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Updated: Dec 16, 2025
Oral Biofilm Analysis of Palatal Expanders by Fluorescence In-Situ Hybridization and Confocal Laser Scanning Microscopy
Published on: October 20, 2011
Bacteriologic status of non-cavitated proximal enamel caries lesions. A histologic and histobacteriologic study
Domenico Ricucci1, José F Siqueira2
1Private Practice, Cetraro, Italy.
Objectives:
This histologic and histobacteriologic study evaluated non-cavitated interproximal white spot lesions in human teeth for the 1) presence and morphology of bacterial aggregations at the enamel-dentinal junction (EDJ), and 2) reactions in the subjacent pulp tissue.
Methods:
The material comprised 16 third molars diagnosed with early interproximal caries lesions obtained consecutively in a single clinical practice. Four third molars with clinically intact proximal surfaces served as controls. Caries activity was categorized as active or arrested. Teeth were prepared for histologic and histobacteriologic analyses.
Results:
Control teeth exhibited normal tissue conditions with no bacteria. Macroscopic discoloration of the superficial dentin occurred in 14/16 teeth with early caries lesions. Bacterial aggregations resembling biofilms were observed in 10/16 teeth (six with active and four with arrested lesions). Bacterial cells were observed superficially in some of the underlying dentinal tubules, while in a few cases a deeper penetration was evident. Pathologic changes of varying degrees were observed in the pulps of all 16 teeth, regardless of the caries activity (active or arrested). Pulp reactions varied from disruption of the odontoblast layer, with loss of odontoblasts, to formation of tertiary dentin.
Conclusions:
Bacterial biofilms associated with white-spot caries lesions may traverse the enamel and reach the underlying dentin in both active and arrested lesions. In all teeth with early lesions, the pulps showed changes in response to the very superficial biofilm challenge.
Clinical Significance:
In non-cavitated, active or arrested, enamel caries lesions, bacteria traverse the enamel and may establish structured biofilms at the enamel-dentinal junction, causing early pulp changes. These new findings may stimulate clinicians to rethink the rationale for treatment methods that are based on the assumption that bacteria are absent in white-spot lesions.
