Pathologies of immature temporary and permanent teeth
- Pathologies of temporary teeth:
- Introduction :
The oral pathology of children seems, at first sight, less rich than that of adults, and in fact, the lesions that we discover in this area are limited in number and also in extreme severity.
In addition, reactions that are usually localized can affect neighboring territories and take on a regional appearance, or, in rare cases, have repercussions on the child’s general condition.
- Caries pathologies of temporary teeth:
- Definition :
Tooth decay is a multifactorial, transmissible, chronic infectious disease characterized by localized destruction of dental tissues by acids produced by bacterial fermentation of dietary carbohydrates.
- Etiopathogenesis:
In children, as in adults, the etiology of caries is essentially due to interactions between cariogenic bacteria, a diet rich in carbohydrates and the susceptibility of the host; other factors further increase the risk of caries.
The appearance of caries is linked, regardless of age, to well-known conditions:
- Presence of bacteria, mainly mutans streptococci;
- Presence of sugar and any food causing a decrease in salivary pH;
- The value of the resistance of dental tissues to possible aggression;
- Time, both duration of contact and frequency of food intake;
- Clinical manifestations:
There is a potential window of infection between 18-36 months where the risk of vertical transmission is significant and which is due to:
Appearance of temporary molars with their occlusal relief conducive to the retention of caries.
Parental habits of tasting children’s foods before feeding them.
The child puts his finger in his mother’s mouth.
Ineffective or non-existent brushing at this age
Before 5 years of age, the most frequent location is the occlusal surface of the molars.
Mandibular molars are more affected than maxillary molars.
During this period, there are no proximal contacts yet, and the proximal surfaces of the molars are generally not carious.
On the other hand, during growth, proximal contacts are established and the frequency of caries increases.
The distal surface of the second primary molar becomes more susceptible to caries from the eruption of the first permanent molar.
Generally, caries progression and pulp involvement are more rapid for proximal caries than for occlusal caries.
The high frequency of caries in the maxillary central incisors is due, in part, to the position of the inter-incisive papilla, favoring the accumulation of dental plaque at this level.
Pit and fissure caries observed in molars are mainly due to the difficulty of properly cleaning these areas of high plaque retention.
- Active caries and arrested caries:
Depending on the speed of the carious process and the type of surface affected, Fortier and Demars-Fremault distinguish two types of carious involvement:
- Progressive caries , (active) the dentine is very demineralized and the bottom of the lesion, of a brownish yellow color, is easily penetrated by the probe and excavated. It is not very extensive on the surface, spreads quickly in depth; This carious lesion quickly leads to pulp necrosis and is not accompanied by the formation of reactive dentine.
- The inflammatory response of the pulp is generally greater than in permanent dentition, and may be the cause of internal resorption phenomena. This pulp is also less sensitive to painful stimuli, probably due to a lower density of nerve fibers.
- Arrested (inactive) caries (very rare) is located preferentially on the occlusal surfaces and is very extensive. Unlike the previous lesion, clinical examination reveals the presence of reactive dentine, hard, smooth, shiny, of variable yellow, brown or black color.
- Pulp retraction is often demonstrated radiologically.
- Polycaries or complex forms (caries or baby bottle syndrome):
In this category it is classic to describe 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 persistent bottle feeding. The latter is then considered by the parents or the nurse as a factor promoting the child’s falling asleep. The bottle contains sweetened or unsweetened milk, sweetened water or fruit juice.
This pathology is characterized by an initial attack on the vestibular and palatal surfaces of the upper incisors, leading to very rapid destruction of the crown and accompanied by exposure, most often painless, of the dentine. As they erupt, the other teeth are also affected according to the same process. The mandibular incisors, protected by the tongue which remains in contact with the lower lip, are generally spared.
- Septum syndrome:
Septal syndrome is a particular form of alveolar osteitis 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, it manifests itself with more or less intensity, as long as the coronary destruction of the proximal zones is not sufficient to ensure automatic cleaning.
- 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 damage may be of low thickness and will be of a progressive type.
- The interdental papilla is inflamed and congested.
- The inflammation can spread to the entire epithelial attachment.
- The application of current clinical tests such as thermal or percussion tests do not provide any important element in the search for these lesions.
- Radiological signs:
Confirm
- Proximal carious cavitations.
- Possible slight ligament thickening.
- The integrity or not of the alveolar and bony areas, given that septum syndrome can occur both in temporary teeth free of pulpal damage and in necrotic teeth, septum syndrome will always be suspected in proximal caries, whatever the pulp pathology.
- 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, pulsating pain is frequently the expression of septal syndrome. Differential diagnosis is sometimes difficult.
- 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.
- Pulp necrosis:
- This is the most common pathology of an untreated decayed temporary tooth. This necrosis, most often painless, follows pulp damage. In 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.
- Apical periodontitis:
- This pathology represents the most complex form of damage to the temporary tooth; it can not only lead to extremely severe clinical situations, but also disrupt the formation and development of the underlying germ.
- Two clinical forms are commonly observed:
- 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: are not necessarily related to the clinical picture, the involvement of the alveolar bone can exist at an early stage without radiological signs, this periodontitis is most frequently observed at the level of the temporary molars at stage II.
- Chronic form:
- more frequent at the level of the temporary tooth at stage III, the tooth represents at this period a widely 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, the gingival mucosa present a congested appearance, but the signs may be totally non-existent apart from the sole presence of a carious lesion.
- 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.
- 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 and limits our possibilities of conservation by endodontic therapy; it remains outside of considerations of general condition one of the major reasons for extraction of temporary molars.
- Clinical examination: a thorough clinical examination in the oral cavity allows the observation of 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 when there is complete disappearance of the architecture of the inter-radicular bone, early signs and widening at the level of the inter-radicular surface or bone loss limited to one side of the inter-radicular septum.
- The parulias:
- Parulia is defined as a purulent collection located in a cavity formed by tissue destruction.
- The best-known etiology of parulia is the impact of a small object: brush bristles, end of a toothpick, fish bone, in the sulcular groove.
The diagnosis is based on a localized abscess, developed rapidly, very painful, associated with an edema of the marginal or papillary gingiva without evidence of ulceration, desquamation, surface necrosis or loss of attachment. - The tooth or neighboring teeth are painful to percussion but without radiographic evidence of bone lysis.
Pathologies of immature temporary and permanent teeth
- Pathology of temporary teeth of non-carious and non-traumatic origin (ANOMALIES):
- Eruption anomaly
- Early eruption
- Eruption anomaly
One or two incisors may be present at birth (one in 1,400 cases). Their shape is normal but the deficiency of their periodontium causes them to fall out quickly. Otherwise, their extraction will facilitate breastfeeding.
Although they do not exist from birth, temporary teeth can erupt early on the arch. Their development is most often normal.
- Delayed eruption
Delayed eruption can affect one tooth, a group of teeth or the entire dentition. We will only speak of “delayed eruption” when there is a delay of more than 12 months compared to the normal date of development.
- Teething accidents
They are of 3 orders: 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: they are explained by the triple process of local irritation, reflex disorder, organic predisposition.
Local irritation is related to infection of the pericoronal cavity (pericoronitis).
Irritation of the mucosa and the gingivoalveolar filaments of the trigeminal nerve is transmitted reflexively. This irritation can affect various systems.
Accidents are of the type:
Hyperthermia for 3 days;
Dental bronchitis;
Various digestive disorders.
- Anomalies of numbers and morphologies
a- Agenesis is the defect in the development of a tissue or organ due to the absence of maturation or lack of its embryonic outline linked to an anomaly of hereditary origin or embryopathy.
b – Dysgenesis is an abnormality in the development of an organ or tissue in the process of formation, whatever the cause, and resulting in insufficiency, atropia or an absence of differentiation linked to embryopathy or a defect in hereditary information.
c- total anodontia: Anodontia is due either to a hereditary factor or to an illness of the mother or child preventing the formation of dental germs; if the absence of teeth is total, a dental prosthesis is essential.
d- Hypodontia: This number anomaly affects permanent teeth more often than temporary teeth, it concerns two or more teeth and is often asymmetrical, on the same arch, preferably affecting the teeth at the end of the series of general condition disorders is accompanied by agenesis
Hereditary ectodermal dysplasia characterized by the triad; anodontia, anhidrosis, hypotrichosis
Down syndrome in which agenesis of the end-of-series teeth is frequent
Christ, Siemens and Touraine syndrome, an anomaly of development of ectomesodermal structures, includes complete agenesis or anodontia is exceptional.
e- hyperdontia supernumerary teeth, anomalies characterized by a number of teeth greater than normal and a rarer condition, it manifests itself mainly in permanent dentition
supernumerary teeth are observed in all sectors of the arch, but are often median, in the majority of cases, they are dysmorphic and conoid and remain included.
The etiologies mentioned are:
- Cleavage of the tooth germ during odontogenesis;
- Further evagination of the blade caused by local irritation or cellular induction
- Heredity
- Association with general pathological conditions; eg: craniofacial dysostosis or Crouson’s disease (acrocephaly “malformation of the skull which is elongated upwards” with a high forehead and a median frontal boss.
f- anomaly of shape and structure
F-1 * volume anomalies;
Macrodontia is observed symmetrically on a single tooth or on all the teeth of an arch or on the entire dentition, often of hereditary origin, it can be associated with a dysfunction of the pituitary or thyroid gland it is also frequent in trisomy 21
Root volume anomalies, rhizomegaly is sometimes seen in permanent canines, mainly affecting PM and DDS
When the anomaly is extensive throughout the teeth, it is linked to a global alteration of the dental structures dentinogenesis or imperfect odontogenesis, of which it is one of the important elements of the diagnosis.
f2 * conformation anomalies
Coronal-radicular laceration: characterized by the non-alignment of the root in relation to the axis of the crown, most often located on single-rooted teeth, this anomaly is caused by trauma occurring before the mineralization of the root; it can prevent the normal eruption of the tooth.
Gemination is the attempt of a germ to subdivide, it is often abortive and is only indicated by a simple notch on the incisive edge.
- Structural anomalies:
We distinguish those that affect the enamel and others the dentin.
Enamel structural abnormalities:
Enamel structural abnormalities may have acquired or hereditary origins.
Acquired
Partial enamel hypoplasia: very common, temporary teeth are less often affected than permanent teeth. If all teeth are affected, it is necessary to look for a general disorder that may have left scars. Depending on the location of the hypoplasia, the time of the pathological damage can be determined.
Fluorosis: If the daily dose of fluoride is too high, the teeth may show structural abnormalities. The enamel is dull with chalky spots. The teeth may be whitish and, depending on the level of fluoride absorbed, their color may vary from yellow to dark brown. If exposure to fluoride has lasted a very long time, all the teeth are affected.
Neurological disorders: abnormalities of the maxillary incisors may be associated with malformations of the forebrain
Hereditary
Beltrami Romieu’s infantile lamelanodontia
Alteration of the enamel of the temporary tooth which is seen in children from twelve months.
It was described in 1939 by Beltrami and Romieu.
This is a dysplasia (anomaly of the formation) of the enamel whose origin is unknown but which is probably 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.
The extent of the destruction and the number of affected teeth vary from child to child.
Affected teeth become fragile, brittle and less resistant to shocks.
Amelogenesis imperfecta: This is a hereditary disease that is transmitted in an autosomal dominant manner. It affects all teeth. It can present several clinical forms.
Hereditary enamel hypoplasia: the enamel is hard, shiny, the alteration is the same on all teeth. It can for example be located at the neck: it 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.
Dentin structural abnormalities:
Dentinogenesis imperfecta or Cap de pont dysplasia: this is a hereditary disease with autosomal dominant transmission. Both sets of teeth are affected. Clinical observation may suggest an alteration of the enamel. The teeth are orange barley sugar colored, translucent, opalescent. The structural abnormality of the dentin comes from anomalies in the synthesis of the collagen molecule which result in abnormal ratios of its different constituents. 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 a corono-radicular striction, the root is slender due to dentin hypoplasia. During the evolution of the tooth there is a rapid obliteration of the corono-radicular pulp lumen
- Tooth color anomalies or dyschromia
- genetic dyschromias
*porphyria (a condition characterized by the presence in the body of massive quantities of porphyrin which gives the red color to the red blood cell)
Which manifests itself through other signs (urinary, cutaneous and ocular) gives temporary or permanent teeth of pinkish hues.
*neonatal jaundice, due to its hemolytic nature, releases greenish pigments linked to biliverdin (green pigment contained in bile and coming from hemoglobin) which stain the teeth green.
Milky enamel, with the presence of milky white opacities appearing included immediately under the surface of the enamel. Histology reveals in the altered enamel the presence of large apatite crystals on the periphery of the prisms as well as the existence of abnormally wide interprismatic spaces.
B- acquired dyschromias
1* pathological dyschromias: they result from dental caries and accompany all its stages ranging from the simple chalky whitish spot or leukoma or alarm dyschromia for MUGNIER to reach the whole range of grays, browns and blacks following caries, treatment, pulp loss or pulp necrosis.
2*traumatic dyschromias (also pathological) they lead to changes in the shade of the permanent incisors following trauma suffered by the temporary teeth which preceded them, varying from internal chalky white with smooth enamel on its surface to internal and external white and yellowish brown with a tear in the enamel.
3* drug-induced dyschromia: tetracyclines administered to pregnant women and young children aged 8 years and older cause unsightly and indelible staining of dental tissues in the form of light yellow or brownish bands depending on the class of antibiotic.
At roughly rectilinear limits, parallel to the free edge of the tooth, the situation of the affected area corresponding to the part of the crown developing during the period of administration of the antibiotic; the height of the bands being related to the duration of action of the antibiotic, at high doses enamel may be hypoplastic
Fluorosis or DRMOUS is observed in subjects who were born and lived during their early childhood (up to 8 years) in regions where drinking water contains a natural fluoride content greater than 1.5 mg/liter.
The lesions have very polymorphic aspects; the enamel is dull, without chips, opaque, with the presence of marbling or irregular whitish spots on the surface. The outermost layer of enamel is hypermineralized; it rests on an internal layer characterized by hypomineralization of the interprismatic substance, in these two layers the path of the prisms is very irregular.
Dental anomalies:
The diagnosis of a dental anomaly must be made as early as possible. Indeed, the earlier the treatment, the more
this will be easy and the practitioner’s work will be easier.
6.1. Number anomaly:
÷ Agenesis: These are frequent and affect permanent teeth more than temporary teeth. Screening
of agenisis in temporary dentition or fusion of two teeth is often revealing, in 20 to 40% of cases,
of agenisis in permanent teeth.
÷ Supernumerary teeth: These anomalies are rarer and are most often located in the incisor region. In case
delayed evolution of ectopic eruption of a permanent tooth (usually in the upper jaw), a
X-ray screening is necessary. Treatment consists of tooth extraction.
6.2. Shape anomalies:
÷ Double teeth: they are the result of a disorder during organogenesis and are the result of two processes
distinct: fusion and gemination. Fusion consists of the joining of two different germs; it can be
coronal, radicular or total (usually with a single pulp chamber). Gemination consists of the
subdivision of a germ. Tooth counting and radiological examination are sufficient to make the diagnosis. We can
However, there is no confusion between gemination and the fusion of a germ and a supernumerary tooth. Clinically,
The practitioner must ensure that these teeth do not disturb the occlusion and seal the coronal groove with a sealant.
or a fluid resin.
÷ Invaginated teeth (or dens in dente): They are discovered incidentally during the radiological examination and
result from a disorder of organogenesis.
÷ Taurodentism: This root malformation shows a pulp chamber that has developed abnormally
with very short channels.
6.3 Structural anomalies: They are very varied, either of hereditary origin (amelogenetic and dentinogenesis
imperfect) or acquired (regional odontodysplasia, dental fluorosis, dyschromia).
÷ Amelogenesis imperfecta: This condition affects all teeth and consists of either insufficient enamel or
in a qualitative imperfection of this enamel.
÷ Dentinogenesis imperfecta: All teeth in the same dentition are affected. They are brownish in appearance and
abrade rapidly. Roots are generally short with pulp retraction as opposed to dentine
reaction which closes the channels in the long term.
÷ Regional odontodysplasia: This disease affects several teeth of one or more quadrants (generally
maxillary and most often at the anterior level), which are also called “phantom teeth” because of their appearance
radiologically not very visible. Permanent teeth remain retained most of the time and, when they evolve, are the
seat of frequent abscesses.
÷ Dental fluorosis: This is a common disease today due to the widespread use of fluoride prevention.
and the varied contributions of this element. An overdose of fluoride leads to damage to the enamel, the stages of which are
function of the overdose. The damage is always symmetrical but may not affect all the teeth (function
of the period of overdose and therefore of tooth formation). Orthodontic treatments by multi-treatments
attachments are not recommended in advanced stages.
÷ Dyschromia: They are of very diverse etiologies and can be either of transmitted origin or of acquired origin.
(most often medicinal).
6.4. Volume anomalies:
÷ We distinguish between macrodontia (characterized by a size greater than normal) and microdontia (where the teeth
appear small in size). They can be localized or generalized (usually during dysendocrinia).
must make the differential diagnosis with “false” microdontia or macrodontia where the teeth are in fact
normal and the jaws are either too small or too large.
÷ When the volume abnormality affects the roots, we speak of rhizomegaly (root amplification) or
rhizomicria (by root reduction, example in dentinogenesis imperfecta).
Dental anomalies:
The diagnosis of a dental anomaly must be made as early as possible. Indeed, the earlier the treatment, the more
this will be easy and the practitioner’s work will be easier.
6.1. Number anomaly:
÷ Agenesis: These are frequent and affect permanent teeth more than temporary teeth. Screening
of agenisis in temporary dentition or fusion of two teeth is often revealing, in 20 to 40% of cases,
of agenisis in permanent teeth.
÷ Supernumerary teeth: These anomalies are rarer and are most often located in the incisor region. In case
delayed evolution of ectopic eruption of a permanent tooth (usually in the upper jaw), a
X-ray screening is necessary. Treatment consists of tooth extraction.
6.2. Shape anomalies:
÷ Double teeth: they are the result of a disorder during organogenesis and are the result of two processes
distinct: fusion and gemination. Fusion consists of the joining of two different germs; it can be
coronal, radicular or total (usually with a single pulp chamber). Gemination consists of the
subdivision of a germ. Tooth counting and radiological examination are sufficient to make the diagnosis. We can
However, there is no confusion between gemination and the fusion of a germ and a supernumerary tooth. Clinically,
The practitioner must ensure that these teeth do not disturb the occlusion and seal the coronal groove with a sealant.
or a fluid resin.
÷ Invaginated teeth (or dens in dente): They are discovered incidentally during the radiological examination and
result from a disorder of organogenesis.
÷ Taurodentism: This root malformation shows a pulp chamber that has developed abnormally
with very short channels.
6.3 Structural anomalies: They are very varied, either of hereditary origin (amelogenetic and dentinogenesis
imperfect) or acquired (regional odontodysplasia, dental fluorosis, dyschromia).
÷ Amelogenesis imperfecta: This condition affects all teeth and consists of either insufficient enamel or
in a qualitative imperfection of this enamel.
÷ Dentinogenesis imperfecta: All teeth in the same dentition are affected. They are brownish in appearance and
abrade rapidly. Roots are generally short with pulp retraction as opposed to dentine
reaction which closes the channels in the long term.
÷ Regional odontodysplasia: This disease affects several teeth of one or more quadrants (generally
maxillary and most often at the anterior level), which are also called “phantom teeth” because of their appearance
radiologically not very visible. Permanent teeth remain retained most of the time and, when they evolve, are the
seat of frequent abscesses.
÷ Dental fluorosis: This is a common disease today due to the widespread use of fluoride prevention.
and the varied contributions of this element. An overdose of fluoride leads to damage to the enamel, the stages of which are
function of the overdose. The damage is always symmetrical but may not affect all the teeth (function
of the period of overdose and therefore of tooth formation). Orthodontic treatments by multi-treatments
attachments are not recommended in advanced stages.
÷ Dyschromia: They are of very diverse etiologies and can be either of transmitted origin or of acquired origin.
(most often medicinal).
6.4. Volume anomalies:
÷ We distinguish between macrodontia (characterized by a size greater than normal) and microdontia (where the teeth
appear small in size). They can be localized or generalized (usually during dysendocrinia).
must make the differential diagnosis with “false” microdontia or macrodontia where the teeth are in fact
normal and the jaws are either too small or too large.
÷ When the volume abnormality affects the roots, we speak of rhizomegaly (root amplification) or
rhizomicria (by root reduction, example in dentinogenesis imperfecta).
Dental anomalies:
The diagnosis of a dental anomaly must be made as early as possible. Indeed, the earlier the treatment, the more
this will be easy and the practitioner’s work will be easier.
6.1. Number anomaly:
÷ Agenesis: These are frequent and affect permanent teeth more than temporary teeth. Screening
of agenisis in temporary dentition or fusion of two teeth is often revealing, in 20 to 40% of cases,
of agenisis in permanent teeth.
÷ Supernumerary teeth: These anomalies are rarer and are most often located in the incisor region. In case
delayed evolution of ectopic eruption of a permanent tooth (usually in the upper jaw), a
X-ray screening is necessary. Treatment consists of tooth extraction.
6.2. Shape anomalies:
÷ Double teeth: they are the result of a disorder during organogenesis and are the result of two processes
distinct: fusion and gemination. Fusion consists of the joining of two different germs; it can be
coronal, radicular or total (usually with a single pulp chamber). Gemination consists of the
subdivision of a germ. Tooth counting and radiological examination are sufficient to make the diagnosis. We can
However, there is no confusion between gemination and the fusion of a germ and a supernumerary tooth. Clinically,
The practitioner must ensure that these teeth do not disturb the occlusion and seal the coronal groove with a sealant.
or a fluid resin.
÷ Invaginated teeth (or dens in dente): They are discovered incidentally during the radiological examination and
result from a disorder of organogenesis.
÷ Taurodentism: This root malformation shows a pulp chamber that has developed abnormally
with very short channels.
6.3 Structural anomalies: They are very varied, either of hereditary origin (amelogenetic and dentinogenesis
imperfect) or acquired (regional odontodysplasia, dental fluorosis, dyschromia).
÷ Amelogenesis imperfecta: This condition affects all teeth and consists of either insufficient enamel or
in a qualitative imperfection of this enamel.
÷ Dentinogenesis imperfecta: All teeth in the same dentition are affected. They are brownish in appearance and
abrade rapidly. Roots are generally short with pulp retraction as opposed to dentine
reaction which closes the channels in the long term.
÷ Regional odontodysplasia: This disease affects several teeth of one or more quadrants (generally
maxillary and most often at the anterior level), which are also called “phantom teeth” because of their appearance
radiologically not very visible. Permanent teeth remain retained most of the time and, when they evolve, are the
seat of frequent abscesses.
÷ Dental fluorosis: This is a common disease today due to the widespread use of fluoride prevention.
and the varied contributions of this element. An overdose of fluoride leads to damage to the enamel, the stages of which are
function of the overdose. The damage is always symmetrical but may not affect all the teeth (function
of the period of overdose and therefore of tooth formation). Orthodontic treatments by multi-treatments
attachments are not recommended in advanced stages.
÷ Dyschromia: They are of very diverse etiologies and can be either of transmitted origin or of acquired origin.
(most often medicinal).
6.4. Volume anomalies:
÷ We distinguish between macrodontia (characterized by a size greater than normal) and microdontia (where the teeth
appear small in size). They can be localized or generalized (usually during dysendocrinia).
must make the differential diagnosis with “false” microdontia or macrodontia where the teeth are in fact
normal and the jaws are either too small or too large.
÷ When the volume abnormality affects the roots, we speak of rhizomegaly (root amplification) or
rhizomicria (by root reduction, example in dentinogenesis imperfecta).
- Trauma in children (immature temporary and permanent teeth):
Traumas constitute real pedodontic emergencies requiring a precise diagnosis and consideration which allows the choice of a therapy oriented towards the favorable development of the dento-alveolar structures concerned and towards the harmony of the growth of the jaws.
A distinction is made between trauma to temporary teeth and trauma to immature permanent teeth .
Trauma to temporary incisors:
Occurs at a very young age, posing multiple problems in terms of diagnosis, therapy and prognosis.
The practitioner’s decision will depend on the following factors:
– age and cooperation of the child.
– physiological stage of the temporary tooth.
– degree of damage to surrounding tissues.
-need to maintain space and hold temporary teeth in place to ensure arch length, and not to disrupt function and aesthetics.
* Trauma to temporary incisors is linked to learning to walk in balanced positions and results in dislocation or reintrusion of a barely erupted incisor.
1-Intrusion or ingression:
This is the usual result of a shock directed from below upwards on the upper temporary incisor block, the intrusion can be observed at the level of one or two incisors, its frequency is highest in children under 4 years old.
2- Partial dislocation:
Is the result of an anteroposterior shock with frequent interposition of an object (pencil, toy), can affect one or more teeth of the maxilla but also antagonist teeth, associated or not with wounds of the lip, palate and supporting tissues.
The diagnosis is firstly clinical, we evaluate the mobility of the traumatized tooth, its position in relation to the adjacent teeth.
3- coronary fractures:
They are not very common in temporary incisors if there is no pulp damage. They are unfortunately neglected by parents unless the fracture line is sharp and causes irritation of the lip or tongue. If there is pulp damage, the clinical and radiological examination will allow the treatment to be chosen according to the pathology and the stage of root resorption.
4- root fractures:
Rare in temporary dentition, they can be observed in the stability phase (stage 2), it is the mobility of the coronal fragment which will motivate the consultation.
5-Total dislocation :
Premature loss of temporary incisors due to trauma can occur in very young children and poses major problems in replacing missing teeth. It is necessary to maintain the aesthetics, function, phonation and space necessary for the development of permanent teeth and the growth of the premaxilla.
Sequelae of trauma to temporary teeth
- Pathologies of immature permanent teeth (IPD):
- CARIES PATHOLOGY OF DPI:
8
6. Dental anomalies:
The diagnosis of a dental anomaly must be made as early as possible. Indeed, the earlier the treatment, the more
this will be easy and the practitioner’s work will be easier.
6.1. Number anomaly:
÷ Agenesis: These are frequent and affect permanent teeth more than temporary teeth. Screening
of agenisis in temporary dentition or fusion of two teeth is often revealing, in 20 to 40% of cases,
of agenisis in permanent teeth.
÷ Supernumerary teeth: These anomalies are rarer and are most often located in the incisor region. In case
delayed evolution of ectopic eruption of a permanent tooth (usually in the upper jaw), a
X-ray screening is necessary. Treatment consists of tooth extraction.
6.2. Shape anomalies:
÷ Double teeth: they are the result of a disorder during organogenesis and are the result of two processes
distinct: fusion and gemination. Fusion consists of the joining of two different germs; it can be
coronal, radicular or total (usually with a single pulp chamber). Gemination consists of the
subdivision of a germ. Tooth counting and radiological examination are sufficient to make the diagnosis. We can
However, there is no confusion between gemination and the fusion of a germ and a supernumerary tooth. Clinically,
The practitioner must ensure that these teeth do not disturb the occlusion and seal the coronal groove with a sealant.
or a fluid resin.
÷ Invaginated teeth (or dens in dente): They are discovered incidentally during the radiological examination and
result from a disorder of organogenesis.
÷ Taurodentism: This root malformation shows a pulp chamber that has developed abnormally
with very short channels.
6.3 Structural anomalies: They are very varied, either of hereditary origin (amelogenetic and dentinogenesis
imperfect) or acquired (regional odontodysplasia, dental fluorosis, dyschromia).
÷ Amelogenesis imperfecta: This condition affects all teeth and consists of either insufficient enamel or
in a qualitative imperfection of this enamel.
÷ Dentinogenesis imperfecta: All teeth in the same dentition are affected. They are brownish in appearance and
abrade rapidly. Roots are generally short with pulp retraction as opposed to dentine
reaction which closes the channels in the long term.
÷ Regional odontodysplasia: This disease affects several teeth of one or more quadrants (generally
maxillary and most often at the anterior level), which are also called “phantom teeth” because of their appearance
radiologically not very visible. Permanent teeth remain retained most of the time and, when they evolve, are the
seat of frequent abscesses.
÷ Dental fluorosis: This is a common disease today due to the widespread use of fluoride prevention.
and the varied contributions of this element. An overdose of fluoride leads to damage to the enamel, the stages of which are
function of the overdose. The damage is always symmetrical but may not affect all the teeth (function
of the period of overdose and therefore of tooth formation). Orthodontic treatments by multi-treatments
attachments are not recommended in advanced stages.
÷ Dyschromia: They are of very diverse etiologies and can be either of transmitted origin or of acquired origin.
(most often medicinal).
6.4. Volume anomalies:
÷ We distinguish between macrodontia (characterized by a size greater than normal) and microdontia (where the teeth
appear small in size). They can be localized or generalized (usually during dysendocrinia).
must make the differential diagnosis with “false” microdontia or macrodontia where the teeth are in fact
normal and the jaws are either too small or too large.
÷ When the volume abnormality affects the roots, we speak of rhizomegaly (root amplification) or
rhizomicria (by root reduction, example in dentinogenesis imperfecta).
- Clinical forms:
- Depending on the stage:
The ICDAS classification, International Caries Detection and Assessment System, makes it easier to differentiate remineralizable lesions (initial caries, enamel caries) from irreversible lesions (cavity caries of the dentin).
Pathologies of immature temporary and permanent teeth
- Rapidly progressing caries:
In young people, who have a high caries risk (RCI), immature enamel and very permeable dentin (immature permanent teeth), the carious lesion progresses very quickly. Cavitary destruction of the enamel and dentin then occurs more quickly, over periods of weeks and months rather than years. The pulp inflammatory reactions in response will be more intense. They may or may not be accompanied by symptoms (the innervation is immature). In the absence of treatment, pulp lesions appear permanently and the inflammation spreads to the entire pulp.
- Depending on location:
-Caries lesions are mainly located on pits and fissures.
-Situations on smooth surfaces indicate a high caries risk.
-Mesial caries of the first permanent molar constitutes the majority of proximal lesions; it is particularly correlated with proximal lesions of temporary molars.
- Caries during orthodontic treatment:
-The appearance of these cavities is most often linked to a lack of brushing.
-These lesions are generally located on smooth surfaces and more precisely at the cervical level
- PULPO-PERIODONTAL PATHOLOGIES OF DPI:
- Complications of carious lesions can be pulpal (chronic, acute inflammation) and periodontal (chronic or acute apical periodontitis).
- -Their evolution is faster on young permanent teeth, due to the immaturity of the tissues (dentin immaturity and an open apex)
- Reversible pulp inflammation:
- Reversible pulpitis is by definition a mild pulp inflammation.
- Eliminating the irritant allows the inflammation to disappear and a return to healthy pulp.
- Reversible pulpitis on the DPI is usually asymptomatic. However, specific signs may occur.
- Application of stimuli such as the cold test can produce acute, transient pain.
- Irreversible inflammation:
- Irreversible pulpitis is a severe inflammation that does not regress if the initial cause is not removed.
- For immature permanent teeth, the pulp rapidly progresses to necrosis (widely open dentinal tubules).
- It is usually asymptomatic and slowly progresses to necrosis.
- The patient may report slight pain.
- However, the classic picture associated with irreversible pulpitis is spontaneous, radiating pain. The pain ranges from a short, sharp thrust to a continuous, dull ache, evolving into a severe, stabbing pain.
- Pulp necrosis:
- Pulp necrosis is the death of pulp tissue, the etiology of which is often traumatic or bacterial.
- It can be partial or total, septic or aseptic.
- The immature tooth is exposed by its crown to carious attacks and dental trauma.
- These attacks can lead to necrosis.
- Endodontic treatment allowing root closure is carried out (apexification, revascularization).
- Complications of pulp necrosis:
- -The pulp necrosis stage leads to the cessation of root growth and apical closure and is complicated by the appearance of a periapical bone infection. Apical periodontitis (AP) is an inflammatory lesion of the deep periodontium, mainly in the periapical region, resulting from pulp necrosis (chronic or acute apical periodontitis).
- -Their evolution is faster on young permanent teeth, due to tissues.
- – Complications of pulp necrosis can also lead, in the acute phase, to damage to the child’s general condition.
- This one is feverish and presents all the general signs of infection (adenopathies). It is important to monitor this condition closely, even after carrying out emergency procedures and antibiotic therapy.
- MIH: Molar-incisor hypomineralizations:
- Definition :
- Molar and incisor hypomineralization is an anomaly characterized by qualitative defects of the enamel, of systemic origin; affecting one or more first permanent molars, associated or not with lesions of the permanent incisors.
- Etiology:
- Different etiologies have been proposed:
- General problems
- Antibiotics
- Certain major syndrome
- Premature birth
- Dioxin in breast milk
- Diagnosis:
- -The enamel has normal thickness (the structural defect being qualitative not quantitative), and the surface of the defects is smooth and hard.
- -The enamel affected by MIH is however more fragile, and enamel loss can occur. Teeth decay more easily.
- – Hypomineralized areas are not necessarily symmetrical
- – Well-defined opacities ranging from white to yellow-brown
- Differential diagnosis:
- -Amelogenesis imperfecta
- – Enamel hypoplasia
- -Dental fluorosis
- -The initial lesion of the enamel
- Problems and complications associated with MIH:
- -Dental hypersensitivity
- -Severe enamel loss
- – Vulnerability to carious lesion
- -Technical difficulties for restorations.
Pathologies of immature temporary and permanent teeth
- CONCLUSION:
- The structures that make up immature permanent teeth are fragile, making them particularly vulnerable to carious disease and trauma.
- In young people, who have a high risk of caries, the carious lesion progresses very quickly.
- This cariosusceptibility, increased in the event of a structural anomaly such as molar-incisor hypomineralization (MIH), is therefore directly linked to the immature character
Pathologies of immature temporary and permanent teeth
Baby teeth need to be taken care of to prevent future problems.
Periodontal disease can cause teeth to loosen.
Removable dentures restore chewing function.
In-office fluoride strengthens tooth enamel.
Yellowed teeth can be treated with professional whitening.
Dental abscesses often require antibiotic treatment.
An electric toothbrush cleans more effectively than a manual toothbrush.