Bacterial infection is the most frequent cause of pulp
and periapical diseases.
96-101
Bacteria may enter the
tooth via caries,
102-105
dental anomalies (e.g., dens
invaginatus, deep lingual and palatal grooves), exposed
lateral canals or damaged cementum as a result of
periodontal diseases, tooth cracks or fractures,
and marginal breakdown at the restoration-tooth
interface.
Bacterial infections of the pulp space consist of
It has been found that Streptococcus mutans by itself
will not induce pulp inflammation.
Although
several species of bacteria have been identified, there is
no absolute correlation with clinical signs and
symptoms; and it is noteworthy that the pulp may
become inflamed long before the bacteria physically
reach the pulp.
Superficial caries in pits and fissures
may cause pulp inflammation.
Substances such as
bacterial toxins, enzymes, antigens, chemotoxins,
organic acids and products of tissue destruction may
diffuse through the dentinal tubules to cause pulp
irritation.
The response of pulp to bacteria depends on many
factors, such as the speed of bacterial ingress and the
speed of progress of caries, which can be slow, rapid or
completely inactive (caries tends to be an intermittent
process, with periods of rapid activity alternating with
periods of quiescence). Caries progresses quickly
through demineralized enamel, but will progress more
slowly in demineralized but more organic dentine.
In young teeth, bacteria may cause the early death of
odontoblasts, and those dentinal tubules devoid of
odontoblast cell processes become dead tracts. These
tracts are highly permeable, and therefore they are a
potential threat to the integrity of the pulp. Fortunately,
the healthy pulp responds by depositing a layer of
reparative dentine over its pulp surface, thus walling it
off. The pulp response is also related to the thickness
and degree of calcification of the remaining dentine,
since dentine permeability can be reduced by dentinal
sclerosis and reparative dentine formation.
If the distance between the caries and the pulp is 1.1mm or
more, pulp inflammation may be negligible. When the
caries reaches within 0.5mm of the pulp, there is a
significant increase in the extent of inflammation, but
the pulp becomes acutely inflamed only when the
reparative dentine is invaded by irritants such as
bacteria or their toxins.
Bacterial entry via periodontal pockets is less likely
to cause pulp inflammation unless the main apical
foraminae are involved in the pocket which contains
bacterial plaque.