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<p>Odontogenic keratocysts (OKCs) exhibit paradoxical biological behavior, displaying both cystic architecture and neoplastic potential. Their recurrence and local aggressiveness are believed to stem from epithelial plasticity and aberrant keratinization. This study introduces the concept of KeratoDynamics, a molecular framework integrating the processes of transdifferentiation and dyskeratosis in OKCs, through the analysis of three key biomarkers—Ki-67, c-Myc, and CK19. Formalin-fixed, paraffin-embedded samples of recurrent and non-recurrent OKCs were examined histologically and immunohistochemically. Quantitative assessment revealed significantly higher Ki-67 (42%) and c-Myc (38%) expression in recurrent lesions compared with non-recurrent cases (25% and 20%, respectively; <i>p</i> &lt; 0.05). CK19 exhibited diffuse cytoplasmic positivity, with greater intensity in recurrent OKCs, indicating disrupted epithelial differentiation. A strong correlation between Ki-67 and c-Myc (<i>r</i> = 0.68, <i>p</i> &lt; 0.01) reflected a proliferative–transcriptional coupling, while CK19 expression correlated moderately with delayed recurrence (<i>r</i> = 0.52, <i>p</i> &lt; 0.05). Histologically, recurrent lesions demonstrated epithelial budding, dyskeratosis, and focal thickening, consistent with molecular reprogramming and epithelial instability. The collective expression of these markers defines the KeratoDynamics panel, which encapsulates the continuum between proliferation, lineage reprogramming, and keratinization that underlies OKC pathogenesis. This integrative approach enhances diagnostic precision, aids in recurrence prediction, and offers new perspectives for biologically guided management of odontogenic keratocysts.</p>

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KeratoDynamics of transdifferentiation and dyskeratosis in odontogenic keratocysts

  • 期刊论文

  • 发表日期：

    2026年2月17日

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  • Krishnasamy Nitya,
  • Ramadoss Ramya,
  • Suresh Vemuri

摘要

Odontogenic keratocysts (OKCs) exhibit paradoxical biological behavior, displaying both cystic architecture and neoplastic potential. Their recurrence and local aggressiveness are believed to stem from epithelial plasticity and aberrant keratinization. This study introduces the concept of KeratoDynamics, a molecular framework integrating the processes of transdifferentiation and dyskeratosis in OKCs, through the analysis of three key biomarkers—Ki-67, c-Myc, and CK19. Formalin-fixed, paraffin-embedded samples of recurrent and non-recurrent OKCs were examined histologically and immunohistochemically. Quantitative assessment revealed significantly higher Ki-67 (42%) and c-Myc (38%) expression in recurrent lesions compared with non-recurrent cases (25% and 20%, respectively; p < 0.05). CK19 exhibited diffuse cytoplasmic positivity, with greater intensity in recurrent OKCs, indicating disrupted epithelial differentiation. A strong correlation between Ki-67 and c-Myc (r = 0.68, p < 0.01) reflected a proliferative–transcriptional coupling, while CK19 expression correlated moderately with delayed recurrence (r = 0.52, p < 0.05). Histologically, recurrent lesions demonstrated epithelial budding, dyskeratosis, and focal thickening, consistent with molecular reprogramming and epithelial instability. The collective expression of these markers defines the KeratoDynamics panel, which encapsulates the continuum between proliferation, lineage reprogramming, and keratinization that underlies OKC pathogenesis. This integrative approach enhances diagnostic precision, aids in recurrence prediction, and offers new perspectives for biologically guided management of odontogenic keratocysts.