EUROPEAN JOURNAL OF INFLAMMATION Vol. 5, no.

3,115-119 (2007)

REVIEWARTICLE
MICROBIOLOGICAL ASPECTS AND INFLAMMATORY RESPONSE OF PULP TISSUE
IN TRAUMATIC DENTAL LESIONS

D. TRIPODI, M. LATROFA and S. D'ERCOLE 1

Department ofStomatology and Oral Science, University ofChieti-Pescara, 'Laboratory ofClinical

Microbiology, Department ofBiomedical Sciences, University ofChieti-Pescara, Chieti, Italy

Received June 4, 2007 - Accepted August 3, 2007

Traumatic dental lesions are more frequently found in the pediatric population, with a major involve-
ment, in 80% of the cases, ofthe superior central incisors. The exposure ofthe dental pulp leads to major
morphological changes in dental tissue, such as discolouring, acute pulp inflammation, chronic inflam-
mation and necrosis. This article reviews the various studies published on the different types of inflam-
matory response of the pulp tissue following traumatic events, from the microbiological and histological
point of view of various techniques.

Traumatic dental lesions are found at all ages,
but most frequently in the paediatric population, in
an age range of 2-5 years, a time period in which
the muscle co-ordination and mental faculties of the
child have still not been fully developed (1-2).
At the age of 5, 1/3 of children have already
suffered trauma of the deciduous teeth with fractures
of the corona (26%), radicular fractures (3%),
intrusive luxation (26%), non-intrusive luxation
(13%), evulsions (52-69%), concussions (10%),
dislocation, especially of the upper incisors (84% of
the deciduous against 87% of the permanent teeth),
possible bud alteration in permanent teeth (48-68%),
and ankylosis (5%) (3-4). On the other hand, in
children between the ages of 8-12 years, due to
their high physical activity during games (58.5%)
and sports, there is an increase in the incidence
of trauma. In fact, at 12 years of age, 25% of the
pediatric population show some damage to their
permanent teeth.(1-4). 18% of dental fractures, as
has been observed in many studies, is represented
by fractures to the corona of the permanent incisors
(the majority, 80%, are ofthe upper central incisors),
and especially those (9.6%) which do not show
complications of trauma to the hard dental tissue
(5-7). Studies on germ-free animals have shown
that healing of the pulp oq,c.urs independently of the
grade of exposure of the same
Pulp exposure induces major morphological
changes in tooth tissue, such as discolouring, acute
pulp inflammation, chronic inflammation and, if the
exposed pulp in not treated, necrosis. This happens
even in the case of dental intrusion, since the pulp
tissue, during displacement, undergoes a severe
shock, which might be seen at a later stage, with
clinical indications that go from colour alteration,
to inflammation and subsequently to pulp necrosis
(8). Following exposure, the pulp suffers from
haemorrhage in the underlying tissue followed
by a secondary superficial inflammation, the start
of coagulation mechanisms and afterwards the
alteration of the tissues in a detrimental (abscesses
and necrosis) or proliferate (hyperplasia) manner (9).
During histological examination of deciduous

Key words: dental trauma, pulp iriflammation, bacteria

Mailing address: Dr. Domenico Tripodi,

Dipartimento di Scienze Odontostomatologiche,
Universita "G. d'Annunzio" Chieti- Pescara,
Via dei Vestini, 31 - Chieti, Italy
Tel: ++39 08713554063 Fax: ++39 08713554063
e-mail: tripodi@unich.it
1721-727 (2007)
Copyright © by BIOLIFE. s.a.s.
This publication andlor article is for individual usc only and may not be further
reproduced without written permission from the copyright holder.
115 Unauthorized reproduction may result in financial and other penalties
116 D. TRIPODI ET AL.
teeth having post-traumatic discolouration, with or
without the presence of abscesses, both clinically
and through radiographs or pain and mobility, it has
been seen that these teeth show histological changes
which go from total pulp necrosis to dystrophic
calcification, with a partial necrosis associated to
inflammation (10).
Evaluating the pulp reaction to the traumatic
event through an optic microscope, it has been seen
that the inflammation decreased, starting from the
pulp chamber at the third apical and medial of the
root canal in which the following changes were
noticed: haemorrhage, damage to the odontoblast
strata and the presence of inflammatory infiltration,
made up mainly polymorphonucleate leukocytes
(11-15).
From the histological examination of animal teeth
having pulp exposure at 48 hand 72 h, it was seen
that in both periods of observation there was an area
of superficial inflammation, with an accumulation
of polimorphonucleate leucocytes in the pulp
cornua and in the third coronal, that the depth of the
inflammation is greater at 48 h{46,33.33 urn) than at
72 h (3933.33 urn), maybe coinciding with a major
chamber opening, (xI332.14 urn a 48 h vs. x 479.52
urn a 72 h), that the strata of odontoblasts near the
exposed pulp results as being completely destroyed
or reduced to a small number of cells, that the
amount of inflammatory infiltration reduces towards
the apex, and that the periradicular area results free
from inflammatory cells (16-17).
Inflammation results as being inferior in teeth
where the exposure of the pulp occurred exclusively
following a traumatic event in respect to those where
the trauma followed an insurgence of a carious
process (11).
Pulp necrosis with an inflammatory cell infiltration
has also been seen in teeth having radicular fractures.
and vertical fractures, in the first case mostly in the
coronal part of the fracture, since the more apical
one is filled by collagen fibre, while in the second
case only on one side of the pulp due to the presence.
of a plasma cell barrier between the portions of
necrotic pulp and inflamed pulp (18). In agreement
with previous studies, Caliskan et. al. obtained the
same results in teeth with complex radicular coronal
fractures where the radicular pulp tissue resulted
normal, having dilated and functioning blood vessels
(19-22).
Disintegration of the pulp tissue may give rise to
inflammation of the periapical tissue which could
induce problems in the development ofthe permanent
tooth's gem, as well as determining ankylosis of the
deciduous tooth, in the case of parodontal damage
and, consequently, delay in the ectopic eruption of
the following permanent tooth (23).
Some authors have observed, in teeth having
fractured enamel and dentine and without any pulp
exposure, during the first post traumatic stages
(17 h), the presence of myelinic degeneration,
surrounding the axis, and of oedema, while in
subsequent stages (4-20 days) tissue inflammation,
neuron degeneration, intramyelinic oedema, axial
tumescence and an aberrant synthesis of the myelin
were observed (24).
From the histological examination of the dental
nerve fibres subgroup which contain the calcitonin
gene related peptide (CGRP), it was possible to
evaluate the progressive evolution stages of the
pulp abscess and of the necrosis in relation to the
proliferation of the same fibre, in the interface
between the abscess and the viable pulp, in the
periapical area during the lesion and around the
chronic abscesses in granulomatosis parodontal
tissue (25).
By classifying dental damage into 3 different
stages it has been seen that for slight damage, 4
days after trauma, CGRP fibres proliferated on
the odontoblast and dentine strata, returning to
normality after 3 weeks. At an intermediate level
of damage, there was damage on the odontobalst
strata, with the formation of micro abscesses and
a proliferation of CGRP around the abscess, with
a consequent formation of repairing dentine and a
successive healing. As regards severe damage with
an exposure of the pulp there was a pulp necrosis
. followed by a probable development of periapical
lesions (26).
CGRP-IR fibres which are immunoreactive
(IR) towards the peptide relative calcitonin gene,
innervate the coronal dentine in sites populated
by primary odontoblasts and by associated pulp
cells. In the case of dental trauma such cells are
lost, in this way reducing the innervating CGRP-
IR and provoking changes in dimension, form, and
immunoreaction of their root endings in relation to
 Eur, J. Inflamm.
the different patterns of inflammation and healing
(27-28).
Vascular changes which occur in the pulp,
following an acute pulpitis condition, consist in an
increase of vascular permeability which affects first
the rete vasculosum and afterwards the capillaries,
while in the case of chronic pulpitis numerous
morphological changes have been noticed, with a
formation of tissue similar to granuloma in the rete
vasculosum around the abscess (29). The nerve fibres
ha'le an important effect on the pulp blood flow and
on inflammation, while cytochemical changes which
are seen following dental damage occur in response
to the alterations which take place in the pulp itself or
are an indication of the pulp status (30).
There are two key components in an inflammatory
process: microcirculation and sensory nerve activity.
According to literature, the excitation of the A-delta
fibre seems to have an insignificant effect on the
pulp blood flow (PBF), the activation of the C fibre
provokes an augmentation caused by the action of
neuro-quinine. On the other hand, the increase of
pulp blood flow (PBF) provokes the excitation ofA-
delta and C fibres and the increase of tissue pressure
(31-34).
Various authors have reported that light damage
gives rise to changes in the pain receptor circuit and
increases the possibility of the neurotrophic system;
derived from the brain, contributing to the persistent
pain even after dental therapy. In fact, the kinase
tyrosine receptor B (TrkB) seems to be present at
a high percentage (54%) of the isolechital neurons
B4+ following tooth damage, suggesting a presence
in the ascending pain receptors (35).
From histological studies conducted on TrkB
reactivity and the connection with the B4 isolechtin,
it was seen that the TrkB receptors are present in
36.6% of the trigeminal ganglion neurons and that
this percentage decreases during the first 48 hand
then increases up to 41% after 7 days from the dental
damage.
In the case of chronic inflammation, an
irreversible destruction ofthe parenchymal tissue has
been noticed, and the restructuring with connective
and fibrous tissue of the resulting defect, as well as
the activation of the cell-mediated bacterial lysase
with the activation of the T and B cells and of the
cytokine system (36-37)
117
Periapical inflammation occurs as a consequence
of pulp inflammation following trauma, carious
process or iatrogenic damage, and such inflammation
stimulates the formation ofgranulomae and cysts with
consequent bone inflammation. The inflammatory
response consists of an initial vasodilatation, an
increase of the vascular permeability, infiltration
of leucocytes regulated by endogenic mediators
such as neuropeptide quinine, migration of
polimorphonuclear leucocytes and monocytes,
cytokines.(Interleukin-l prostaglandin-l) (38).
Binomial bacterial pulp-infection inflammation has
been widely demonstrated (39-40).
A coronal fracture exposes a great number of
dental tubules: the main path towards the pulp of a
wide variety of dangerous agents present in the oral
cavity, including bacteria and bacterial products.
Invasion might be followed; by pulpitis, necrosis,
infection of the radicular canal . and periapical
lesions. Of the approximately.Sfn) different types of
bacteria present in the oral cavity, only a small and
select group manages to invade the, dental tubules.
The one mostly found is Streptococcus spp., thanks
to the capability of recognising ~h~c~.mponents of
the dental tubules, such as type Icollagen, which
stimulates bacterial adhesion and intra-tubular
growth.The environment' also .' stiniulates the
growth of anaerobae, such as Eub'acterium spp.,
Propionibacterium spp., Bifidobacterium spp.,
Peptostreptococcus micros 'and Veillonella spp.
Gram-negative bacillus, for example Porphyromonas
spp., have been less frequently found (41).
In teeth where the viable pulp is functional,
dentine has a considerable resistance towards
bacterial infiltration and inflammatory changes
are transient. Dental pulp defends itself by using
a "passive" mechanism made up of an increase
in the flow of dentinal fluid, which removes the
bacteria through hydrostatic pressure, and with an
active mechanism. This latter consists of the pulp's
capacity, through the blood flow, of developing an
immediate inflammatory response which removes
stimuli, bacterial toxins or bacteria. Alterations
in these mechanisms, for example in the case of
concurrent displacement which alters the pulp's
circulation, or the teeth's age, with a consequent
reduction of the healing potential, changes the
prognosis of the fractured tooth (42). The dental
118 D. TRIPODI ET AL.

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