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自己能抠掉牙结石吗? 第1页

  

user avatar   yi-bei-ku-ka-pei-37 网友的相关建议: 
      

手指头当然是偶尔可以抠掉牙石的。为什么说是偶尔呢?这牙结石在牙齿上面粘的是很紧的,除非块头比较大,正好用手指甲可以抠到牙石的边缘,指甲用力抠几下就下来了。如果指甲抠不到牙石的边缘,就算牙石在厚也很难抠的。强行抠,就会感觉很不舒服。抠出的牙石有时候是深黄色的,有时候是棕色的,放在鼻子上闻一下,那味道是特别酸爽的。不过,这牙石也有自己掉下来的时候。

顺便说一下,吧牙石抠下来以后,原来的地方就会感觉很不平整,甚至用舌头舔那个位置都会感到刺舌头。这时候去刷牙,你就会看到牙膏的泡沫里面有很多血。这种出血无需担心,只有一次。

最后,还是建议大家别用手指头去抠牙石,否则真的会伤到牙齿的。牙石过多,还是要去正规牙科诊所或者医院进行洁牙的。

那位说我怎么知道这些的呢?那是因为这都是我亲身体验。


user avatar   mai-wen-xue-67 网友的相关建议: 
      

抠不掉。

严格地说, 您可以折断牙结石, 但是您很可能抠不掉所有的牙结石。

牙结石和牙面的接触存在化学连接。


细说起来, 真的可能有一匹布那么长。

但是,可喜的是用某些牙膏刷牙可以更有效地预防牙结石。


补充一点, 有器械(Dental Scaler)的帮助, 徒手也是能刮掉牙结石的。上面说的抠不掉指的是用牙签或者指甲来抠。 您要认真杠,您就赢了。所以,还是说,“一般抠不掉, 二般能抠掉”,比较稳阵。




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牙结石是什么?

牙结石是硬化(钙化)的菌斑。

牙结石能保护和促进细菌的定居和繁殖。牙结石的英文是 Calculus ,和数学里面的微积分是一个字, 看起来很高大上。实际上牙结石是很脏的, 和大便差不多。


牙菌斑在牙齿表面逐渐沉积,牙菌斑通常是透明无色,变厚时会呈现黄或棕黄色,如果使用牙菌斑显示剂可以比较容易地发现牙菌斑在口腔内的分布。

口腔(消化道开口)是一个细菌和人共生的微生态环境。菌斑需要定时清除(因此普通人每天要刷牙)。

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牙菌斑是牙齿上形成的一种粘性无色薄膜。牙菌斑上生长着可能诱发龋齿和牙周疾病的微生物或者说细菌。牙结石是钙化/硬化的牙菌斑。


牙菌斑对牙齿的危害随其沉积时间而增长,应该定期清除。牙菌斑的质地很软,可以用物理和化学的方法例如牙刷加上牙膏(摩擦剂+表面活性剂+某些药物和添加剂+水)来有效清除。

刷牙是去除菌斑的最有效的办法。但是在去除以后,菌斑在一天内又会堆积起来。菌斑事实上形成了一个培养基。




牙菌斑的形成机制里面很重要的一个东西就是 “获得性膜”(Dental Pellicle,Acquired Pellicle)。获得性膜(acquired pellicle)是牙齿表面的一个结构。牙萌出到口腔之后,牙冠被釉质表皮(牙胚残留组织)覆盖,釉质表皮很快因摩擦活动消失。 唾液成分和口腔内部细菌的酶的作用下来会形成牙釉质表面的一层具有保护作用的液态层,这就是所谓的获得性膜或唾液薄膜。获得性膜的成分是唾液糖蛋白(salivary glycoproteins,缩写 SG),它选择性吸附在牙齿釉柱的羟基磷灰石结晶(hydroxyapatite crystal,缩写 HC)上。获得性膜是无细胞无定形的非溶解半透明有光泽的软沉淀。它除了可以粘粘在牙齿表面,也可以附着在牙结石或修复体(dental restoration)上。

获得性膜可以形成一个抑制链球菌产的酸对牙齿的去矿化(demineralization)的保护屏障。 除此之外,获得性膜起润滑的作用、保持牙齿表面湿润、减小[牙合]面磨损,同时获得性膜也成为微生物膜的前体。

一般情况下获得性膜不会在简单的口腔清洗之后脱离牙齿表面,即使清除后也会迅速重新形成。 因HC(羟基磷灰石结晶)的钙磷离子和SG(唾液糖蛋白)之间有着稳定的离子相互作用,在口腔环境里短时间里立即又会恢复。获得膜在牙齿表面的厚度为0.1~0.8微米, 最厚为近龈缘部分。

获得性膜形成后,成为口腔微生物定居的第一位置,接着就形成了牙菌斑(dental plaque)。 因为获得性膜富含微生物必需的营养物质。


获得性膜表面有结合位点(binding sites),只和那些具有相应特殊受体的微生物连接。口腔微生物族群中具有这些特殊的细胞膜受体的有变形链球菌(streptococcus mutans),血链球菌(streptococcus sanguis)常见于龈上菌斑,唾液链球菌(streptococcus salivarius)等。

SG的碳水化合物部分也可以提供连接受体予具备粘附素(adhesins)的口腔微生物,变形链球菌和血链球菌具有名为外凝集素(lectin)的粘附素可选择性识别碳水化合物部分受体,进而与之形成化学连接。



口腔是一个细菌和人共生的环境, 认识这个事实也很重要。

有助于大家破除幻想或者避免纠结沉迷于杀死口腔内所有的细菌这个念头。。。。。。。


从预防牙周病的角度来看,菌斑在牙龈处堆积会刺激牙龈,引起免疫反应,也可能发展成炎症。当炎症波及牙齿周围的支持组织时就称为牙周病。

例如以下情形,可能提示牙周组织受影响:

牙龈自发或者非自发出血、牙周溢脓或挤压后有脓液出现、牙周退缩、牙周肿胀或触痛等表现、牙齿松动或移位呼吸时口腔发出异味(口臭)等等。


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牙结石主要由矿物以及无机和有机成分组成。

牙龈上和牙龈下的牙结石分别含有37%和58%的矿物成分。

龈上结石的基质占结石干重的15.7%,含有54.9%的蛋白质和10.2%的脂质。在总脂质中,61.8%是中性脂质,包括高含量的游离脂肪酸和少量的甘油三酯。糖脂占总脂质的28%,由17.2%的简单糖鞘脂,主要是乳糖基和葡糖基甘油胺,以及82.8%的中性和硫酸化甘油糖脂组成。磷脂,占总脂质的10.2%,包含34.2%的磷脂酰乙醇胺,25.5%的二磷脂酰甘油,2.3%的磷脂酰肌醇,和1.7%的磷脂酰丝氨酸。磷脂酰肌醇和磷脂酰丝氨酸是两类重要的酸性磷脂,但只是细菌细胞膜的次要磷脂成分,其富含磷脂酰乙醇胺和二磷脂酰甘油(中性磷脂)。值得注意的是,牙结石含有总磷脂和酸性磷脂,其浓度远高于腮腺唾液。此外,重度结石形成者的唾液中磷脂的浓度明显高于轻度结石形成者。这些发现表明,磷脂在牙结石的形成中起着重要作用。

牙结石总是被一层柔软而松散的微生物所覆盖。在龈上结石上,该层主要是丝状微生物。这些丝状物大约与下层致密的牙结石垂直,并与之直接接触。相比之下,覆盖在龈下结石上的球菌、杆菌和丝状物的混合物没有明显的方向性。然而,用次氯酸钠处理后,龈上结石表面的丝状物消失了,在扫描电子显微镜下,龈上结石呈现出蜂窝状的外观。经过钠盐水清洗的龈下牙结石表面的孔洞不如龈上牙结石表面的孔洞规则。在微生物层的下面是钙化区,由于深色和浅色染色带的交替出现,看起来是层状的。由于非钙化层的存在,龈上结石的钙化区是异质性的。这些非钙化层通常是不规则的,类似于被钙化物质部分隔开的空洞带。此外,已经证明斑块矿化发生在许多单独的病灶中。牙结石的矿物沉积既存在于微生物之间,也存在于微生物内部,这取决于沉积年龄;也就是说,矿物最初沉积在牙菌斑的基质中,随着结石年龄的增加,一些牙菌斑的微生物逐渐钙化。

磷酸八钙[Ca8(PO4)4(HPO4)25HO](OCP)、羟基磷灰石[Ca10(PO4)6(OH)2](HAP)和β-磷酸三钙或白锁石[Ca10(HPO4)(PO4)6](WHT)构成龈上和龈下结石的无机部分。刷石[CaHPO4-2H2O:磷酸二钙二水合物](DCPD)仅存在于早期的龈上结石中。在上述的磷酸钙晶体中,只有WHT含有镁,它可以代替WHT中的部分钙。

龈上结石和龈下结石在主要晶体成分和无机元素成分方面有所不同;也就是说,龈上结石中WHT与HAP和钙与磷的比率低于龈下结石。

在牙齿萌出或牙齿预防后,唾液蛋白迅速并有选择地吸附在牙釉质表面,形成后天的牙釉质膜。随后是各种口腔微生物的粘附。革兰氏阳性的球状生物是第一批粘附在形成的釉质皮层上的定居者,随后,丝状细菌逐渐主导了成熟的斑块生物膜。

牙菌斑从唾液中吸收钙和磷酸盐以形成龈上结石,从牙缝液中吸收钙和磷酸盐以形成龈下结石。磷酸钙的过饱和度、某些与膜相关的成分以及成核抑制剂的降解是斑块和细菌初始矿化的必要条件。牙结石的形成始于磷酸钙前体相、OCP和DCPD的沉积,这些前体相逐渐水解并转化为较难溶解的HAP和WHT矿物相。

已经观察到三种类型的唾液蛋白的时间依赖性吸附。一些唾液蛋白,如富含脯氨酸的蛋白-3(PRP-3)、PRP-4和石蜡蛋白,在HAP上的吸附速度非常快,而淀粉酶、糖基化富含脯氨酸的蛋白(PRG)和胱氨酸的结合速度很慢。第三种类型的蛋白质吸附可以在PRP-1、PRP-2和组蛋白的情况下看到。它的特点是两步过程-快速吸附(蛋白质与HAP的直接结合),然后是缓慢吸附(蛋白质-蛋白质相互作用)。关于酸性PRPs和石蜡素的吸附的研究经常出现在文献中。酸性PRPs和石蜡素具有极性,因为它们的氨基端域带电性很强,这也是这些蛋白质在牙齿表面吸附的原因。带电区域的磷酸丝氨酸残基被认为是静电相互作用的关键。

微生物对固体表面(如牙齿表面和各种植入物表面)的粘附可能是一个四阶段的序列。

第一阶段是细菌最初接近表面,可能发生随机接触,如布朗运动和液体流动,或微生物的主动运动。有吸引力的范德瓦尔斯力和排斥性的静电力负责微生物粘附的第二阶段,这是一个可逆的过程。微生物的牢固附着,即第三阶段是不可逆的,随后是附着的第四阶段,即细菌定居。

微生物附属物参与细菌粘附在涂有毛皮的牙齿表面的过程。在细菌的fimbrillin蛋白中存在三个或更多的结合位点,所有这些结合位点的组合将是稳定结合唾液蛋白的关键。鞭毛蛋白,另一种微生物表面蛋白,也参与了微生物的粘附。鞭毛可能有四个不同的功能。

  • 首先,鞭毛可能参与趋化作用,使浮游细菌游向与表面相关的营养物质或由附着在表面的细胞产生的信号。
  • 第二,鞭毛介导的运动可以克服介质-表面界面的排斥力,使细菌到达表面。
  • 第三,鞭毛介导的运动可能是发展中的生物膜中的细菌沿着表面移动所必需的,从而促进生物膜的生长和传播。
  • 最后,鞭毛本身可能需要通过粘附在非生物表面来形成生物膜。在大肠杆菌模型系统中,用抑制鞭毛功能的这些方面的突变来确定哪个方面对生物膜的形成至关重要。非化能型的运动细胞形成的生物膜与野生型的对应细胞没有区别。相反,缺乏鞭毛或拥有瘫痪的鞭毛的细胞在生物膜的形成上有严重的缺陷。因此,很明显,趋化作用对生物膜的形成是不需要的,而鞭毛介导的运动对这个过程至关重要。

总的来说,鞭毛介导的运动使细菌能够通过克服静电界面的排斥力而达到离表面足够短的距离,这样绒毛就能通过粘附素-受体的相互作用和/或抽动运动将它们推到表面上。附着的细菌可以在鞭毛产生的力的推动下再次沿着表面移动。除流苏和鞭毛外,许多其他表面蛋白也参与细菌粘附。

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钙和磷酸盐是唾液中的两种离子,是形成牙结石的 "原料"。

理论上,唾液,特别是牙菌斑液中磷酸钙盐的过饱和度是牙菌斑矿化的驱动力。离子积(Ip)和溶解度积(Ksp)对于估计特定盐的饱和度(SD)非常重要。如果Ip>Ksp,液体是过饱和的,盐的沉淀会发生;如果Ip=Ksp,液体对盐只是饱和的,如果Ip<Ksp,盐有溶解的趋势,因为液体对盐没有饱和。

事实上,腮腺和颌下腺的唾液对HAP、OCP和WHT来说通常是过饱和的。下颌分泌物在HAP方面的过饱和度甚至比腮腺分泌物还要高。在pH值高于4.0时,HAP是最不容易溶解的相,其溶解度随pH值的变化比DCPD更快(Barone和Nancollas,1978)。因此,唾液和牙菌斑液对HAP的过饱和度更高,因此,与其他磷酸钙相比较,HAP的沉淀更容易发生。然而,在最近的一项研究报道,在未受刺激和受刺激的唾液中,唾液中的磷酸钙过饱和度与牙结石的形成率之间不存在显著的相关性。然而,牙结石的形成受到多种因素的影响,如唾液流速,以及除唾液中磷酸钙盐过饱和度以外的牙结石形成的抑制剂和促进剂。不幸的是,所有这些因素在本研究中都没有作对照研究。

过饱和度和结石形成之间缺乏相关性可能是由这些因素的影响造成的。例如,如果一组的受试者具有较高的磷酸钙过饱和度,但与另一组的受试者相比,唾液流速较低,这两组可能具有相似的结石水平;也就是说,过饱和度和结石形成之间的相关性被组间唾液流速的差异所掩盖了。唾液流速影响腺体唾液中磷酸钙的饱和度。尽管在所有测试的流速下,从0.1到2.0毫升/分钟,腮腺唾液对HAP和WHT是过饱和的,但在流速低于0.2毫升/分钟时,腮腺唾液对OCP是不饱和的。对于DCPD,在所有的流速下,腮腺唾液都是不饱和或刚刚饱和的,而且饱和程度只受流速的影响很弱。较高的唾液pH值或可能是腺体唾液中磷酸钙盐的分泌量增加,可能有助于唾液流速对唾液中磷酸钙饱和程度的影响。

pH值对腮腺唾液中磷酸钙饱和度的影响也被调查过。在不同的流速下,HAP、OCP和DCPD的饱和度随着唾液pH的增加而增加。腮腺唾液在pH值高于5.5、6.4和6.9时,对HAP、WHT和OCP都是过饱和的。唾液pH值和过饱和程度之间有密切的相关性(r = 0.91)。以HAP为例。下一个方程式显示了为什么磷酸钙的饱和程度会受到pH值的影响。Ca10(PO4)6 ↔ (OH)210Ca2++6PO43-+2OH-。当溶液中的磷酸钙晶体处于动力学平衡状态时,沉淀的速度与溶解的速度相等。如果溶液中的pH值下降(氢离子浓度增加),OH-和PO43-倾向于被H+去除,分别形成水和更酸性的磷酸盐形式。结果,平衡被打破并被拉向右边;也就是说,溶解的速度超过了沉淀的速度,净结果是HAP晶体的溶解和HAP饱和度的降低。如果溶液中的pH值上升,将发生相反的事件。OH-迫使方程中的平衡向左移动,从而导致溶液中的HAP饱和度增加。


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刷牙在清除牙菌斑方面相对有效,

但对于维护牙龈健康仍是不够的。


化学治疗剂已被用于补充机械性清除牙菌斑。

早期使用化学治疗剂的尝试主要集中在去除牙齿上的牙结石。使用粘液酶就是一个例子。

人们认为,用酶溶解结石中的有机物可以帮助破坏结石结构。已知螯合剂可以通过形成稳定和可溶性的钙复合物来封存和溶解钙盐。例如Ex347,一种螯合剂,已被证实能有效防止结石的形成。然而,螯合剂可能会导致釉质损伤。抗菌剂也被用于减少牙结石,因为微生物是形成牙结石的重要因素。然而,由于对抗生素产生耐药性的潜在问题,作用被削弱了。自20世纪70年代以来,主要的抗结石策略集中在抑制晶体生长和防止矿化斑的发展。目前,使用的抗结石剂包括三氯生(抗菌剂)与聚乙烯甲醚(PVM)和马来酸(MA)共聚物,以及晶体生长抑制剂,包括焦磷酸与PVM/MA共聚物、柠檬酸锌和氯化锌。

进一步讨论抗结石剂之前,必须阐明几个重要的问题。

  • 首先,晶体生长抑制剂,如焦磷酸盐和锌盐,已被证明只对控制龈上结石有效,对龈下结石无效。第二,使用晶体生长抑制剂是为了防止沉积物的形成。
  • 第三,晶体生长抑制剂如焦磷酸盐和锌离子通常会降低化学吸附表面的溶解率。如同氟化物的情况一样,溶解率的降低可以为处理过的牙齿提供防龋效果。因此,晶体生长抑制剂通过与磷灰石表面结合可能同时表现出两种功能--防止再矿化和防止脱矿。
  • 第四,目前市场上销售的抗钙化牙膏和漱口水并不只包括晶体生长抑制剂,还含有某种形式的氟化物作为抗钙剂。
  • 最后,值得注意的是,在牙膏和漱口水中使用的晶体生长抑制剂的浓度实际上比根据结晶率的Langmuir 分析计算的HAP、OCP和DCPD相上生长点的最大覆盖率所需的浓度高2-3个数量级。晶体的过度生长和抑制剂的降解已被证明会阻碍这些药剂的功能。因此,在两次治疗之间,保留在斑块液体中作为 "储存器 "的抑制剂的剩余作用是必要的。来自 "库 "的残留抑制剂可以包裹斑块基质内新形成的晶体,从而抵消晶体过度生长的影响。


三氯生是一种广谱抗菌剂,对革兰氏阳性和阴性微生物都有活性。其目标是细胞质膜。在抑菌浓度下,三氯生会阻止细菌吸收必需的氨基酸,而在杀菌浓度下,三氯生会破坏细胞质膜的完整性并导致细胞内容物的泄漏。除了作为一种抗菌剂外,三氯生还可能具有抗炎功能,因为它可以中和可能引发炎症的细菌产物。它也是环氧化酶和脂氧化酶途径的有效抑制剂。为了使三氯生有效,有必要采用一种递送系统来增加其在口腔中的停留时间。PVM/MA共聚物(商品名Gantrez)已被用作三氯生的传递系统。PVM/MA共聚物可促进牙釉质和口腔上皮细胞对三氯生的吸收。当使用含有三氯生和PVM/MA共聚物的牙膏时,在牙菌斑和唾液中也观察到三氯生的保留量增加。PVM/MA共聚物增强三氯生传递的机制已被阐明。该共聚物由两个基团组成:一个附着基团和一个增溶基团。增溶基团将三氯生保留在表面活性剂胶束中,这样附着基团就有足够的时间通过液体附着层中的钙与牙齿表面发生反应。然后,三氯生通过与唾液环境的相互作用缓慢释放。除了上述功能外,该共聚物还具有微弱的晶体生长抑制特性,并能有效地防止结石的形成。该共聚物可以强烈地复合和封存镁,从而抑制碱性磷酸酶对焦磷酸盐的水解。三氯生和共聚物对牙结石形成的影响已被临床研究证实。研究发现,与安慰剂牙膏相比,完全预防后,0.3%的三氯生和2.0%的PVM/MA共聚物在0.243%的氟化钠/二氧化硅基础牙膏中可显著降低牙龈上结石的严重程度和发生率。



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【未完待续】




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       三氯生已经在消费品中使用了数十年,经过全球监管机构的广泛审查并允许进行使用。 数年来多项科学研究,为抗菌成分的安全和效果进行了佐证。 2016 年 9 月,美国食品药品管理局 (FDA) 颁布了一条新规,表示含有特定 成分(包括三氯生)的非处方消费类抗菌洗涤产品(抗菌皂)不得继续销售,因为 生产商并没有证明这些成分在这种产品中的效果。该规定仅适用于作为洗手液或 沐浴露的消费类抗菌洗涤产品/肥皂,并不影响消费类洗手液或医疗保健及食品处理环境中使用的抗菌产品。 FDA 还对三氯生可能有助于形成抗药性细菌而感到担忧。      


** 备注: 是否使用含有“三氯生”等成分的药物牙膏,敬请咨询您自己的牙医, 如果您罹患牙周疾病。本文不对药物牙膏作任何推荐。




  

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