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Objective <p>Turner teeth are developmental defects of permanent teeth commonly associated with disturbances affecting the corresponding primary predecessors, particularly infection or trauma. Although their clinical features have been described in previous reports, detailed histopathological characterization of severe Turner teeth, especially with respect to pulp tissue alterations, remains limited. This case-control study compared severe Turner teeth with normal teeth, focusing primarily on structural and molecular alterations in pulp tissue and descriptively on periodontal tissue morphology. Enamel structure and composition were not directly investigated.</p> Materials and methods <p>Ten extracted severe Turner teeth and ten extracted normal teeth from orthodontic patients were included. Hematoxylin and eosin staining and Masson trichrome staining were used to evaluate pulp, apical, and periodontal tissue morphology. Immunofluorescence staining was performed in pulp tissue sections to assess markers related to stemness (CD105), vascularization (CD31), innervation (βIII-tubulin), dentinogenesis (DSPP and RUNX2), extracellular matrix organization (Vimentin and FN1), inflammation (IL-1β and TNF-α), and Wnt/β-catenin signaling (β-catenin, AXIN1, and AXIN2).</p> Results <p>Compared with controls, severe Turner teeth showed a thinner odontoblast layer, a less continuous dentin-pulp interface, disorganized apical pulp fibers, reduced vascular distribution, irregular periodontal fiber arrangement, and a thinner cementum layer. In pulp tissue, CD105, CD31, βIII-tubulin, DSPP, RUNX2, Vimentin, FN1, and β-catenin expression levels were lower in Turner teeth, whereas IL-1β, TNF-α, AXIN1, and AXIN2 expression levels were higher (all <i>P</i> &lt; 0.05).</p> Conclusion <p>Severe Turner teeth were associated with coordinated histopathological alterations in pulp tissue architecture, marker expression, and periodontal morphology. These findings provide tissue-level evidence that severe Turner teeth are accompanied by an altered pulp microenvironment and provide a histopathological basis for future mechanistic and clinical studies.</p>

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A histopathological case-control study of severe turner teeth and normal teeth: structural and compositional alterations in pulp and periodontal tissues

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月10日

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  • Tiankai Di,
  • Yuhan Liu,
  • Jinlong Xu,
  • Xiaodong Zhang,
  • Jun Li,
  • Lulu Wang,
  • Yujiang Chen

摘要

Objective

Turner teeth are developmental defects of permanent teeth commonly associated with disturbances affecting the corresponding primary predecessors, particularly infection or trauma. Although their clinical features have been described in previous reports, detailed histopathological characterization of severe Turner teeth, especially with respect to pulp tissue alterations, remains limited. This case-control study compared severe Turner teeth with normal teeth, focusing primarily on structural and molecular alterations in pulp tissue and descriptively on periodontal tissue morphology. Enamel structure and composition were not directly investigated.

Materials and methods

Ten extracted severe Turner teeth and ten extracted normal teeth from orthodontic patients were included. Hematoxylin and eosin staining and Masson trichrome staining were used to evaluate pulp, apical, and periodontal tissue morphology. Immunofluorescence staining was performed in pulp tissue sections to assess markers related to stemness (CD105), vascularization (CD31), innervation (βIII-tubulin), dentinogenesis (DSPP and RUNX2), extracellular matrix organization (Vimentin and FN1), inflammation (IL-1β and TNF-α), and Wnt/β-catenin signaling (β-catenin, AXIN1, and AXIN2).

Results

Compared with controls, severe Turner teeth showed a thinner odontoblast layer, a less continuous dentin-pulp interface, disorganized apical pulp fibers, reduced vascular distribution, irregular periodontal fiber arrangement, and a thinner cementum layer. In pulp tissue, CD105, CD31, βIII-tubulin, DSPP, RUNX2, Vimentin, FN1, and β-catenin expression levels were lower in Turner teeth, whereas IL-1β, TNF-α, AXIN1, and AXIN2 expression levels were higher (all P < 0.05).

Conclusion

Severe Turner teeth were associated with coordinated histopathological alterations in pulp tissue architecture, marker expression, and periodontal morphology. These findings provide tissue-level evidence that severe Turner teeth are accompanied by an altered pulp microenvironment and provide a histopathological basis for future mechanistic and clinical studies.