Tables 2 and 3 outline the length of the specific time intervals. Following the initial procedure, two subjects did not return for extraction and two other subjects agreed to the extraction of only one tooth; two teeth were lost in the process of histological preparation. The number of samples evaluated was 14.

Samples capped with mineral trioxide aggregate.

• One-week sample: No bridge was formed and mild chronic inflammation at the exposure site plus slight hyperaemia and necrosis were observed. Lymphocytes and few polymorphonuclear leucocytes (PMNLs) were seen.
• Two-month samples: Dentine bridges of maximum 0.28 mm thickness with underlying mild chronic inflammation were found (Fig.1). Lymphocytes dominated the inflammatory zone. Mild hyperaemia and necrotic areas could be seen in only one sample. The other sample had calcifications and a few odontoblasts.
• Three-month samples: Dentine bridges of maximum thickness of 0.25 mm and odontoblasts were registered for all samples (Fig. 2). Mild chronic inflammation, mild hyperaemia and necrosis were observed underneath the bridge of one sample. Calcifications and dominating lymphocytes also could be seen.
• Four-month sample: Dentinal bridges of 0.37 mm thickness were seen. Inflammation, hyperaemia, necrosis, calcification or odontoblastic layer were not observed.
• Six-month sample: A 0.43 mm-thick dentine bridge and a nearly regular odontoblastic layer were noted. No inflammation, necrosis or calcifications were registered.

Table 2. Samples capped with MTA.



Table 3. Samples capped with calciumhydroxide.



Figure 1. A view of the pulp cap area of a 2-month sample capped with MTA, H&E stained, x31.25.
(1) MTA;
(2) dentinal bridge;
(3) pulp;
(4) calcification.



Figure 2. A view of the pulp cap area of a 3-month sample capped with MTA, H&E stained, x312.5.
(1) MTA;
(2) dentinal bridge;
(3) odontoblasts.

Samples capped with calcium hydroxide.

• One-week sample: No dentinal bridges were present. Chronic and acute inflammation at the exposure site and hyperaemia were noted. PMNLs and to a lesser extent lymphocytes were the dominant inflammatory cells. There were no calcifications.
• Two-month sample: No dentine bridges had formed. Acute and chronic inflammation, hyperaemia and calcifications were prominent with dominating PMNLs and lymphocytes.
• Three-month samples: Both samples showed moderate chronic inflammation, mild hyperaemia and necrosis. Lymphocytes were the dominant inflammatory cells (Figs 3 and 4). An irregular bridge of maximum 0.02 mm thickness was reported. No calcifications or odontoblastic layers could be seen.
• Four-month sample: A bridge of maximum 0.04 mm thickness had formed with mild chronic lymphocytedominated inflammation and mild hyperaemia underneath. No calcifications or odontoblastic layer were present.
• Six-month sample: Calcification and necrosis were seen underneath a bridge of maximum 0.15 mm thickness. No odontoblastic layer was showed. Lymphocytes dominated the mild chronic inflammation and there was mild hyperaemia.

Figure 3. A view of the pulp cap area of a 3-month sample capped with calciumhydroxide, H&E stained, x31.25.
(1) Calcium hydroxide;
(2) pulp.
A few vessels can be seen (arrows) indicating mild hyperaemia.



Figure 4. A view of the pulp-cap area of a 3-month sample capped with calciumhydroxide, H&E stained, x312.5.
(1) calcium hydroxide;
(2) dentine-like structures;
(3) pulp.
Polymorphonuclear leucocytes dominate the superficial layers (top), whereas lymphocytes are more frequently dispersed in the deeper parts (bottom).Mild hyperaemia is also present (arrows).