Dens invaginatus-type malformation without pulpal involvement

Abstract

Dens invaginatus is a developmental abnormality in which there is a communication from surface of tooth toward pulpal tissue or root. There are several theories to explain this type of phenomenon. Gustafson and Sundberg 1 believed that if there are no ameloblasts at some point over dental papilla, then no dentin will be formed because inductive stimulus is absent. Therefore, in absence of enamel and dentin, there will be a direct channel through dental papil la that will remain patent after mineralization of normally formed enamel and dentinal matrix. Connective tissue occupies defect and restricts further development; at same time, this causes infolding of normal dental tissues adjoining defect. Kronfeld ~ has suggested that mechanism of formation of dens invaginatus may not be by actual ingrowth of enamel into underlying pulp, but rather by a relative retardation in growth of a portion of enamel. The surrounding dental tissues continue to grow normally so that final result is similar to intussusception of a portion of tooth into another portion. On other hand, KiUey and associates a said that invagination may result from proliferation of ameloblasts since, the large size achieved by some invaginations would be irapossible by a mechanism of local growth arrest with continued growth of epithelial component of tooth form around it. The morphology of crown of tooth may differ from normal morphology depending on size of invagination. Thus, if crown is dilated, malformation may be described as a dilated odontoma. OmneU and his co-workers 4 studied unerupted specimens of dens invaginatus since decomposition of any uncalcified tissue within invagination might occur when tooth erupts into mouth. The value of histological investigation then would be diminished. They concluded that aberrant cells contained in dental lamina are destined to become keratinized squamous epithelial cells rather than ameloblasts. These aberrant cells are situated at internal enamel epithelial layer. Thus, formation of normal enamel matrix is impossible at such sites. Channels extending from base of invagination to pulp have been described. 1,~,6 Bacteria obtaining access through such channels could be cause of pulpaI death. Kramer 7 found an absence of enamel at base of defect; he thought microorganisms could obtain access to pulp via unprotected dentin, and thus give rise to infection and eventual necrosis of pulp. Clinical evidence supports concept that death of pulp may occur in absence of caries or trauma, s In following case report, infection occurred in lateral periodontal space as a result of a dens invaginatus-type malformation. The vitality of pulp was not affected either before or after treatment.