complication:

This is the most common pathology of an untreated decayed temporary tooth.
Most often painless, it can affect all or part of the radicular 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.

⇒ Pulp necrosis 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 temporary teeth (stage II). The clinical signs are the same as for permanent teeth.
Radiographic examination allows the extent of bone destruction in the inter-radicular and periapical areas to be assessed.
The chronic form is more common when the temporary 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.

⇒ Furcation damage

Due to the low thickness of the floor of the pulp chamber and the multitude of pulpo-periodontal canals, we observe a very frequent attack of the inter-radicular zone which is

gradually destroyed. In the advanced stage, the appearance of a parula is the clinical sign.

⇒ Cellulite:

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

Complications involving the underlying tooth germ

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

Of dyschromia; of hypoplasia;
From a stoppage in the development of the permanent tooth;
From a follicular cyst which can cause the permanent tooth germ to be pushed out;
Pericoronitis which may be responsible for early exfoliation of the germ

General complications : Pain caused by carious lesions can be the cause of

Sleep disturbances.
An impairment of the child’s general condition (fever, swollen lymph nodes).
It is important to monitor this condition closely, even after emergency procedures and antibiotic treatment have been performed. If the infection persists, the patient should be referred to a hospital.

Conclusion

Carious lesion is a pathological process leading to the destruction of the hard tissues of the dental organ by acid demineralization. It can become complicated if left untreated and lead to premature extractions in children.

Early tooth loss in growing children induces a decrease in the masticatory coefficient and can therefore influence craniofacial development .

Prevention and early treatment of dental caries is one of the major objectives in order to avoid and control the development of carious lesions.