histological evaluationof teethwith
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CASE REPORT
Histologicalevaluationof teethwithhyperplasticpulpitiscausedby traumaorcaries: casereports
M. K. Calskan1, F. O« ztop2 & G. Calskan3
1Department of Endodontology, School of Dentistry, Ege University, 2Department ofPathology, Faculty of Medicine, Ege University, 3Dental Health and Oral Hygiene Centre,Alsancak, Izmir, Turkiye
Abstract
Calskan MK, O« ztop F, Calskan G. Histological evaluation of teeth with hyperplastic pulpitis caused
by trauma or caries: case reports. International Endodontic Journal, 36, 64^70, 2003.
Aim The purpose of this histological study was to examine teeth with hyperplastic
pulpitis caused by trauma or caries.
Summary The pulp tissue of one young permanent incisor with a complicated crown-
root fracture and a hyperplastic pulpitis, which had been contaminated with oral
microflora for 40 days, and pulp polyps from four permanent first molars whose crowns
were destroyed by extensive caries were prepared for standard histological examination.
Histologically, normal pulp tissue organization was observed in the tooth with a
complicated crown-root fracture in the cervical radicular region. Irregular calcification
was seen in the coronal and radicular portion of the pulp in the four carious teeth with
pulp polyps. Radicular pulp tissue in the middle and apical third of root canals beneath
irregular calcification showed intensive fibrosis but was free from inflammatory cells.
Key learning points� Hyperplastic pulpitis is a type of irreversible chronic open pulpitis.
� Young permanent teeth with hyperplastic pulpitis caused by trauma or caries have a great
inherent defensive capacity to heal.
Keywords: caries, histologic evaluation, hyperplastic pulpitis, trauma
Received 17 January 2002; accepted 12 July 2002
Introduction
Hyperplastic pulpitis is a type of irreversible chronic open pulpitis that occurs usually in
young teeth where the pulp has been exposed by caries or trauma. It is asymptomatic,
except during mastication, when pressure of the food bolus may cause discomfort. Thermal
Correspondence: Mehmet Kemal Calıskan, Ege Universitesi, Dis Hekimligi Fakultesi, Endodonti Bilim Dalı,
Bornova Kampusu 35100, Izmir, TURKIYE (Tel.: þ90 232 3880328; fax: þ90 232 3880325;
e-mail: calıskan@dishekimligi.ege.edu.tr).
64 International Endodontic Journal, 36, 64^70, 2003 � 2003 Blackwell Publishing Ltd
and electrical sensitivity tests may elicit normal responses. Sometimes, it may be confused
with proliferating gingival tissue. Radiographs generally show a large open cavity with direct
access to the pulp chamber (Walton et al. 1985, Grossman et al. 1988, Smulson & Sieraski
1989, Calıskan 1993; 1995).
Histopathologically, a blood clot, fibrin and inflammatory cells may be present at the pulp
surface immediately after traumatic or carious pulp exposure, due to tissue trauma and
microbial irritation. If treatment is delayed, the pulp may develop a proliferative (hyper-
plastic) pulpitis (Brannstrom 1982). The surface of the polyp usually shows epithelialization
and even para-keratinization depending upon the age of the polyp. The tissue in the pulp
chamber is often transformed into granulation tissue, which projects from the pulp into the
carious lesion. There may be fibrosis and calcific degeneration in some areas of the coronal
pulp, whilst the radicular pulp tissue may be healthy or contain few chronic inflammatory
cells (Walton et al. 1985, Grossman et al. 1988, Smulson & Sieraski 1989, Calıskan et al.
1997). However, no histological report of human pulp reaction to exposure, after compli-
cated crown fracture has been published in the literature and there are only two experi-
mental histological studies in monkeys on this subject. In these studies, pulpal changes
were characterized by a proliferative response, invariably associated with only superficial
inflammation extending not more than 2 mm from the exposure site after 7 days (Cvek et al.
1982, Heide & Mjor 1983).
The depth of pulp inflammation is a critical factor for pulp healing after pulpotomy (Cvek
1994) because calcium hydroxide has no beneficial effect on the healing of inflamed pulp
(Tronstad & Mjor 1972). Depending on the size of the exposure, time elapsed after injury
and type of pulp exposure (cariously or traumatically), different levels of pulpal amputation
have been recommended, i.e. partial or cervical (Stanley 1989, Cvek 1994).
The purpose of this study was to examine the histological changes in a complicated
crown-root fractured tooth with hyperplastic pulpitis which had been previously contami-
nated by the oral microflora and in four teeth with pulp polyps whose crowns had been
completely destroyed by caries.
Materials and method
The report describes five teeth with hyperplastic pulpitis, in patients ranging in age from
10 to 20 years, who presented at the Dental Clinic of Ege University, Izmir, Turkey for
examination and treatment. Clinical examination of one case revealed hyperplastic
pulp tissue growing from a traumatic exposure site in a left maxillary central incisor,
40 days after an untreated crown-root fracture (Fig. 1a). The other four teeth, all permanent
mandibular first molars, had pulp polyps after complete coronal destruction by caries
(Fig. 2a).
Patients and/or parents stated that carious lesions had appeared in the molars several
years before, but they had not previously received any treatment. The teeth responding to
electrical pulp testing were not mobile or tender to percussion, and gave no history of
spontaneous prolonged pain. Internal resorption or periradicular pathological changes were
not observed on radiographs (Fig. 1b). Whilst three of the carious teeth with pulp polyps
showed normal, mature roots, the fourth case showed short root formation without
radiographic signs of periapical involvement (Fig. 2b). These carious teeth had been seen
by an orthodontist who had recommended extraction. The patient with the complicated
crown-root fracture was advised to undergo orthodontic or surgical extrusion and root canal
treatment followed by a post, core and crown, but preferred extraction.
The teeth were extracted and fixed in 10% neutral buffered formalin, decalcified in 1 N
nitric acid and embedded in paraffin wax. Sections of 5–6 mm were cut in a buccal–lingual
plane and stained with haematoxylin and eosin for nuclear differantiation, Weigert von
� 2003 Blackwell Publishing Ltd International Endodontic Journal, 36, 64^70, 2003 65
Figure 1 (a) Lacerated gingival tissue and hyperplastic pulp tissue around the site of the maxillary left central
incisor in a case with complicated crown-root fracture untreated for 40 days after accident. The polyp is
covered by plaque. (b) Radiographic view of same tooth. (c) There is granulation tissue of pulp through the
exposure (H&E stain: � 32). (d) Laminated matrix on the surface of the proliferated pulp tissue (H&E
stain: � 100). (e) Chronic pulp inflammation was found just beneath the exposure site (H&E stain: � 170).
(f) Cervical radicular pulp tissue beneath the region shown in Fig. 1(e) demonstrating normal tissue organization
with odontoblastic layer and dilated functioning blood vessel (H&E stain: � 170).
66 International Endodontic Journal, 36, 64^70, 2003 � 2003 Blackwell Publishing Ltd
Gieson for connective tissue, and Gram stain according to the method of Brown & Brenn
(1931) for bacteria.
Sections of the pulp tissue of each tooth were evaluated subjectively by light microscopy
for pulpal inflammation, presence and location of necrosis, fibrosis, calcification and
resorption and for the presence of bacteria.
Results
Histologic pulp reactions in the complicated crown-root fractured tooth with hyperplastic
pulpitis
Hyperplastic pulp tissue was protruding above the exposure level (Fig. 1c). The surface of
polypoid overgrowth was not covered with epithelium and there was capillary proliferation
and a dense infiltration of polymorphonuclear leucocytes. Foci of microabscesses were
present in some areas of proliferated pulp tissue (Fig. 1d). A chronic inflammatory cell
infiltration was present just underneath the exposure site (Fig. 1e), but the cervical radicular
pulp tissue appeared normal with dilated functioning blood vessels (Fig. 1f).
The dentine walls of the fracture site containing the pulp polyp were lined with bacteria.
Most of the bacteria were Gram positive and penetrated deeply into dentine. No stained
bacteria were seen in the pulp tissue.
Histologic pulp reactions in carious teeth with hyperplastic pulpitis
The surface of the polypoid outgrowth in all four cases showed histologic evidence of
epithelialization. Pulp polyps consisted of proliferated capillary blood vessels, a dense
infiltration of polymorphonuclear leucocytes and foci of microabscesses (Fig. 2c). In the
coronal pulps of all teeth, there was extensive irregular calcification, which tended to
separate the pulp polyp from the radicular pulp and fill the coronal pulp at the root canal
orifices. The pulp tissue stayed in contact with the polypoid overgrowth by means of many
tunnels of various diameters that ran through this irregular calcification (Fig. 2d). The middle
and apical third of radicular pulp tissue beneath the calcified barrier tissue in three teeth was
generally less vascular and more fibrotic, with absence of inflammatory cells. The pulp
tissue at the apices of roots appeared normal and included nerve fibres. Irregular calcifica-
tion extended to the apical third of the mesial root canals in the case with short roots.
Although there was insufficent root formation with a normal periodontal ligament space and
no signs of root resorption radiographically, the periapical surfaces of the roots showed
cementum and dentine resorption (Fig. 2e). Moreover, the radicular pulp tissue showed
fibrosis along with a group of denticles of different size (Fig. 2f). The middle third of the
distal radicular pulp tissue of the same tooth showed fibrosis (Fig. 2g).
On the surface of the pulp polyp, colonies of Gram-positive bacteria were observed
where ulcerative change had caused loss of the epithelium. A Gram-positive bacterial
staining was observed on the wall of the cavity containing the pulp polyp. No bacterial
colonies were seen in radicular pulp tissue or in the periapical tissues.
Figure 2 (a) Hyperplastic pulp tissue in carious cavity of mandibular left first molar. (b) Periapical radiograph
showing a normal periodontal ligament space without sign of apex root resorption. Note insufficient
development of roots. (c) Stratified squamous epithelium covering polypoid overgrowth (H&E stain: � 100). (d)
Inflamed pulp tissue filling tunnels in the calcified tissue (H&E stain: � 100). (e) Extensive irregular calcification
in the apical third of the mesial root and a significant resorption around apical cementum and dentine (H&E
stain: � 32). (f) Radicular pulp tissue beneath calcified barrier showing fibrosis free from inflammatory cells
with a group of denticles (H&E stain: � 100). (g) Fibrosis of pulp tissue in the middle third of distal root canal of
the same tooth (H&E stain: � 200).
� 2003 Blackwell Publishing Ltd International Endodontic Journal, 36, 64^70, 2003 67
68 International Endodontic Journal, 36, 64^70, 2003 � 2003 Blackwell Publishing Ltd
Discussion
In one of our cases, hyperplastic pulp was observed clinically without any sign of tissue
necrosis. Histologically, pulp inflammation was limited in the cervical radicular region
40 days after trauma. Similar tissue reactions were found after 7 days in experimentally
exposed primate pulps (Cvek et al. 1982, Heide & Mjor 1983). Although the time elapsed
after injury was different, similar findings of these studies may reflect the defensive
capacity of the human pulp, which may be greater in humans than primates. The previous
clinical studies of pulp exposures resulting from trauma to human teeth in 7–20-year-olds
found that an exposure of between 45 days and 6 months did not significantly affect the
prognosis of partial pulpotomy treatment (Cvek 1978, Calıskan & Sabah 1992, Calıskan &
Sepetcioglu 1993).
Four carious teeth with hyperplastic pulpitis in the present study had unrestorable
crowns, irregular calcification and reactive fibrosis, frequently tended to separate the
grossly inflamed area in the polyp from the middle and/or apical portion of the pulp which
remained apparently normal. It was likely that this process was promoting intrinsic defence
of the pulp.
Calıskan et al. (1997) demonstrated that radicular pulp tissue in cases of chronic
hyperplastic pulpitis with periapical osteosclerosis also showed fibrosis with absence of
inflammatory cells. They suggested that development of periapical osteosclerosis was
probably a reaction to the stimulant effect of inflammation within the root canal. In the case
of a hyperplastic pulpitis with short roots reported here, compromised root development
might have been a reaction to long-standing inflammation within the root canal resulting
from dental caries.
A hyperplastic response of the pulp to acute inflammation occurs in young teeth (Stanley
1965), but never in teeth of old patients (Seltzer & Bender 1976). This may be indicative of a
good pulpal response. Presumably the young pulp does not become necrotic following
exposure, because its natural defences and rich supply of blood allow it to resist bacterial
infection (Kim & Trowbridge 1987). This reaction is probably favoured by free exposure of
the pulp in complicated crown fracture or in teeth whose crowns are completely destroyed
by caries, permiting continuous salivary rinsing and preventing impaction of contaminated
debris (Cvek et al. 1982, Calıskan et al. 1997). Transudate and exudate which are
inflammatory response products in open chronic pulpitis, drain into the oral cavity and
do not accumulate. Thus, intrapulpal pressure, which may consequently cause tissue
damage and destruction of the microcirculation does not develop (Walton et al. 1985).
Masterton (1966) claimed that one reason why the wound did not heal might be the
absence of epithelium on the pulp. Therefore, an active dressing was considered necessary
for healing. However, the epithelial layer over the surface of the polyp protects the
underlying granulation tissue from the harmful effects that will disturb wound healing in
the oral cavity (Calıskan et al. 1997). These defensive reactions probably contribute to the
inherent healing potential of a young dental pulp in which hyperplastic pulpitis develops.
Conclusions
According to the favourable histologic results of this study, it may be concluded that young
permanent teeth with hyperplastic pulpitis caused by caries or trauma have a great inherent
defensive capacity to heal despite adverse conditions.
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