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Статья

Comparative Cytotoxicity and Inflammatory Profiles of CeraSeal Versus AH Plus in Periodontal Tissue Repair: An In Vitro and In Vivo Study

Gulnihol SharipovaDepartment of Hygiene No. 2, Bukhara State Medical Institute Named After Abu Ali Ibn Sino, Bukhara 200100, UzbekistanJasur RizaevDepartment of Public Health and Healthcare Management, Samarkand State Medical University, Samarkand 140100, UzbekistanShuxrat BoymuradovDepartment of Maxillofacial Surgery and Dentistry, Tashkent State Medical University, Tashkent 100000, UzbekistanMirzaakbar KamolovDepartment of Maxillofacial Surgery, Andijan State Medical Institute, Andijan 170100, UzbekistanAdolat MamadiyorovaDepartment Prevention of Dental Diseases, Tashkent State Medical University, Tashkent 100000, UzbekistanLatipov JavdatDepartment of Medicine, Termez University of Economics and Service, Termez 190100, UzbekistanUmarov DoniyorDepartment of Clinical Sciences, Ma’mun University, Urgench 220100, UzbekistanNozimjon IbrokhimovDepartment of Social Sciences, Bukhara State Pedagogical Institute, Bukhara 200100, Uzbekistan
2026en
ABI

Аннотация

Background/Objectives: Endodontic perforation repair requires biomaterials that balance sealing ability with minimal cellular injury. AH Plus (epoxy resin-based) remains widely used despite cytotoxicity concerns. CeraSeal (calcium silicate-based bioceramic) is a potentially more biocompatible alternative. However, comparative data on sealer-induced cytotoxicity and inflammatory responses remain limited. This study compared the cytotoxicity and inflammatory profiles of CeraSeal and AH Plus using in vitro and in vivo approaches. Methods: Human periodontal ligament stem cells (hPDLSCs) were exposed to sealer extracts (1:4 AH Plus, 1:8 CeraSeal) for 120 h. Cell death was assessed by MTT, Live/Dead, LDH release, and Annexin V/PI flow cytometry. Oxidative stress was quantified via ROS generation (DCFH-DA). In a rat furcation perforation model (n = 8 teeth/group), inflammatory markers (TNF-α, IL-1β, CD68), osteogenic activity (ALP), and osteoclasts (TRAP) were evaluated. Results: AH Plus was associated with significantly greater necrotic cell death (357.6 ± 47.6% LDH release vs. CeraSeal 128.8 ± 37.5%; p = 0.0079) and reduced hPDLSC viability at all time points (p < 0.0001). ROS generation was comparable between sealers (~32–35%, p > 0.05). In vivo, IL-1β was higher in AH Plus-treated tissues (52.25 vs. 24.88 cells/mm2; p = 0.0002), while TNF-α and CD68 were greater in CeraSeal (p ≤ 0.0011). ALP was higher in AH Plus (median 6.15 vs. 3.68; p = 0.0002), with no difference in TRAP-positive osteoclasts. Morphometric analysis showed superior cellular preservation with CeraSeal (p = 0.0079), while inflammatory infiltration was higher in CeraSeal (p = 0.0002). Conclusions: AH Plus was associated with a necrotic-inflammatory profile with elevated IL-1β and higher ALP expression. CeraSeal demonstrated better cellular preservation, lower LDH release, and a distinct inflammatory signature (higher TNF-α and CD68). These findings establish comparative response profiles for the two sealers and support CeraSeal as a potentially biocompatible alternative, though further mechanistic studies are warranted.

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