BACKGROUND: The most common problems for a patient with molar incisor hypomineralization (MIH) are the collapse of enamel and cavitations, loss of fillings, and secondary caries, but most of all, severe hypersensitivity. OBJECTIVE: The aim of this paper was therefore to histologically study possible bacterial invasion of dentinal tubules beneath apparently intact, but hypomineralized enamel in permanent molars with MIH. MATERIAL AND METHODS: Five extracted permanent first molars diagnosed with MIH were fixated, demineralized, and sagittally serially sectioned in a bucco-lingual direction in a microtome with a thickness of 4-5 microm. Sections were stained with a modified Brown and Benn staining for bacteria, unstained sections were analysed in field emission SEM. RESULTS: Stained sections from the cuspal areas, below the hypomineralized enamel, the staining indicated the presence of bacteria in the dentinal tubules. The HTX staining showed that the pulp in sections without any findings was normal and free from bacteria or infiltrates from inflammatory cells. In sections where bacteria were found in the cuspal areas or deeper in the dentin, a zone of reparative dentin was found, and in sections from one tooth, the coronal pulp showed an inflammatory reaction with inflammatory cells. In sections adjacent to those without any bacterial staining, the SEM analyses revealed empty dentinal tubules without any odontoblast processes or signs of bacteria. When odontoblast processes were found, the dentinal tubules were filled with bacteria located on the surface of the odontoblast processes. In some areas, a large number of tubules were found with bacteria. No bacteria were found close to the pulp. The odontoblast processes appeared larger in areas where bacteria were found. CONCLUSIONS: The presence of bacteria in the dentinal tubules and inflammatory reactions in the pulp indicate that oral bacteria may penetrate through the hypomineralized enamel into the dentin, thus possibly contribute to hypersensitivity of teeth with MIH.
BACKGROUND: The most common problems for a patient with molar incisor hypomineralization (MIH) are the collapse of enamel and cavitations, loss of fillings, and secondary caries, but most of all, severe hypersensitivity. OBJECTIVE: The aim of this paper was therefore to histologically study possible bacterial invasion of dentinal tubules beneath apparently intact, but hypomineralized enamel in permanent molars with MIH. MATERIAL AND METHODS: Five extracted permanent first molars diagnosed with MIH were fixated, demineralized, and sagittally serially sectioned in a bucco-lingual direction in a microtome with a thickness of 4-5 microm. Sections were stained with a modified Brown and Benn staining for bacteria, unstained sections were analysed in field emission SEM. RESULTS: Stained sections from the cuspal areas, below the hypomineralized enamel, the staining indicated the presence of bacteria in the dentinal tubules. The HTX staining showed that the pulp in sections without any findings was normal and free from bacteria or infiltrates from inflammatory cells. In sections where bacteria were found in the cuspal areas or deeper in the dentin, a zone of reparative dentin was found, and in sections from one tooth, the coronal pulp showed an inflammatory reaction with inflammatory cells. In sections adjacent to those without any bacterial staining, the SEM analyses revealed empty dentinal tubules without any odontoblast processes or signs of bacteria. When odontoblast processes were found, the dentinal tubules were filled with bacteria located on the surface of the odontoblast processes. In some areas, a large number of tubules were found with bacteria. No bacteria were found close to the pulp. The odontoblast processes appeared larger in areas where bacteria were found. CONCLUSIONS: The presence of bacteria in the dentinal tubules and inflammatory reactions in the pulp indicate that oral bacteria may penetrate through the hypomineralized enamel into the dentin, thus possibly contribute to hypersensitivity of teeth with MIH.