Alani Nooruldeen Ammar, Abdullah Bashar Hamid
Department of Oral Diagnostic Sciences, College of Dentistry, Baghdad University, Baghdad 10071, Iraq.
Diagnostics (Basel). 2025 Jul 19;15(14):1819. doi: 10.3390/diagnostics15141819.
Pulp inflammation impairs healing, yet the underlying vascular and neural mechanisms remain poorly understood. This study investigated the differential regulation of lymphatic vessels, blood vessels, and neural tissue in pulpitis to elucidate healing limitations in inflamed dental pulp. This study evaluated 38 pulp samples (14 symptomatic irreversible pulpitis, 13 asymptomatic irreversible pulpitis, and 11 healthy controls) via immunohistochemistry, using D2-40 to identify lymphatic vessels, CD31 to mark blood vessels, and PGP9.5 to detect neural tissue. Vessel counts and neural tissue scoring were performed by blinded examiners and analyzed using appropriate statistical tests. Dental pulp with symptomatic irreversible pulpitis exhibited significantly increased blood vessel density (50.3 vs. 39.2 in asymptomatic irreversible pulpitis and 25.8 in controls, = 0.001, Cohen's d = 1.82), while lymphatic vessel density remained unchanged across all groups ( ≥ 0.05), indicating impaired lymphangiogenesis despite inflammation. Neural tissue density was consistent across conditions, with a significant negative correlation between PGP9.5 expression and age (r = -0.5, = 0.001). CD31 and D2-40 expression showed a positive correlation (r = 0.389, = 0.016), suggesting coordinated vascular development. Our findings reveal a critical imbalance between enhanced angiogenesis and impaired lymphangiogenesis during pulpitis, potentially explaining the compromised healing capacity of inflamed dental pulp. This vascular dysregulation, combined with persistent neural tissue density, creates an environment in which inflammatory exudates accumulate with limited clearance. These insights indicate a need for new therapeutic strategies aimed at enhancing lymphangiogenesis to improve endodontic outcomes.
牙髓炎症会损害愈合，但其潜在的血管和神经机制仍知之甚少。本研究调查了牙髓炎中淋巴管、血管和神经组织的差异调节，以阐明炎症牙髓愈合的局限性。本研究通过免疫组织化学评估了38个牙髓样本（14个有症状的不可逆性牙髓炎、13个无症状的不可逆性牙髓炎和11个健康对照），使用D2-40识别淋巴管，CD31标记血管，PGP9.5检测神经组织。血管计数和神经组织评分由不知情的检查人员进行，并使用适当的统计测试进行分析。有症状的不可逆性牙髓炎的牙髓血管密度显著增加（无症状的不可逆性牙髓炎为50.3，对照为39.2，对照组为25.8， = 0.001，科恩d = 1.82），而所有组的淋巴管密度保持不变（≥ 0.05），表明尽管有炎症，但淋巴管生成受损。神经组织密度在各条件下一致，PGP9.5表达与年龄呈显著负相关（r = -0.5， = 0.001）。CD31和D2-40表达呈正相关（r = 0.389， = 0.016），表明血管发育协调。我们的研究结果揭示了牙髓炎期间血管生成增强与淋巴管生成受损之间的关键失衡，这可能解释了炎症牙髓愈合能力受损的原因。这种血管调节异常，加上持续的神经组织密度，创造了一个炎症渗出物清除有限而积累的环境。这些见解表明需要新的治疗策略来增强淋巴管生成以改善牙髓治疗效果。
