Offenbacher Steven, Barros Silvana P, Beck James D
Center for Oral and Systemic Disease, Department of Periodontology, University of North Carolina at Chapel Hill, Manning Drive and Columbia Street, Chapel Hill, NC 27599, USA.
J Periodontol. 2008 Aug;79(8 Suppl):1577-84. doi: 10.1902/jop.2008.080220.
Clinical signs and symptoms, as well as medical and dental history, are all considered in the clinical determination of gingival inflammation and periodontal disease severity. However, the "biologic systems model" highlights that the clinical presentation of periodontal disease is closely tied to the underlying biologic phenotype. We propose that the determination and integration of subject-level factors, microbial composition, systemic immune response, and gingival tissue inflammatory mediator responses will better reflect the biology of the biofilm-gingival interface in a specific patient and may provide insights on clinical management. Disease classifications and multivariable models further refine the biologic basis for the increasing severity of periodontal disease expression. As such, new classifications may better identify disease-susceptible and treatment-non-responsive individuals than current classifications that are heavily influenced by probing and attachment level measurements alone. New data also suggest that the clinical characteristics of some complex diseases, such as periodontal disease, are influenced by the genetic and epigenetic contributions to clinical phenotype. Although the genetic basis for periodontal disease is considered imperative for setting an inflammatory capacity for an individual and, thus, a threshold for severity, there is evidence to suggest an epigenetic component is involved as well. Many factors long associated with periodontitis, including bacterial accumulations, smoking, and diabetes, are known to produce strong epigenetic changes in tissue behavior. We propose that we are now able to rethink periodontal disease in terms of a biologic systems model that may help to establish more homogeneous diagnostic categories and can provide insight into the expected response to treatment.
在临床确定牙龈炎症和牙周疾病严重程度时，会考虑临床体征和症状以及医学和牙科病史。然而，“生物系统模型”强调牙周疾病的临床表现与潜在的生物表型密切相关。我们提出，确定并整合个体水平因素、微生物组成、全身免疫反应和牙龈组织炎症介质反应，将能更好地反映特定患者生物膜-牙龈界面的生物学特性，并可能为临床管理提供见解。疾病分类和多变量模型进一步完善了牙周疾病严重程度增加的生物学基础。因此，与仅受探诊和附着水平测量严重影响的当前分类相比，新的分类可能能更好地识别易患疾病和对治疗无反应的个体。新数据还表明，一些复杂疾病（如牙周疾病）的临床特征受遗传和表观遗传对临床表型的影响。尽管牙周疾病的遗传基础被认为对于确定个体的炎症能力以及严重程度阈值至关重要，但有证据表明表观遗传成分也参与其中。许多长期与牙周炎相关的因素，包括细菌堆积、吸烟和糖尿病，已知会在组织行为中产生强烈的表观遗传变化。我们提出，现在我们能够根据生物系统模型重新思考牙周疾病，这可能有助于建立更同质化的诊断类别，并能深入了解预期的治疗反应。
