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).