Study of aging system in Pulpal and periodontal tissue

1. 巨噬细胞在幼鼠根尖周围病变中产生IL-1α，病变缓慢增大。根尖周围病变的愈合随着年龄的增长而延迟。大鼠牙髓中抗原提呈细胞的反应随年龄的增长而减弱，但巨噬细胞和单核细胞的反应不减弱。牙龈分解系统的抑制是幼龄大鼠牙龈过度生长的原因之一。牙髓化学刺激引起的颌骨肌肉活动随年龄变化而变化。人牙髓碱性磷酸酶活性随年龄增长而降低。随着年龄的增长，牙周韧带的增殖能力下降，SPARC表达增加，参与了牙周韧带代谢的衰老改变。牙周韧带细胞的活力随供体年龄的增加而降低，细胞增殖也随之减少。由于达到衰老的细胞不能表达c-fos，因此与细胞衰老相关的机制可能是老年细胞低迁移的潜在机制。牙髓和牙龈血流随年龄变化而变化。慢性炎症性牙周炎患者IL-17的产生受个体免疫反应的影响，而不受年龄的影响。牙周健康妇女的腰椎和下颌骨骨密度高于无牙妇女。

1. Macrophages produced IL-1α in periapical lesions in young rat, and lesion increased slowly.2. Healing in periapical lesions was delayed with aging.3. Reaction of antigen presenting cells was weakened in quantity with aging in rat dental pulp, but that of macrophages and monocytes were not weakened.4. Inhibition of breakdown system in gingiva was one of the reasons of gingival overgrowth in young rat.5. Jaw muscle activity induced by dental pulp chemical stimulation was changed with aging. Activity of alkaline phosphatase in dental pulp was decreased with aging in human.6. Decrease in proliferative ability and the increase in the SPARC expression with aging are involved in the aging alterations of metabolism in periodontal ligament.7. Cellular motility of periodontal ligament cells decreased with donor age as well as cell proliferation. Since the cells reaching senescene fail to express c-fos, the mechanisms linked to cellular senescence may be a possible underlying mechanism for low migration seen in the older cells.8. Blood flow in dental pulp and gingiva changed with aging.9. Production of IL-17 in chronic inflamed periodontitis was effected by immunological response of individual man, not effected by aging.10. Bone mineral density of the lumbar vertebra and the mandible in periodontally healthy women was higher than that in edentulous women.