Morphology, histophysiology and pathophysiology of the immature permanent tooth

Morphology, histophysiology and pathophysiology of the immature permanent tooth

1.  Definition:

•   A tooth is immature until the apical cemento-dentin junction is in place.
•   3 – 4 years after eruption of the tooth on the dental arch and occlusion
•  Immature tooth , immature periodontium and dental arches are immature

1. Amelogenesis:

• Enamel organ of epithelial origin
•  Differentiation of adamantoblasts (or ameloblasts)
•  Secretion of the organic matrix of enamel (amelogenins, enamelins, tuft proteins)
• Mineralization of this matrix: hydroxyapatite crystals (enamel prisms)

Acellular tissue incapable of regeneration, Terminated before eruption 

Morphology, histophysiology and pathophysiology of the immature permanent tooth

1. Email immaturity:

When the tooth erupts, the enamel is immature and then undergoes a process of post-eruptive maturation (secondary mineralization)

during which water and proteins are gradually replaced by calcium and phosphate, so-called demineralization-remineralization cycles.

In its mature form, enamel consists of numerous hydroxyapatite crystals and contains: more than 96% mineral phase, little water (3.2%) and only traces of organic matrix (0.4%). 

While its immature form consists of a larger organic matrix (19%), a reduced mineral phase (37%) and a much larger aqueous phase (44%). 

Immature enamel:

1- Post-Eruptive Maturation

•  Completed amelogenesis ≠ Ameloblasts
•  Irregular surface
•  Permeable pores: water, bacteria, acids
• Ionic exchanges: Post-eruptive maturation

• Increase in mineral phase, decrease in organic phase
• Exogenous mineral intake (saliva: Ca, P, F)
• Sensitivity to acid attacks

2- Coalescence of enamel prisms

•  Molars formed by welding 4 to 5 cusps
• Independent evolution of these cusps
•  Coalescence of enamel at the bottom of the grooves
•  98% persistence of a crack, a split

real weakness of DPI

• Numerous furrows, pits and cracks
• Immature enamel Sensitivity to acid attacks

• Occlusal grooves
• Brushing the Furrows!
• Progressive Caries
• Surprise Cavities!

II/ Dentin immaturity:

• The immature permanent tooth also shows immaturity at the level of the dentin.
•  Dentinogenesis continues throughout tooth formation.
• During tooth development, three types of dentin are produced:
•   Primary dentin is normal dentin, composed of regularly spaced tubules. § root apical closure
•   Secondary dentin: throughout the life of the tooth, on the periphery of the pulp chamber, floor, pulp horns.

 is deposited in response to biomechanical factors, such as

temperature changes, mechanical shocks or even chemical irritations.

•   Tertiary dentin, also called reactional or irregular dentin, is deposited
• after major pulp irritation such as attrition, caries, etc. It forms exclusively in the areas adjacent to the irritation.
• From a morphological point of view, the immature permanent tooth:
• has an absence of secondary dentin . In addition, immature permanent teeth do not yet benefit from the deposition of pericanalicular dentin, which gradually allows the obliteration of the tubules. These widely open tubules make the dentin very permeable.
• This results in the rapid proliferation of caries once the enamel-dentin junction is reached.

B) Dentin Sensitivity:

• Three theories:

• Dentin contains sensory nerve fibers
• Odontoblasts = receptors

• coupled to nerve fibers,
• cell junctions exist
• Pulp receptors stimulated by fluid movements

C) Immature innervation:

• Subodontoblastic Raschkow plexus is only established when the tooth is mature
• Teeth not very sensitive even if severely affected
• Unreliable vitality tests
• The innervation is also immature, which contributes to making it less sensitive to various external stimuli. The absence of apical constriction means that the nerve pathways are not compressed during possible inflammation, which explains a reduction or even absence of pain.
•  No apical compression during pulp inflammation
•  Reversible pulp inflammation in the early stages
• Pulp defense potential +++
• The therapeutic decision must take into account the stage of root and apical formation. Interventions on immature permanent teeth must allow for the most physiological dental and alveolar development possible.

III. Pulpo-radicular immaturity:

• The tooth erupts into the oral cavity when the root has reached 2/3 of its total length (Nolla stage 8). It will take between 03 and 04 years to reach stage 10. 
• between these 2 stages, the tooth will be considered immature.
• The immature tooth is characterized by an apical region that is not completely formed. The
• The vascular-nervous bundle is voluminous in a flared endodontic canal, thus revealing a widely open apex. With thin and fragile dentinal walls, the root appears thin and more or less short depending on the degree of evolution. 

   NOLLA Stadiums     

Stage 0. Dental blade stage 

Stage 1. Crypt: Buds, cups and dental bells 

Stage 2. Initial calcification 

Stage 3. One third crown completed 

Stage 4. Two thirds of the crown completed 

Stage 5. Crown almost complete 

Stage 6. Crown completed: Beginning of intra-osseous  eruption

Stage 7. One third root built 

Stage 8. Two-thirds of the root built: CB eruption 

Stage 9. Root erect but apex open 

Stage 10. Cemento-dentin junction in place

Table I: The NOLLA stages (according to NOLLA 1996)  .

Morphology, histophysiology and pathophysiology of the immature permanent tooth

VI/ Root formation:

• is done by epithelial proliferation in the connective tissue called the HERTWIG sheath which allows the differentiation of the cells of the radicular pulp into odontoblasts
• ensuring the dentinogenesis of the apical end of the root. Once the definitive length of the root has been acquired , the disintegration of the HERTWIG sheath is observed, thus putting
• exposed dentin in direct contact with the surrounding connective tissue. This process then leads to the
• formation of cementoclasts which will develop the primary cementum (which participates in the closing of the apical orifices) and the secondary cementum (which covers the apical part of the root), the latter
• predominant at the apical third of the roots and thus contributes to the formation of the apex. 

Root building:

Hertwig’s epithelial sheath,

• expansion of the enamel organ
• Induction of mesenchymal papilla cells: Dentin odontoblasts

• Apposition in apical direction
• Degeneration, Malassez epithelial debris 

Morphology, histophysiology and pathophysiology of the immature permanent tooth

Cementogenesis: 

• Differentiation of internal SF fibroblasts under induction of root dentin
• Organic cement frame developed then mineralized
•  Direction: Collet to Apex
•  Incorporation of SF fibers, anchoring of the tooth

Alveolar bone: 

• Differentiation of external SF fibroblasts into osteoblasts
• Organic bone structure developed then mineralized at the same time as the root
• Incorporation of SF fibers, anchoring of the tooth

Desmodont: 

• Fibroblasts intermediate zone of SF
• Collagen fibers organize, thicken
•  Incorporation of these fibers, anchoring of the tooth
• Final orientation of fibers occurs after eruption as opposed to mechanical and functional constraints

• Fibroblasts          
• Cementoblasts Conservation Secretory Potential 
• Osteoblasts 

Morphology, histophysiology and pathophysiology of the immature permanent tooth

  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.
 

Morphology, histophysiology and pathophysiology of the immature permanent tooth