Pulp necrosis
I- Terminology
Pulp necrosis is the death of pulp tissue accompanied by its destruction; it can be partial or total.
There are two main anatomo-pathological forms:
- Aseptic necrosis
- Septic necrosis
Aseptic necrosis of the pulp: also called necrobiosis or coagulation necrosis
Septic necrosis of the pulp : also called pulp gangrene or liquefaction necrosis: this is the microbial invasion of the entire pulp parenchyma.
Pulp gangrene is said to be open when, after spontaneous trepanation, there is communication between the pulp cavity and the oral environment. Otherwise, it is said to be closed .
There are intermediate forms , indirectly open: decalcified dentine closes the trepanation orifice, but allows salivary moisture to pass through; biologically it is similar to open gangrene, but clinically to a closed form.
- Coagulation necrosis:
- It is seen especially when blood circulation is interrupted in a tissue area
- It occurs rapidly and is accompanied by massive coagulation of the cytoplasm.
- In such foci, the tissue architecture is more or less preserved
- Liquefaction necrosis : Autolysis plays an important role in the mechanism of liquefaction necrosis.
II- Clinical and anatomo-pathological forms of pulp necrosis
- 1: Necrobiosis
This is a pulpal lesion without any presence of pathogenic germs; in this case, it is a factor other than caries which is responsible for the coagulation necrosis. There is traumatic rupture of the vascular-nervous bundle.
When faced with a dyschromic tooth, without caries or often bearing traces of trauma, mainly in young people, especially at the level of the maxillary incisors, necrobiosis should be considered.
Etiologies
- Mechanical or traumatic causes are the most frequent: contusion, dislocation, etc. the vascular-nervous bundle suffers significant damage or even ruptures. Repeated microtraumas due to certain occlusal disorders can also cause pulp mortification in the long term.
- Physical or thermal causes: such as untimely grinding of teeth which can cause a real burn of the pulp
- Chemical causes: such as fillings with composite resins and certain cements which have an acidic pH.
Pulp necrosis
Anatomical pathology
In necrobiosis, the pulp can only be seen after trepanation of the pulp chamber. We then encounter a grayish mass that is not very moist or dry, with little or no odor,
Symptomatology
Physical signs;
- Inspection shows that the pulp chamber is closed .
- the loss of translucency of the crown , the color of which becomes opaque or even grayish.
Objective signs
- the percussion is negative ;
- Pulp vitality test is negative
- No odor
Subjective signs
- Absence of pain,
- Absence of radiological signs
- Evolution
All clinical signs may remain silent for a long time, but the quiet evolution may be towards septic necrosis.
- 2: Pulp gangrene
It is the invasion of the pulp by a septic process without crossing the apex. The pulp tissue undergoes real degradation in the presence of strict anerobes.
Etiologies
- Carious lesions: In fact, pulp gangrene is the terminal form of pulpopathies
- Transformation of aseptic necrosis into septic necrosis
- Periodontal diseases with retrograde septic seeding
- Blood contamination by septic route in the context of general diseases (rarer).
Anatomical pathology
In open and wet gangrene, the pulp appears as a very nauseating black putrescence. A development takes place towards pulpolysis, that is to say the complete disappearance of the pulp tissue;
Symptomatology
- Physical signs; Dyschromia ; grayish coloration of the corona which can be explained by;
- According to Buckley: Ammonia acts on the iron in hemoglobin to give the grayish iron sesquioxide.
- According to Pont: The intradentine albumins, when decomposed, give rise to tyrosine which oxidizes, giving the dentine a grayish tint.
- Objective and subjective signs;
- The percussion is negative,
- thermal tests do not cause any reaction.
- Probe exploration is insensitive and absent.
- Presence of putrid, nauseating odor when opening the tooth.
- No radiological signs.
Evolution: The evolution leads to acute then chronic apical periodontitis, cellulitis, osteitis, etc.
Pulp necrosis
III-Bacteriology
- The flora of open gangrene is essentially the same as that of the oral cavity since the pulp cavity is open to the oral environment, and we find mainly aerobic/facultative anaerobic germs there.
- The flora of closed gangrene is essentially made up of strict anaerobes , with gram + bacteria (Clostridium and Corynebacterium) and gram – bacteria (bacteroides, spirochetes and actinomyces) largely dominating.
IV- Biochemistry of pulp gangrene
The disintegration of pulp tissue occurs through two essential pathways: glycolysis and proteolysis
Glycolysis: The aerobic pathway is that of the Krebs carboxylic cycle which takes place in an acidic environment. Lactic and alcoholic fermentation constitute the term for the degradation of carbohydrates in an anaerobic environment.
The catabolism products of this glycolysis are acids (lactic, acetic), alcohol, CO2, and water.
Proteolysis: First, amino acids are released, then they are catabolized by two different pathways:
- Deamination in alkaline medium
- Decarboxylation in acidic medium
To end up as waste in acid amines, volatile basic amines, ammonia and CO2.
PH:
- Open gangrene has an acidic pH (6.6 and 6.8)
- Closed gangrene has a basic pH (8.2 and 8.4)
Pulp necrosis
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