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 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, Caliskan 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 (hyperplastic) 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, Caliskan et al. 1997). However, no histological report of human pulp reaction to exposure, after complicated crown fracture has been published in the literature and there are only two experimental 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 contaminated 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 differentiation, Weigert von 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.

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 iscovered by plaque.
(b) Radiographic view of same tooth.
(c) There is granulation tissue of pulp through the exposure (H&E stain: x 32).
(d) Laminated matrix on the surface of the proliferated pulp tissue (H&E stain: x 100).
(e) Chronic pulp inflammation was found just beneath the exposure site (H&E stain: x 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: x 170).



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: x 100).
(d) Inflamed pulp tissue filling tunnels in the calcified tissue (H&E stain: x100).
(e) Extensive irregular calcification in the apical third of the mesial root and a significant resorption around apical cementum and dentine (H&E stain: x 32).
(f) Radicular pulp tissue beneath calcified barrier showing fibrosis free from inflammatory cells with a group of denticles (H&E stain: x100).
(g) Fibrosis of pulp tissue in the middle third of distal root canal of the same tooth (H&E stain: x 200).

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 calcification extended to the apical third of the mesial root canals in the case with short roots. Although there was insufficient 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.

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, Caliskan & Sabah 1992, Caliskan & Sepetc¸iog˘ lu 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 defense of the pulp.
Caliskan 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 defenses 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, permitting continuous salivary rinsing and preventing impaction of contaminated debris (Cvek et al. 1982, Caliskan 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 (Caliskan et al. 1997). These defensive reactions probably contribute to the inherent healing potential of a young dental pulp in which hyperplastic pulpitis develops.

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