Pulp mortifications

Pulp mortifications

PLAN

Introduction

1. Terminology
   1. Pulp mortification
   2. Pulp necrobiosis
   3. Pulp gangrene
2. Pulp necrobiosis
   1. Definition
   2. Etiologies
   3. Pathogenesis
   4. Pathological anatomy
   5. Symptoms and clinical signs
   6. Diagnosis
   7. Evolution and prognosis
3. Pulp gangrene
   1. Definition
   2. Etiology
   3. The different types of pulp gangrene
   4. Pathological anatomy
   5. Histopathology
   6. Bacteriology
   7. Biochemistry of pulp gangrene
   8. Symptoms and diagnosis
   9. Diagnosis
   10. Evolution 

Conclusion.

Pulp mortifications

Introduction 

Pulp mortification is a sequela of pulp inflammation in the absence of treatment or of a sudden cessation of circulation following a traumatic lesion which has caused rupture of the vascular-nervous bundle at the level of the canal entrance of the apical foramen.

1. Terminology
   1. Pulp mortification (pulp necrosis) 

It is a mortification of the pulp tissue accompanied by its destruction, it can be partial or total, septic or aseptic.

2. Pulp necrosis (ischemic necrosis)

It is a total sterile, aseptic necrosis, caused by a stoppage of blood supply, without associated infection. Of ischemic and/or toxic origin

  1.3. Pulp gangrene (total septic necrosis): Possibly 

• Primary if the infection causes inflammation of the tissue.
• Secondary following septic inoculation of necrobiosis.
• Closed (dry), open (wet) or intermediate (indirectly open).

2. Pulp necrobiosis

2.1. Definition

• Total, sterile, aseptic necrosis of ischemic and/or toxic origin, without participation of germs.
• Following a chemical, physical or traumatic attack

2.2. Etiologies

• Mechanical: represented by the trauma which can be: 

• Severe trauma: a single violent shock can cause rupture of the vascular-nervous bundle at the apical foramen, which creates a state of hypoxia or even anorexia leading to ischemic necrosis.
• Low trauma: but repeated, 
• Trauma to the vascular-nervous bundle: or during surgical intervention can be the cause of ischemic necrosis.
• Orthodontic treatment: subjecting the teeth to fairly significant forces
• Thermal:

• Whatever the thermal source, physical or chemical; a temperature which exceeds the limits of tissue tolerance always causes damage to the pulp-dentin complex.
• According to some authors, a temperature increase of 11°C causes or can cause pulp necrosis.

These thermal causes may possibly be due to:

• Exothermic reactions when taking certain catering products.
• A size without cooling or polishing.
• The conductivity of restorative materials.
• Chemical:

• This is the toxicity of products used in dentistry.
• The degree of toxicity depends on the chemical composition of the product and especially on the concentration of the toxic elements which compose them, acid and base e.g. silicates.

2.3. Pathogenesis

– When the vascularization of the pulp is interrupted, the pulp cells die due to lack of O2 (hypoxia) and nutrients.

– Cellular metabolism will not cease immediately after interruption of blood flow, but will continue at a gradually decreasing rate for at least 4 to 5 days.

– Intracellular enzymes instead cause coagulation of the cytoplasm and the nuclear material is often condensed into a small mass.

Tissue necrotized by ischemia loses its structural details but the general architectural configuration of the pulp remains identifiable.

2.4. Pathological anatomy

Histologically characterized by: 

• Plasma cell infiltration
• A fibrous degeneration of pulp tissue.
• The tissue appears as a solid mass, sometimes of a caseous consistency, composed mainly of coagulated proteins.

Pulp mortifications

2.5. Symptoms and clinical signs

• Beginning or installation phase: Painful or not 
• With pain:

• Blood circulation is interrupted. 
• The pulp tissue slowly but not completely necrotizes. 
• Histologically, the nerve fibers die last, hence the painful phenomena.
• Without pain 

– Section of the vascular-nervous bundle in one go

• State phase

• Complete loss of pulp sensitivity.
• The change in color of the dead tooth can be noted. 
• Exploratory trepanation of the tooth reveals no sensitivity or foul odor.
• The extirpation of the pulp does not cause any hemorrhage and the pulp architecture is more or less preserved.
• The X-ray does not reveal anything, sometimes a desmodontal thickening can be seen.

2.6. Diagnosis

• Differential diagnosis: is done with

1. Dentinitis (deep + superficial)

2. Asymptomatic pulpitis.

3. Pulp gangrene.

4. Post-traumatic hypoesthesia.

5. Pulp degeneration

• Positive diagnosis: based on

• History of the disease.
•  Clinical signs: No sensitivity
• Vitality test (-)
• No smell
• Rx: no pulp chamber breach
• No response to percussion.

2.7. Evolution and prognosis

• Without TRT: it progresses to gangrene (it becomes infected secondarily and ends in the stage of pulp gangrene due to septic colonization)
• Noticed :
• It is very rare to find necrobiosis because it remains a histopathological stage

3. Pulp gangrene
   1. Definition

It is a mortification of the pulp parenchyma with the participation of germs leading to a degradation and putrefaction of the different constitutional elements of this tissue.

It is a total and septic necrosis, it can be:

• Primary: The infection causes inflammation of the tissue 
• Secondary: Resulting from septic inoculation of necrobiosis.

2. Etiology

Septic inoculation of the pulp has double origin: coronal and radicular

• Coronary:

– Dental exposure through abrasion, cracks and fractures

– Dental exposure due to caries (more frequent)

– Lack of sealing of coronal fillings

• Root: apical or latero-radicular.

– From a periodontal pocket: ascending or retro pulpitis which can lead to necrosis.

– Septic inoculation of a previously necrotic pulp (necrobiosis).

3. The different types of pulp gangrene

• It can be open or closed depending on whether the pulp chamber has a trephination orifice and whether or not it is open on the CB.
• Open pulp gangrene: PH = 6.6_6.8 (acidosis)

• This form is found when there is a solution of continuity between the pulp chamber and the oral environment after spontaneous trepanation.
• It evolves in an aerobic (acid) environment although the aerobic flora gradually disappears as one progresses deeper into the canal or the anaerobic flora then becomes predominant (humid).
• Closed gangrene: 8.2_ 8.4 (alkalosis):

• When there is no communication between the pulp cavity and the oral environment.
•  It evolves in an anaerobic (alkaline) environment. It is dry.
• Intermediate form 
• Clinically 

   The trepanation orifice of the pulp chamber is closed by an operculum of decalcified dentin.

• Bacteriologically

It is “open” because the canalicular structure of the decalcified dentin allows salivary impregnation of the pulp.

4. Pathological anatomy

• Open, wet gangrene (necrotic liquefaction gangrene):

Proteolytic enzymes transform the pulp tissues into a softened mass to form a very foul-smelling blackish putrilage.

• Closed (or dry) gangrene: necrotic coagulation

Pulp tissue will undergo precipitation and transform into a product of firm or semi-solid consistency (caseum) giving the pulp the appearance of a grayish coagulated mass.

Pulp mortifications

5. Histopathology

• Gangrenous pulp appears as a disorganized, amorphous tissue with numerous microbial clusters located mainly on the canal walls and in the canaliculi.
• The products of gangrene can be very foul-smelling and are toxic to periapical tissues.

6. Bacteriology

• More important in open than closed gangrene.
• According to Demars in 1977: gangrene does not have a specific flora.

3.6.1. Flora of open gangrene:

– Is substantially the same as the oral flora 

– Mainly aerobic towards the pulp chamber and becomes facultative anaerobic in the depth of the canals.

– We mainly find:

Streptococcus mitis; Enterococcus; Lactobacillus; Staphylococcus; Neissirea; Mixed corynebacterium; Actinomycetes.

3.6.2. Flora of closed gangrene:

– 78% of species are strict anaerobes.

– There are also micrococci, veillonella, neisseria

– Anaerobic B G – generally dominate, these are actinomyces, and even condida-type yeast, bacteroids, spirillae and spirochetes.

7. Biochemistry of pulp gangrene

• Whatever the nature of the infected canal environment, the germs, through the enzymes they release, will cause the destruction of the pulp via a catabolic pathway.
• Two pathways of connective tissue degradation dominate: glycolysis and proteolysis:
• Glycolysis: Or fermentation of carbohydrates

The products of aerobic or anaerobic catabolism are essentially:

Acids (lactic, acetic); Alcohol, CO2, H2O

• Proteolysis

First: release of amino acids, then these are catabolized to end up, as waste in: amino acids, in volatile basic amines, in ammonia (NH2) and in CO2.

The intermediate products will be Putrecine and Cadaverine (the nauseating smell)

8. Symptoms and diagnosis

• The diagnosis of closed gangrene is sometimes tricky but is obvious for open gangrene.
• The pain

• Absence of pulp response to vitality tests (thermal and electrical).
• It is advisable to be wary of a possible desmodontal response by passage of the electric current to the apex because of the humidity of the canal.
• The shade:

• The change in tooth color is indeed characteristic but is not systematic.
• The tooth turns gray this is due to: (different theories)
• Theories of Hue Modification

• DELIBEROS: transformation of hemoglobin into Hematoidin during putrefaction = orange tint.
• BUCKLY: it is the ammonia which acts on the iron in the hemoglobin, and forms iron dioxide = gray tint.
• BRIDGE: the albumin decomposes: birth of a series of AA, including thyrosine which will oxidize in the presence of oxidase = brownish dentin.
• FS Weine: Tooth discoloration, if present, is due to hemolysis of blood cells or decomposition of pulp tissue.
• HESS: dentin impregnation by blood pigment decomposition products:

• Hemin: bluish black; 
• Hematoidin: ornage;
• Hematidine: dark brown.
• The color examination is done in relation to that of neighboring or homologous teeth.
• The smell:
• The foul odor of gangrene is evident when the gangrene is open, it only appears in closed gangrene after trephination of the pulp chamber,
• The X-ray:
• The radio does not provide information on the state of the pulp, however sometimes a widening of the desmodontal space can be noted.

9. Diagnosis

• Differential diagnosis:

• Deep dentinitis.
• Post-traumatic hypoesthesia
• Asymptomatic pulpitis.
• Necrosis associated with chronic apical periodontitis (R(x) + positive percussion)
• Grayish dental discoloration (amalgam filling/taking tetracyclines which are widespread in this case)
• Positive diagnosis

• Inspection shows a caries cavity, or a coronal fracture, the change in color.
• Vitality tests are negative.
• Negative percussion test.
• The presence of a foul odor.
• The X-ray shows nothing if there is no associated periapical pathology .

Pulp mortifications

10. Evolution 

• The gangrenous condition does not remain limited to the tooth, it spreads through the canals and orifices which connect the pulp cavity to the periodontal ligament.

Conclusion

Necrosis cannot be considered as a particular form of pulp pathology, but as the outcome of inflammatory phenomena, its therapy requires special care to save the tooth on the arch.

Pulp mortifications

  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.
 

Pulp mortifications