histological evaluationof teethwith

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: calı[email protected]).

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).


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).


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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