PULP NECROSIS

PULP NECROSIS

1. Introduction :

Pulp necrosis is the logical outcome of any untreated pulp inflammation; it can also follow trauma that has caused rupture of the vascular-nervous bundle at the apical canal entrance.  

2. Terminology:
   1. Necrosis: This is a death of the pulp tissue accompanied by its destruction. 

It can be partial or total depending on whether it affects all or part of the pulp parenchyma. 

2. Pulp necrobiosis: total, sterile, aseptic necrosis of ischemic and/or toxic origin.
3. Pulp gangrene: septic necrosis:

It can be:

• primary , if the infection causes pulp inflammation;
• secondary: it results from a septic inoculation of necrobiosis.

3. Etiologies of pulp necrosis:
   1.   Infectious origin:

Septic inoculation of the pulp has a dual origin: coronal and radicular (apical).

• Coronary: all losses of coronary substances are at the origin and especially caries which is the most frequent.

Caries external infection causing inflammation of the pulp in the absence of treatment       progression  : necrosis

• Apical or latero-radicular:
  • Pulp necrosis can originate from a periodontal pocket (endo-periodontal lesion).
  • By anachoresis: action of going backwards, the germs find rejection in the already mortified pulp tissue.

2.   Traumatic origin:

Necrobiosis is a coagulation necrosis of ischemic origin: accidental rupture of the vascular-nervous bundle.

3.   Iatrogenic origin: 
   • Surgical curettage in an area involving the apex of one or more neighboring teeth.
   • Following iatrogenic pulp inflammation of a physical or chemical nature, or even drug-related. 
4. Bacteriology of pulp gangrene:

• The flora of pulp gangrene is not specific.
• The flora of open gangrene is essentially the same as the oral flora.
• This flora is mainly aerobic towards the chamber where saliva is circulating, becomes facultative anaerobic in the depth of the canals; this evolution comes from the progressive disappearance of salivary circulation in the canals.
• The facultative aerobic and anaerobic germs are mainly: Streptococci (Hemolytic, Viradans, etc.), and Enterococci.
• Staphylococci are rare.
• Anaerobes constitute the majority of the flora of closed gangrene (+ 50%) example: Veillonellae, Neisseriae.
• The canal flora varies according to ecological conditions; there are fewer germs in dry gangrene than in wet gangrene.

5. the biochemistry of pulp gangrene: 

The germs, through the enzymes they release, will cause the destruction of the pulp through a catabolic pathway.

Two pathways of connective tissue breakdown dominate: glycolysis and proteolysis.

5.1 Glycolysis:

The products of aerobic or anaerobic carbohydrate catabolism are essentially:

• acids (lactic, acetic).
• Alcohol.
• Co2, H2O.

5.2 Proteolysis:

First there is the release of amino acids, then these are catabolized by 02 different pathways:

• Deamination in Alkaline Medium.
• Decarboxylation in acidic medium.

    To end up, as waste: in Amino-acids, volatile basic amine, Ammonia (NH2) and in CO2.

The pH of pulp gangrene: 

• Open gangrene: PH between:     6.6    and   6.8   (PH close to that of saliva) Acid PH.
• Closed gangrene: PH between: 8.2    and  8.4 (Alkaline).

6. pulp gangrene clinic: 

6.1 Anatomical pathology:

The appearance of the necrotic pulp varies depending on the nature of the gangrene.

1.  Open and wet gangrene: the pulp appears as a very nauseating black putrescence. A progression takes place towards pulpolysis, that is to say the complete disappearance of the pulp tissue.  
2.  Closed gangrene (Necrobiosis): after trepanation of the pulp chamber, we then encounter a grayish mass that is slightly damp or dry and has little or no odor.

 Histologically, gangrenous pulp appears as disorganized, amorphous tissue with numerous microbial clusters.

PULP NECROSIS

6.2 Symptomatology and diagnosis: 

a. closed gangrene:

• The characteristic sign of pulp necrosis is the absence of response of the pulp to various vitality tests.
• The change in the color of the tooth is in fact characteristic: the tooth becomes gray.
• Foul odor of gangrene is evident (open), it appears only after (closed) trephination of the pulp cavity, but the odor may not exist in dry forms.

2. open gangrene: 

The diagnostic evidence is given by the exploration of the pulp cavity using a fine probe plus (+) the signs mentioned above.

6.3 Evolution:

• the gangrenous condition does not remain localized to the tooth,
• The presence of necrotic tissue increases the potential risk of infections and periapical complications.
• The germs spread through the canals and orifices that connect the pulp cavity to the desmodont (apical periodontitis),     the point of septic inoculation of the organism; it can in turn give rise to other complications: cellulitis, osteitis.

6.4 Therapeutic indications:

• Treatment consists of removing this infectious focus (etiological treatment).
• The most commonly used treatment currently: conservative treatment which consists of disinfecting the pulp cavity.
• Root canal debridement combined with root canal disinfection is the surgical procedure that removes gangrenous tissue.

7. Conclusion: Conservative treatment of teeth affected by pulp gangrene has become a common affair with a good prognosis.

PULP NECROSIS

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An annual checkup helps monitor oral health.
 

PULP NECROSIS