Opercula of teeth delayed in eruption were examined histopathologically and immunohistochemically to determine the possible causes for tooth eruption failure. Specimens were obtained from 58 patients with non-erupted teeth by surgical removal of their gingival opercula. Among the 61 specimens, 31 (50.8%) were diagnosed as pericoronal myxofibrous hyperplasia (PMH), 8 (13.1%) as infantile ameloblastic fibromatosis (IAF), and 19 (31.2%) as odontomas. Histopathologically, PMH is characterized by hyperplasia of odontogenic mesenchymal tissues with a myxoid appearance in which odontogenic epithelial islands and mesenchymal multinucleated giant cells are scattered randomly. Between the mucosal epithelium and the PMH, there is a layer of fibrosis, whose matrix is strongly immuno-positive for tenascin. The PMH seems to induce its overlying gingival mucosa to remodel the connective tissue, which obstructs tooth eruption. IAF is usually located adjacent to the PMH and shows an ameloblastic fibroma-like histology with atrophic ameloblastic components and poor encapsulation. The findings suggest that IAF associated with PMH is not a true neoplasm and should be distinguished from ameloblastic fibromas by the name of IAF, and that both lesions are included in the range of hamartomas formed only in the pericoronal tissue of teeth in eruption. We propose to categorize these lesions into a new disease entity of pericoronal hamartomas of odontogenic origin.