Pulpo-dentin damage

Pulpo-dentin damage

PLAN

Introduction

1. Reminder on the pulp-dentin complex
   1. Dentin 
   2. The pulp
2. Etiological factors of aggression
   1. Bacterial origin
   2. Structural anomalies
   3. Traumatic causes
   4. Iatrogenic origins
3. Histopathology of caries
   1. Dentin caries in precavitary stages
   2. Cavitary stages of dentin caries
4. Pulp reactions to dentin caries
   1. Before bacterial invasion of dentin
   2. After bacterial invasion of dentin
5. Clinical forms of dental cariesdiagnosis in oc/E
   1. Slowly progressing lesion
   2. Severe, rapidly progressive lesion
6. Symptomatology
7. Diagnosis

Pulpo-dentin damage

Introduction 

Carious lesion can be defined as a pathological process leading to the destruction of hard tissues of the dental organ by acid demineralization.

Although this pathological process can be reversed in the initial stages, it is not self-limiting and, without adequate care, it progresses until the tooth is destroyed. 

The progression of caries determines an inflammatory pulp reaction, which can occur from the white spot stage, even before the enamel-dentin junction is reached.

1. Reminder on the pulp-dentin complex

Dentin protects the pulp, which in turn ensures the “vitality” of the tooth (Linde and Goldberg, 1993). 

The pulp-dentin complex is so called because of the very close relationship that binds these two tissues, one mineralized and the other connective. The separation of one from the other is difficult both histologically and functionally.

1. Dentin : Dentin is a mineralized connective tissue: it is made up of 70% hydroxyapatite crystals, 20% organic matter and 10% water.

Predentin, present at the interface between dentin and pulp, constitutes the non-mineralized phase at the origin of the dentin matrix. Its composition is very close to that of dentin, even if some modifications can occur during the mineralization process (Linde, 1984)

Intracanalicular dentin is secreted throughout the life of the tooth and can be accelerated in certain pathophysiological conditions sometimes leading to partial or even complete dentin sclerosis (Senawongse et al., 2008)

• Types of dentin

• Primary dentin 
• This is the dentin secreted first during tooth development. 
• It gives the general shape of the crown and the root and is thus responsible for the morphology of the organ. 
• The outermost layer, relatively thin and immediately underlying the enamel-dentin junction, is secreted by odontoblasts during their terminal differentiation. It has a structure without canaliculi and is called the “mantle dentin”.
• Secondary dentin 
• Secondary dentin, on the other hand, is secreted physiologically after the eruption of the tooth into the oral cavity or after apexogenesis. 
• It is physiological and should in no way be considered a pathological structure. 
• This dentinogenesis is responsible for the progressive and asymmetrical decrease in canal volume during aging, often incorrectly called “calcification” or “mineralization”.

• Tertiary dentin 
• Tertiary dentin is secreted in response to external aggression, such as caries or abrasion, in order to protect the underlying pulp. 
• In the case of moderate stress, which does not lead to the destruction of odontoblasts, the secreted dentin is called “reactionary dentin”; when the stress is more intense and the survival of odontoblasts is compromised, it is then called “reparative dentin”.
• Dentin is a permeable tissue that is traversed by tubular structures called dentinal tubules or canaliculi. These canaliculi cross the dentin from one side to the other, from the enamel-dentin junction (or cemento-dentin junction in the root region) to the canal lumen that contains the pulp tissue.

– Their distribution is uneven in the thickness of the dentin and their density increases near the pulp cavity,

1.2. The pulp : 

The pulp is organized into several layers which are, from the periphery to the interior:

 The odontoblastic layer : it includes the odontoblasts, 

The acellular Weil layer : it includes a significant nerve and capillary network which provides the odontoblasts with all the elements necessary for their synthesis and mineralization activity.

Höhl’s layer : thin area rich in cells, it contains: fibroblasts, undifferentiated mesenchymal cells, dendritic cells.

The central zone rich in cells : it contains: fibroblasts, undifferentiated mesenchymal cells, immunocompetent defense cells (dendritic cells, macrophages, T lymphocytes), large diameter blood vessels and nerves

2. Etiological factors of aggression

 Dentin exposure has very varied origins

2.1. Bacterial origin

• The main process that causes pulp inflammation is caries. 
• These are caused either by direct contact of bacteria with the pulp tissue or indirectly, through bacterial antigens traveling in the dentinal tubules.

Pulpo-dentin damage

2.2. Structural anomalies

Structural abnormalities can directly or indirectly bring pulp tissue into contact with bacteria .

2.3. Traumatic causes

These causes are numerous: they include “accidents” such as fractures with or without pulp exposure, abrasions, attritions, erosions, but also poorly adapted orthodontic or prosthetic devices.

2.4. Iatrogenic origins

During treatment procedures, the various elements (rotating instruments, air spray, dental materials) used by the dental surgeon can cause pulp damage. 

3. Histopathology of dentin caries
   1. Dentin caries in precavitary stages

• Early caries

As long as the lesion has not reached the inner third of the enamel, the dentinal alterations are essentially intracanalicular.

As soon as the lesion concerns the enamel-dentin junction, demineralization of the dentin progresses gradually over time.

• Advanced closed caries or “hidden caries”

The phenomenon of hidden caries is generally explained by the fact that demineralization progresses slowly at the enamel level, delaying cavitation, due to the fluoridated environment.

Dentin demineralization would be triggered from microperforations (generally undiagnosed) exposing the enamel-dentin junction and would progress more rapidly than enamel demineralization.

3.2. The recall examination

Partial or routine examination, which includes a medical interview and a brief history, an intraoral examination, any X-rays deemed necessary, a precise diagnosis, appropriate treatment and a prognosis.

2. Cavitary stages of dentin caries

When the surface enamel is no longer supported by healthy dentin, from a certain degree of weakening it ends up breaking. An enamel cavity, which will eventually expose the dentin, opens, allowing bacterial invasion of the latter.

The caries then acquires a quasi-pathognomonic form described as a dentin carious cone whose base is located near the enamel-dentin junction and which is subdivided into three zones: opaque dentin, transparent dentin, and apparently normal dentin.

• Opaque dentin itself has three zones:

A zone of total disintegration: which corresponds to the most superficial zone of the caries. In this necrotic zone we find bacteria, digested dentin debris and essentially necrotic food debris.

• A zone of bacterial invasion, or infected dentin layer, consisting of “softened”, highly demineralized dentin, contaminated by bacteria present in dilated canaliculi due to the destruction of pericanalicular dentin;
• A demineralized or affected area: at the level where the action of acids and proteolytic enzymes combine. This area, where only pioneer bacteria are infiltrated, is assimilated to an uninfected layer, hence its name of affected dentin layer.
• As one goes deeper into the lesion, one observes the gradual reappearance of the pericanacular dentin, the demineralization affecting only the hydroxyapatite crystals of the intracanalicular dentin and the collagen framework being preserved. the underlying demineralization zone being little or not infected is a zone partly remineralizable and therefore can be preserved
• Transparent or sclerotic or translucent dentin marks the boundary between the area of ​​demineralized dentin and the apparently normal dentin. 

•It is in fact a sclerotic dentin as a result of the mineralization of the canaliculi. This sclerotic zone is a transition zone between the demineralized zone and the healthy dentin, it plays the role of a biological barrier opposing bacterial invasion and the progression of caries.

• Apparently normal dentin

•Under the sclerotic layer, we find almost normal dentin, where the canaliculi are open and contain odontoblastic extensions in continuity with the cell bodies of the odontoblasts. 

•The changes observed at this level are mainly metabolic. Vacuoles of variable size were observed at the level of the odontoblastic extensions.

4. Pulp reactions to dentin caries

The progression of caries determines an inflammatory pulp reaction.

Pulpo-dentin damage

1. Before bacterial invasion of dentin

Pulp changes are detected at an early stage under enamel lesions. 

Even before the enamel-dentin junction is reached, cellular changes in the odontoblastic (change in the size of the odontoblasts) and subodontoblastic (appearance of cells in the acellular zone) layers are observed under the sclerotic dentin, as well as an initial inflammatory reaction and disturbances in the predentin.

When the dentin-enamel junction is reached and the dentin is demineralized, a layer of more or less canalicular tertiary dentin appears at the dentin-pulp border , its structure being affected by the speed of progression of the lesions.

This reaction dentin is deposited by primary odontoblasts (and not by replacement cells) and is only formed if the non-cavitary enamel lesion is active

2. After bacterial invasion of dentin

• As soon as the bacterial invasion of the dentin occurs, the bacterial toxins as well as the peptides resulting from the degradation of the dentin matrix will transit through the canaliculi whose permeability is increased.
• Bacterial antigens are captured by dendritic cells positioned in the odontoblastic region and are presented to antigens, macrophages, and activated B and T lymphocytes directly in the inflamed pulp area.
• When bacteria and their by-products reach the last barrier built against carious progression (the reaction dentin layer underlying the damaged area), the accumulation of macrophages and T and B lymphocytes becomes more significant. At this point, the intradentin defense mechanisms are overwhelmed, the tubules open and the dentin interface destroyed.

5. Clinical forms of dental caries

• Clinically, two types of carious lesions can be observed: active caries where the dentin is pale yellow and softened, and slowly progressing chronic caries where the tissue is brownish and harder.
• When the lesion has caused the destruction of odontoblasts, the formation of reaction dentin cannot occur.
• However, it is still possible to obtain the formation of reparative dentin that insulates and maintains pulp vitality.
• Recent advances in biology have shown that this reparative dentin was secreted by odontoblastic cells, resulting from the differentiation of stem cells from the dental pulp.

1. Slowly progressing lesion

• If the microbial invasion is eliminated by isolating the dentine from the saliva, the activity of the pulp returns to normal, the caries no longer progresses, the reaction dentine persists and takes on its full value as an insulator between the pulp and the aggressiveness of the filling material. 
• The risk of pulp denudation is excluded due to the formation of tertiary dentin.
• Dentin capping is useless; dentinogenesis has never ceased; it has only been disturbed, sometimes it is even aberrant (pulpolith formation).
• Therefore, in the case of slow-developing caries, the tooth must be restored immediately and permanently.

2. Severe, rapidly progressive lesion

• Caries takes on this appearance when it develops on young teeth with widely open tubules. 
• Cavitation of the enamel occurs very quickly and the dentinal base of the cavity becomes less hard to the touch but without any apparent change in color. 
• Pulp inflammation disrupts dentinogenesis; no reactional dentin, sclerodentin or tertiary dentin is formed.
• It is difficult to confirm the diagnosis of juxtapulp caries. 
• The only warning sign was described by Marmasse: when the enamel bordering the carious cavity presents a “yellowish white, milky, opaque ring, whiter and more opaque than the rest of the tooth”, the pulp may be exposed.

6. Symptomatology

Exposed dentin is sensitive: cold, heat, contact, sugary or acidic solutions in particular cause pain.

Painful responses of dentin constitute the “dentin pain syndrome” which is characterized by the existence of pain only provoked, during stimulation with cessation as soon as it disappears, which differentiates it in particular from the pain syndrome of acute pulpitis.

7. Diagnosis

Exposed dentin is diagnosed by observing its denudation with the probe with the different possible characteristics of its surface (hard, smooth, rough, soft) (tables I and II).

Pulpo-dentin damage

                                                                     Table I

Table II

Table II

  Untreated cavities can reach the nerve of the tooth.
Porcelain veneers restore a bright smile.
Misaligned teeth can cause headaches.
Preventative dental care avoids costly treatments.
Baby teeth serve as a guide for permanent teeth.
Fluoride mouthwash strengthens tooth enamel.
An annual checkup helps monitor oral health.
 

Pulpo-dentin damage