Human Root Caries: Histopathology of Advanced Lesions

This study describes cellular and microradiographic findings in thin undemineralized enamel-dentine sections from 36 enamel caries lesions from freshly extracted third molars. Lesions activity was determined by clinical examination and the estimated age of the lesion at extraction time. The cellular reactions to the enamel/dentine lesion complex were measured using computerized histomorphometry under the following conditions: (a) the cytoplasm:nucleus ratio of the odontoblast cell; (b) the odontoblast cell:dentinal tubule ratio, and (c) the adjacent predentine area (μm²). The first cellular reactions were observed beneath superficial enamel lesions before visible alterations in dentine mineralization. The cytoplasm:nucleus ratio of the odontoblast cells was markedly reduced, and only active lesions showed evidence of cellular proliferation into the cell-free zone. In more advanced active lesions the affected odontoblast cells had a significantly lower cytoplasm:nucleus ratio compared with the controls. Similar changes were not seen in arrested or slow-progressing lesions. Before onset of tertiary dentine formation there was a positive correlation between odontoblast cell size and predentine formation. Primary odontoblast cells were involved in early tertiary or reactionary dentine formation without odontoblast cell replacement. Reactionary dentine was only seen in active lesions, suggesting that reactions in the dentine/pulp complex are closely associated with the external environment.

Section: Discussionsupporting

confidence: 79%

A Quantitative Light Microscopic Study of the Odontoblast and Subodontoblastic Reactions to Active and Arrested Enamel Caries without Cavitation

Bjørndal

Darvann²,

Thylstrup

1997

“…Our estimations of different rates of cavitated lesion progress were additionally confirmed, since the active lesions were characterized by yellowish discoloured dentine, previously used as a parameter of lesion activity, whereas the slow-progressing lesions were darker [Massler, 1967;Nyvad and Fejerskov, 1987;Schüpbach et al, 1990]. Moreover, we could distinguish between lesion activity related to closed and open lesion environments on the basis of differences in plaque accumulation covering the cavity.…”

Section: Discussionsupporting

confidence: 79%

A Light Microscopic Study of Odontoblastic and Non–Odontoblastic Cells Involved in Tertiary Dentinogenesis in Well–Defined Cavitated Carious Lesions

Bjørndal

Darvann²

1998

This study examines cellular and microradiographic findings in thin, undemineralized sections of 46 cavitated lesions, that were clinically well–defined with respect to lesion activity and estimated lesion age at extraction time. The progressive stages of surface breakdown ranged from enamel cavitation to larger dentine exposures classified as closed and open lesion environments. Measurements of the following parameters were performed using computerized image processing software: (a) the cytoplasm:nucleus ratio of primary odontoblast cells; (b) the cell:dentinal tubule ratio; (c) the adjacent predentine area (μm²), and (d) the cytoplasm: nucleus ratio of non–odontoblastic cells, and secondary odontoblast–like cells, where estimation of these cell types were based on structural criteria. In active enamel cavitated lesions, reduced odontoblast–predentine regions and indistinct subodontoblastic regions were noted. During initial dentine exposures, non–odontoblastic cells along the pulp–dentinal interface were observed as well. The first indication of tertiary dentine was seen in old lesions with exposed dentine. The tertiary dentine appeared more atubular in the closed/active lesions than in the open/slow–progressing lesions. The involved odontoblastic cells in tubular tertiary dentine in small open/slow–progressing lesions were comparable to the primary odontoblast cells, however, new dentinal tubules were also noted presenting a mixture between reactionary and reparative dentinogenesis. In close/active lesions non–primary odontoblastic cells were aligning the atubular tertiary dentine, whereas well–defined signs of secondary odontoblast–like cells were first seen in larger open lesions, producing tubular tertiary dentine. In conclusion, a strong relationship between external lesion environments and corresponding different formations of tertiary dentine was noted in advanced cavitated lesions. It is additionally suggested that the stimulation of tubular tertiary dentine could be a closely related reaction when an active lesion complex changes into a slower progressing lesion environment.

“…These include a hypermineralised surface layer [Hals and Selvig, 1977], irritation dentine on the pulpal wall [Schüpbach et al, 1990a] and dentine sclerosis beneath a lesion [Schüpbach et al, 1992]. However, enamel 'undermining' at the CEJ noted by Schüpbach et al [1992] was also seen in our study ( fig.…”

Section: Discussionsupporting

confidence: 55%

Fluoride Distribution in Sound and Carious Root Tissues of Human Teeth

Shu

Pearce²,

Sissons³

et al. 1998

Proton probe analysis has been used to provide for the first time quantitative F concentration data in carious root tissues from subjects consuming water containing 1 ppm F. In small lesions at the neck of the tooth with minimal tissue loss the F concentration was significantly higher at the outer lesion edge than at the outer edge of adjacent sound root tissue. In one sample with high F values the lesion edge had 19,000 ppm F and the adjacent sound root surface 5,400 ppm F (μg F/g apatite). In large lesions with extensive cavitation F was again concentrated in the outer edge of the lesion and was significantly higher (1,800–4,100 ppm) than in adjacent sound inner dentine (190–290 ppm). Fluoride concentrations varied markedly along the outer edge of both normal and carious root tissues. Fluoride increase at the lesion edge is not an effect of tissue shrinkage but probably a result of remineralisation events during caries. This additional F may be expected to increase tissue resistance to further acid attacks.