自己能抠掉牙结石吗？

抠不掉。

严酷地说, 您能够折断牙结石， 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毗连。

细说起来， 实的可能有一匹布那么长。

但是，可喜的是用某些牙膏刷牙能够更有效地预防牙结石。

弥补一点， 有器械(Dental Scaler)的帮忙， 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。 您要认实杠，您就赢了。所以，仍是说，“一般抠不掉， 二般能抠掉”，比力稳阵。

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牙结石是什么？

牙结石是硬化（钙化）的菌斑。

牙结石能庇护和促进细菌的定居和繁衍。牙结石的英文是 Calculus ，和数学里面的微积分是一个字， 看起来很高峻上。现实上牙结石是很脏的， 和大便差不多。

牙菌斑在牙齿外表逐步堆积，牙菌斑凡是是通明无色，变厚时会呈现黄或棕黄色，若是利用牙菌斑显示剂能够比力容易地发现牙菌斑在口腔内的散布。

口腔（消化道启齿）是一个细菌和人共生的微生态情况。菌斑需要按时肃清（因而通俗人每天要刷牙）。

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牙菌斑是牙齿上构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堆积时间而增长，应该按期肃清。牙菌斑的量地很软，能够用物理和化学的办法例如牙刷加上牙膏（摩擦剂+外表活性剂+某些药物和添加剂+水）来有效肃清。

刷牙是去除菌斑的最有效的法子。但是在去除以后，菌斑在一天内又会堆积起来。菌斑事实上构成了一个培育基。

牙菌斑的构成机造里面很重要的一件工具就是 “获得性膜”（Dental Pellicle，Acquired Pellicle）。获得性膜（acquired pellicle）是牙齿外表的一个构造。牙萌出到口腔之后，牙冠被釉量表皮（牙胚残留组织）笼盖，釉量表皮很快因摩擦活动消逝。 唾液成分和口腔内部细菌的酶的感化下来会构成牙釉量外表的一层具有庇护感化的液态层，那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卵白（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消融半通明有光泽的软沉淀。它除了能够粘粘在牙齿外表，也能够附着在牙结石或修复体（dental restoration）上。

获得性膜能够构成一个按捺链球菌产的酸对牙齿的去矿化（demineralization）的庇护屏障。 除此之外，获得性膜起光滑的感化、连结牙齿外表潮湿、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离开牙齿外表，即便肃清后也会敏捷从头构成。 因HC（羟基磷灰石结晶）的钙磷离子和SG（唾液糖卵白）之间有着不变的离子彼此感化，在口腔情况里短时间里立即又会恢复。获得膜在牙齿外表的厚度为0.1~0.8微米, 最厚为近龈缘部门。

获得性膜构成后，成为口腔微生物定居的第一位置，接着就构成了牙菌斑（dental plaque）。 因为获得性膜富含微生物必须的营养物量。

获得性膜外表有连系位点（binding sites），只和那些具有响应特殊受体的微生物毗连。口腔微生物族群中具有那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的碳水化合物部门也能够供给毗连受体于具备粘附素（adhesins）的口腔微生物，变形链球菌和血链球菌具有名为外凝固素（lectin）的粘附素可选择性识别碳水化合物部门受体，进而与之构成化学毗连。

口腔是一个细菌和人共生的情况， 认识那个事实也很重要。

有助于各人废除梦想或者制止纠结沉浸于杀死口腔内所有的细菌那个念头。。。。。。。

从预防牙周病的角度来看，菌斑在牙龈处堆积会刺激牙龈，引起免疫反响，也可能开展成炎症。当炎症涉及牙齿四周的撑持组织时就称为牙周病。

例如以下情形，可能提醒牙周组织受影响：

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

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牙结石次要由矿物以及无机和有机成分构成。

牙龈上和牙龈下的牙结石别离含有37%和58%的矿物成分。

龈上结石的基量占结石干重的15.7%，含有54.9%的卵白量和10.2%的脂量。在总脂量中，61.8%是中性脂量，包罗高含量的游离脂肪酸和少量的甘油三酯。糖脂占总脂量的28%，由17.2%的简单糖鞘脂，次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构成。磷脂，占总脂量的10.2%，包罗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）。值得留意的是，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，重度结石构成者的唾液中磷脂的浓度明显高于轻度结石构成者。那些发现表白，磷脂在牙结石的构成中起着重要感化。

牙结石老是被一层柔嫩而松懈的微生物所笼盖。在腿上结石上，该层次要是丝状微生物。那些丝状物大约与下层致密的牙结石垂曲，并与之间接接触。比拟之下，笼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标的目的性。然而，用次氯酸钠处置后，龈上结石外表的丝状物消逝了，在扫描电子显微镜下，龈上结石呈现出蜂窝状的外不雅。颠末钠盐水清洗的龈下牙结石外表的孔洞不如龈上牙结石外表的孔洞规则。在微生物层的下面是钙化区，因为深色和淡色染色带的瓜代呈现，看起来是层状的。因为非钙化层的存在，龈上结石的钙化区是异量性的。那些非钙化层凡是是不规则的，类似于被钙化物量部门离隔的浮泛带。此外，已经证明斑块矿化发作在许多零丁的病灶中。牙结石的矿物堆积既存在于微生物之间，也存在于微生物内部，那取决于堆积年龄；也就是说，矿物最后堆积在牙菌斑的基量中，跟着结石年龄的增加，一些牙菌斑的微生物逐步钙化。

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门。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，只要WHT含有镁，它能够取代WHT中的部门钙。

龈上结石和龈下结石在次要晶体成分和无机元素成分方面有所差别；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，唾液卵白敏捷并有选择地吸附在牙釉量外表，构成后天的牙釉量膜。随后是各类口腔微生物的粘附。革兰氏阳性的球状生物是第一批粘附在构成的釉量皮层上的定居者，随后，丝状细菌逐步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构成龈上结石，从牙缝液中吸收钙和磷酸盐以构成龈下结石。磷酸钙的过饱和度、某些与膜相关的成分以及成核按捺剂的降解是斑块和细菌初始矿化的需要前提。牙结石的构成始于磷酸钙前体相、OCP和DCPD的堆积，那些前体相逐步水解并转化为较难消融的HAP和WHT矿物相。

已经察看到三品种型的唾液卵白的时间依赖性吸附。一些唾液卵白，如富含脯氨酸的卵白-3（PRP-3）、PRP-4和白腊卵白，在HAP上的吸附速度十分快，而淀粉酶、糖基化富含脯氨酸的卵白（PRG）和胱氨酸的连系速度很慢。第三品种型的卵白量吸附能够在PRP-1、PRP-2和组卵白的情况下看到。它的特点是两步过程-快速吸附（卵白量与HAP的间接连系），然后是迟缓吸附（卵白量-卵白量彼此感化）。关于酸性PRPs和白腊素的吸附的研究经常呈现在文献中。酸性PRPs和白腊素具有极性，因为它们的氨基端域带电性很强，那也是那些卵白量在牙齿外表吸附的原因。带电区域的磷酸丝氨酸残基被认为是静电彼此感化的关键。

微生物对固体外表（如牙齿外表和各类植入物外表）的粘附可能是一个四阶段的序列。

第一阶段是细菌最后接近外表，可能发作随机接触，如布朗运动和液体活动，或微生物的主动运动。有吸引力的范德瓦尔斯力和排挤性的静电力负责微生物粘附的第二阶段，那是一个可逆的过程。微生物的安稳附着，即第三阶段是不成逆的，随后是附着的第四阶段，即细菌定居。

微生物从属物参与细菌粘附在涂有毛皮的牙齿外表的过程。在细菌的fimbrillin卵白中存在三个或更多的连系位点，所有那些连系位点的组合将是不变连系唾液卵白的关键。鞭毛卵白，另一种微生物外表卵白，也参与了微生物的粘附。鞭毛可能有四个差别的功用。

起首，鞭毛可能参与趋化感化，使浮游细菌游向与外表相关的营养物量或由附着在外表的细胞产生的信号。第二，鞭毛介导的运动能够克制介量-外表界面的排挤力，使细菌抵达外表。第三，鞭毛介导的运动可能是开展中的生物膜中的细菌沿着外表挪动所必须的，从而促进生物膜的生长和传布。最初，鞭毛自己可能需要通过粘附在非生物外表来构成生物膜。在大肠杆菌模子系统中，用按捺鞭毛功用的那些方面的突变来确定哪个方面临生物膜的构成至关重要。非化能型的运动细胞构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构成上有严峻的缺陷。因而，很明显，趋化感化对生物膜的构成是不需要的，而鞭毛介导的运动对那个过程至关重要。

总的来说，鞭毛介导的运动使细菌可以通过克制静电界面的排挤力而到达离外表足够短的间隔，如许绒毛就能通过粘附素-受体的彼此感化和/或抽动运动将它们推到外表上。附着的细菌能够在鞭毛产生的力的鞭策下再次沿着外表挪动。除流苏和鞭毛外，许多其他外表卵白也参与细菌粘附。

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钙和磷酸盐是唾液中的两种离子，是构成牙结石的 "原料"。

理论上，唾液，出格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）和消融度积（Ksp）关于估量特定盐的饱和度（SD）十分重要。若是Ip>Ksp，液体是过饱和的，盐的沉淀会发作；若是Ip=Ksp，液体对盐只是饱和的，若是Ip<Ksp，盐有消融的趋向，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来说凡是是过饱和的。下颌排泄物在HAP方面的过饱和度以至比腮腺排泄物还要高。在pH值高于4.0时，HAP是最不容易消融的相，其消融度随pH值的变革比DCPD更快（Barone和Nancollas，1978）。因而，唾液和牙菌斑液对HAP的过饱和度更高，因而，与其他磷酸钙比拟较，HAP的沉淀更容易发作。然而，在比来的一项研究报导，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构成率之间不存在显著的相关性。然而，牙结石的构成遭到多种因素的影响，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构成的按捺剂和促进剂。不幸的是，所有那些因素在本研究中都没有做对照研究。

过饱和度和结石构成之间缺乏相关性可能是由那些因素的影响形成的。例如，若是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比拟，唾液流速较低，那两组可能具有类似的结石程度；也就是说，过饱和度和结石构成之间的相关性被组间唾液流速的差别所掩盖了。唾液流速影响腺体唾液中磷酸钙的饱和度。虽然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。关于DCPD，在所有的流速下，腮腺唾液都是不饱和或刚刚饱和的，并且饱和水平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排泄量增加，可能有助于唾液流速对唾液中磷酸钙饱和水平的影响。

pH值对腮腺唾液中磷酸钙饱和度的影响也被查询拜访过。在差别的流速下，HAP、OCP和DCPD的饱和度跟着唾液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值和过饱和水平之间有亲近的相关性（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水平会遭到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形态时，沉淀的速度与消融的速度相等。若是溶液中的pH值下降（氢离子浓度增加），OH-和PO43-倾向于被H+去除，别离构成水和更酸性的磷酸盐形式。成果，平衡被突破并被拉向右边；也就是说，消融的速度超越了沉淀的速度，净成果是HAP晶体的消融和HAP饱和度的降低。若是溶液中的pH值上升，将发作相反的事务。OH-迫使方程中的平衡向左挪动，从而招致溶液中的HAP饱和度增加。

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刷牙在肃清牙菌斑方面相对有效，

但关于维护牙龈安康仍是不敷的。

化学治疗剂已被用于弥补机械性肃清牙菌斑。

早期利用化学治疗剂的测验考试次要集中在去除牙齿上的牙结石。利用粘液酶就是一个例子。

人们认为，用酶消融结石中的有机物能够帮忙毁坏结石构造。已知螯合剂能够通过构成不变和可溶性的钙复合物来封存和消融钙盐。例如Ex347，一种螯合剂，已被证明能有效避免结石的构成。然而，螯合剂可能会招致釉量损伤。抗菌剂也被用于削减牙结石，因为微生物是构成牙结石的重要因素。然而，因为匹敌生素产生耐药性的潜在问题，感化被削弱了。自20世纪70年代以来，次要的抗结石战略集中在按捺晶体生长和避免矿化斑的开展。目前，利用的抗结石剂包罗三氯生（抗菌剂）与聚乙烯甲醚（PVM）和马来酸（MA）共聚物，以及晶体生长按捺剂，包罗焦磷酸与PVM/MA共聚物、柠檬酸锌和氯化锌。

进一步讨论抗结石剂之前，必需阐明几个重要的问题。

起首，晶体生长按捺剂，如焦磷酸盐和锌盐，已被证明只对控造龈上结石有效，对龈下结石无效。第二，利用晶体生长按捺剂是为了避免堆积物的构成。第三，晶体生长按捺剂如焦磷酸盐和锌离子凡是会降低化学吸附外表的消融率。好像氟化物的情况一样，消融率的降低能够为处置过的牙齿供给防龋效果。因而，晶体生长按捺剂通过与磷灰石外表连系可能同时表示出两种功用--避免再矿化和避免脱矿。第四，目前市场上销售的抗钙化牙膏和漱口水其实不只包罗晶体生长按捺剂，还含有某种形式的氟化物做为抗钙剂。最初，值得留意的是，在牙膏和漱口水中利用的晶体生长按捺剂的浓度现实上比按照结晶率的Langmuir 阐发计算的HAP、OCP和DCPD相上生长点的更大笼盖率所需的浓度高2-3个数量级。晶体的过度生长和按捺剂的降解已被证明会障碍那些药剂的功用。因而，在两次治疗之间，保留在斑块液体中做为 "贮存器 "的按捺剂的剩余感化是需要的。来自 "库 "的残留按捺剂能够包裹斑块基量内新构成的晶体，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。其目的是细胞量膜。在抑菌浓度下，三氯生会阻遏细菌吸收必须的氨基酸，而在杀菌浓度下，三氯生会毁坏细胞量膜的完好性并招致细胞内容物的泄露。除了做为一种抗菌剂外，三氯生还可能具有抗炎功用，因为它能够中和可能引发炎症的细菌产品。它也是环氧化酶和脂氧化酶路子的有效按捺剂。为了使三氯生有效，有需要接纳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）已被用做三氯生的传递系统。PVM/MA共聚物可促进牙釉量和口腔上皮细胞对三氯生的吸收。当利用含有三氯生和PVM/MA共聚物的牙膏时，在牙菌斑和唾液中也察看到三氯生的保留量增加。PVM/MA共聚物加强三氯生传递的机造已被阐明。该共聚物由两个基团构成：一个附着基团和一个增溶基团。增溶基团将三氯生保留在外表活性剂胶束中，如许附着基团就有足够的时间通过液体附着层中的钙与牙齿外表发作反响。然后，三氯生通过与唾液情况的彼此感化迟缓释放。除了上述功用外，该共聚物还具有微弱的晶体生长按捺特征，并能有效地避免结石的构成。该共聚物能够强烈地复合和封存镁，从而按捺碱性磷酸酶对焦磷酸盐的水解。三氯生和共聚物对牙结石构成的影响已被临床研究证明。研究发现，与慰藉剂牙膏比拟，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/二氧化硅根底牙膏中可显著降低牙龈上结石的严峻水平和发作率。

Ref： Afflitto J, Patel M, Smith KA, Gaffar A (1990). 113Cd NMR study of the inhibitory effect of PVM/MA copolymer (Gantrez) on the alkaline phosphatase of E. coli (abstract). J Dent Res 69(Spec Iss):118. Aleece AA, Forscher BK (1954). Calculus reduction with a mucinase dentifrice. J Periodontol 25:122–125. Amano A, Sharma A, Lee JY, Sojar HT, Raj PA, Genco RJ (1996). Structural domains of Porphyromonas gingivalis recombinant fimbrillin that mediate binding to salivary proline-rich protein and statherin. Infect Immun 64:1631–1637. Baier R (1982). Conditioning surface to suit the biomedical environment: recent progress. J Biomech Eng 104:257–271. Bánóczy J, Sari K, Schiff T, Petrone M, Davies R, Volpe AR (1995). Anticalculus efficacy of three dentifrices. Am J Dent 8:205–208. Barone JP, Nancollas GH (1978). The seeded growth of calcium phosphates, the kinetics of growth of dicalcium dihydrate on enamel, dentin, and calculus. J Dent Res 57:153–161. Benga G, Holmes RP (1984). Interactions between components in biological membranes and their implications for membrane function. Prog Biophys Molec Biol 43:195–257. Bennick A, Cannon M, Madapallimattam G (1979). The nature of the hydroxyapatite-binding sites in salivary acidic proline-rich proteins. Biochem J 183:115–126. Bercy P, Vreven J (1979). Correlation between calculus index and acid and alkaline pyrophosphatases activities of dental plaque and saliva. J Biol Buccale 7:31–36. Berg JH, Farrell JE, Brown LR (1990). Class II glass ionomer/silver cement restorations and the effect on interproximal growth of mutans streptococci. Pediatr Dent 12:20–23. Bishop DG (1971). The distribution and function of lipids in cells. In: Biochemistry and methodology of lipids, Johnson AR, Davenport JB, editors. New York: J. Wiley and Sons, pp. 424-456. Bollen CML, Papaioannou W, Van Eldere J, Schepers E, Quirynen M, Van Steenberghe D (1996). The influence of abutment surface roughness on plaque accumulation and peri-implant mucositis. Clin Oral Implant Res 7:201–211. Boyan BD, Boskey AL (1984). Co-isolation of proteolipids and calcium-phospholipid-phosphate complexes. Calcif Tissue Int 36:214–218. Briner WW, Francis MD (1962). The effect of enamel fluoride on acid production by Lactobacillus casei. Arch Oral Biol 7:541–550. Brooks W, Demuth DR, Gil S, Lamont RJ (1997). Identification of a Streptococcus gordonii ssp B domain that mediates adhesion to Porphyromonas gingivalis. Infect Immun 65:3753–3758. Brown CM, Hancock EB, O’Leary TJ, Miller CH, Sheldraker MA (1991). A microbiological comparison of young adults based on relative amounts of subgingival calculus. J Periodontol 62:591–597. Brown WH, Schilling K, Giertsen E, Pearson S, Lee SF, Bleiweis A, et al. (1991). Role of a cell surface-associated protein in adherence and dental caries. Infect Immun 59:4606–4609. Brudevold F, Steadman LT, Spinelli MA, Amdur BH, Gron P (1963). A study of zinc in human teeth. Arch Oral Biol 8:135–144. Carey C, Gregory T, Rupp W, Tatevossian A, Vogel GL (1986). The driving force is human dental plaque fluid for demineralization and remineralization of enamel mineral. In: Factors relating to demineralization and remineralization of the teeth. Leach SA, editor. Oxford: IRL Press Ltd., pp. 163-173. Chen C (2001). Periodontitis as a biofilm infection. CA Dent Assoc J 29:362–369. Cisar JO, Kolenbrander PE, McIntire FC (1979). Specificity of coaggregation reactions between human oral streptococci and strains of Actinomyces viscosus or Actinomyces naeslundii. Infect Immun 24:742–752. Collins LM, Dawes C (1987). The surface area of the adult human mouth and thickness of the salivary film covering the teeth and oral mucosa. J Dent Res 66:1300–1302. Cookson AL, Handley PS, Jacob AE, Eatson GK, Allison C (1995). Coaggregation between Prevotella nigrescens and Prevotella intermedia with Actinomyces naeslundii strains. FEMS Microbiol Lett 132:291–296. Corbett TL, Dawes C (1998). A comparison of the site-specificity of supragingival and subgingival calculus deposition. J Periodontol 69:1–8. Cotton FA, Wilkinson G (1966). Advanced inorganic chemistry. A comprehensive text. New York: Interscience Publications. A Division of John Wiley and Sons, pp. 158-166. Damen JJ, ten Cate JM (1989). The effect of silicic acid on calcium phosphate precipitation. J Dent Res 68:1355–1359. Darzins A (1994). Characterization of a Pseudomonas aeruginosa gene cluster involved in pilus biosynthesis and twitching motility: sequence similarity to the chemotaxis proteins of enterics and the gliding bacterium Myxococcus xanthus. Mol Microbiol 11:137–153. Davies DG, Parsek MR, Pearson JP, Iglewski BH, Costerton JW, Greenberg EP (1998). The involvement of cell-to- cell signals in the development of a bacterial biofilm. Science 280:295–298. Dawes C, Watanabe S, Biglow-Lecomte P, Dibdin GH (1989). Estimation of the velocity of the salivary film at some different location in the mouth. J Dent Res 68:1479–1482. Denepitiya L, Kleinberg I (1982). A comparison of the microbial composition of pooled human dental plaque and salivary sediment. Arch Oral Biol 27:739–745. Dibdin GH, Shellis RP, Wilson CM (1976). An apparatus for the continuous culture of micro-organisms on solid surfaces with special reference to dental plaque. J Appl Bacteriol 40:261–268. Donald JW (1997). Dental calculus: recent insight into occurrence, formation, prevention, removal and oral health effects of supragingival and subgingival deposits. Eur J Oral Sci 105:508–522, Eanes ED, Meyer JL (1978). The influence of fluoride on apatite formation from unstable supersaturated solutions at pH 7.4. J Dent Res 57:617–624. Edgerton M, Lo SE, Scannapieco FA (1996). Experimental salivary pellicles formed on titanium surfaces mediate adhesion of streptococci. Int J Oral Maxillofac Implants 11:443–449. Featherstone JD, Rodgers BE (1981). Effect of acetic, lactic and other organic acids on the formation of artificial carious lesions. Caries Res 15:377–385. Fisher SJ, Prakobphol A, Kajisa L, Murray PA (1987). External radiolabelling of components of pellicle on human enamel and cementum. Arch Oral Biol 32:509–517. Fleisch H (1981). Inhibitions of calcium phosphate precipitation and their role in biological mineralization. J Crystal Growth 53:120–134. Fleisch H, Russell RGG, Bisaz S, Mühlbauer RC, Williams DA (1970). The inhibitory effect of phosphonates on the formation of calcium phosphate crystals in vitro and on aortic and kidney calcification in vivo. Eur J Clin Invest 1:12– 18. Francis MD (1969). The inhibition of calcium hydroxyapatite crystal growth by polyphosphates. Calcif Tissue Res 3:151–162. Friskopp J, Hammarström L (1980). A comparative, scanning electron microscopic study of supragingival and subgingival calculus. J Periodontol 51:553–562. Frostell G (1960). Studies on the ammonia production and the ureolytic activity of dental plaque material. Acta Odontol Scand 18:29–65. Frostell G, Söder PÖ (1970). The proteolytic activity of plaque and its relation to soft tissue pathology. Int J Dent 20:436–450. Gaare D, Rølla G, van der Ouderaa (1989). Comparison of the rate of formation of supragingival calculus in an Asian and a European population. In: Recent advances in the study of dental calculus. Oxford: IRL Press at Oxford University Press. Gaffar A, Afflitto J, Nabi N (1997). Chemical agents for the control of plaque and plaque microflora: an overview. Eur J Oral Sci 14:502–507. Gallagher IH, Pearce EI, Hancock EM (1984). The ureolytic microflora of immature dental plaque before and after rinsing with a urea-based mineralizing solution. J Dent Res 63:1037–1039. Ganeshkumar N, Hannam PM, Kolenbrander PE, McBride BC (1991). Nucleotide sequence of a gene coding for a saliva-binding protein (SsB) from Streptococcus sanguis 12 and possible role of the protein in coaggregation with actinomyces. Infect Immun 59:1093–1099. Geddes DA, Weetman DA, Featherstone JD (1984). Preferential loss of acetic acid from plaque fermentation in the presence of enamel. Caries Res 18:430–433. Gilbert P, Das J, Foley I (1997). Biofilm susceptibility to antimicrobials. Adv Dent Res 11:160–167. Gilbert RL, Ingram GS (1988). The oral disposition of zinc following the use of an anticalculus toothpaste containing 0.5% zinc citrate. J Pharm Pharmacol 40:399–402. Goldfine H (1972). Comparative aspects of bacterial lipids. In: Advances in microbial physiology. Vol. 8. Rose AH, Tempest DW, editors. New York: Academic Press, pp. 1-58. Golub LM, Borden SM, Kleinberg I (1971). Urea content of gingival crevicular fluid and its relation to periodontal disease in humans. J Periodontal Res 6:243–251. Grenier D, Mayrand D (1987). Functional characterization of extracellular vesicles produced by Bacteroides gingivalis. Infect Immun 55:111–117. Grossman LI (1954). Clinical evaluation of a salivary calculus preventive agent. Oral Surg Med Oral Pathol 7:607– 608. Hauster H, Chapman D, Dawson RM (1969). Physical studies of phospholipids XI. Ca2+ binding to monolayers of phosphatidlserine and phosphatidyl inositol. Biochim Biophys Acta 183:320–333. Hauster H, Philips MC, Barratt MD (1975). Differences in the interaction of inorganic and organic (hydrophobic) cations with phosphatidyl serine membranes. Biochim Biophys Acta 413:341–353. Hidaka S, Okamoto Y, Abe K (1993). Possible regulatory roles of silicic acid, silica and clay minerals in the formation of calcium phosphate precipitates. Arch Oral Biol 38:405–413. Howell R, Boyan-Salyers B (1980). Composition of calcification between Bacterionema matruchotii and Actinomyces naeslundii. J Dent Res 59:1999–2005. Jenkinson HF (1992). Adherence, coaggregation, and hydrophobicity of Streptococcus gordonii associated with expression of cell surface lipoproteins. Infect Immun 58:1429–1436. Jensen AT, Danø M (1954). Crystallography of dental calculus and the precipitation of certain calcium phosphates. J Dent Res 33:741–750. Johnsson M, Richardson CF, Bergey EJ, Levine MJ, Nancollas GH (1991). The effects of human salivary cystatins and statherin on hydroxyapatite crystallization. Arch Oral Biol 36:631–636. Kazmierczak M, Mather M, Ciancio S, Fischman S, Cancro L (1990). A clinical evaluation of anticalculus dentifrices. Clin Prev Dent 12:13–17. Keevil CW, Bradshaw DJ, Dowsett AB, Feary TW (1987). Microbial film formation: dental plaque deposition on acrylic tiles using continuous culture techologies. J Appl Bacteriol 62:129–138. Kleerebezem M, Quadri LE, Kuipers OP, de Vos WM (1997). Quorum sensing by peptide pheromones and two- component signal-transduction systems in Gram-positive bacteria. Mol Microbiol 24:895–904. Lagerlöf F (1983). Effect of flow rate and pH on calcium phosphate saturation in human parotid saliva. Caries Res 17:403–411. Lamkin MS, Arancillo AA, Oppenheim FG (1996). Temporal and compositional characteristics of salivary protein adsorption to hydroxyapatite. J Dent Res 75:803–808. Le Geros RZ, Bleiwas CB, Retino M, Rohanizadeh R, Le Geros JP (1999). Zinc effect on the in vitro formation of calcium phosphates: relevance to clinical inhibition of calculus formation. Am J Dent 12:65–71. Lear JD, Wasserman ZR, DeGrado WF (1988). Synthetic amphiphilic peptide models for protein ion channels. Science 27:1177–1181. Leskovar P, Hartung R (1977). Inhibition of nucleation and growth of calcium oxalate crystals by aluminium, iron (II), lanthanum, cerium, neodynium, yttrium, europium, magnesium and zinc ions. Fortschr Urol Nephrol 9:30–34. Lindskog S, Friskopp J (1983). Immunoglobulins in human dental calculus demonstrated with the peroxidase- antiperoxidase (PAP) method. Scand J Dent Res 91:360–364. Listgarten MA (1987). Nature of periodontal disease: pathogenic mechanisms. J Periodontal Res 22:172–178. Little MF, Hazen SP (1964). Dental calculus composition (2); subgingival calculus, ash, calcium and sodium. J Dent Res 43:654–651. Little MF, Bowman L, Cascinani CA, Rowley J (1966). The composition of dental calculus 111; supragingival calculus—the amino acid and saccharide component. Arch Oral Biol 11:385–386. Lobene RR, Volpe AR (1987). The anti-calculus effect of dentifrices containing pyrophosphate salts and sodium fluoride. Compend Contin Educ Dent 8(Suppl 8):S272–274. Macpherson LMD, Dawes C (1991). Urea concentration in minor mucous gland secretions and the effect of salivary film velocity on urea metabolism by Streptococcus vestibularis in an artificial plaque. J Periodontal Res 26:395–401. Maitland M, Robinson R (1924). The possible significance of hexose phosphoric esters in ossification. V. The enzymes in the early stages of bone development. Biochem J 18:1354–1357. Mandel ID, Eisenstein A (1969). Lipids in human salivary secretion and salivary calculus. Arch Oral Biol 14:231–233. Mandel ID, Levy BM, Wasserman BH (1957). Histochemistry of calculus formation. J Periodontol 28:132–137. Margolis HC, Varughese K, Moreno EC (1982). Effect of fluoride on crystal growth of calcium apatites in the presence of a salivary inhibitor. Calcif Tissue Int 34:S33–S40. Marsh PD, Bradshaw DJ (1990). The effect of fluoride on the stability of oral bacterial communities in vitro. J Dent Res 69:668–671. McIntire FC, Vatter AE, Baros J, Arnold J (1978). Mechanism of coaggregation between Actinomyces viscosus T14V and Streptococcus sanguis 34. Infect Immun 21:978–988. Melani F, Ramponi G, Farnanaro M (1967). Regulation by phosphate of alkaline phosphatase in rat kidney. Biochim Biophys Acta 138:411–420. Moorer WR, ten Cate JM, Buijs JF (1993). Calcification of a cariogenic Streptococcus and of Corynebacterium (Bacterionema) matruchotii. J Dent Res 72:1021–1026. Moreno EC, Aoba T, Gaffar A (1989). Physical chemistry of calculus formation. In: Recent advances in the study of dental calculus. Oxford: IRL Press at Oxford University Press, pp. 129-142. Morita M, Watanabe T (1986). Relation between the presence of supragingival calculus and protease activity in dental plaque. J Dent Res 65:703–705. Morrison DA (1997). Streptococcal competence for genetic transformation: regulation by peptide pheromones. Microb Drug Resist 3:27–37. Nabi N, Mukerjee C, Schmid R, Gaffar A (1989). In vitro and in vivo studies on triclosan/PVM/MA copolymer NaF combination as an anti-plaque agent. Am J Dent 2:197–206. Nakazato G, Tsuchiya H, Sato M, Yamauchi M (1989). In vivo plaque formation on implant materials. Int J Oral Maxillofac Implants 4:321–326. Nakou M, Mikx FHM, Oosterwaal PJM, Kruijsen JCWM (1987). Early microbial colonization of permucosal implants in edentulous patients. J Dent Res 66:1654–1657. Nelsons DGA, Jongebloed WL, Arends J (1984). Crystallographic structure of enamel surfaces treated with topical fluoride agents: TEM and XRD considerations. J Dent Res 63:6–12. O’Toole GA, Kolter R (1998). Flagella and twitching motility are necessary for Pseudomonas aeruginosa biofilm development. Mol Microbiol 30:295–304. Oppenheim FG, Yang YC, Diamond RD, Hyslop D, Offner GD, Troxler RF (1986). The primary structure and functional characterization of the neutral histidine-rich polypeptide from human parotid saliva. J Biol Chem 261:1177– 1182. Oppermann R, Rølla G, Johansen J (1980). Thiol groups and reduced acidogenicity of dental plaque in the presence of metal ions in vivo. Scand J Dent Res 88:389–396. Parfitt G (1959). A survey of the oral health of Navajo Indian children. Arch Oral Biol 1:193–205. Pearce EI, Sissons CH (1987). The concomitant deposition of strontium and fluoride in dental plaque. J Dent Res 66:1518–1522. Pearce EI, Wakefield J, Sissons CH (1991). Therapeutic mineral enrichment of dental plaque visualized by transmission electron microscopy. J Dent Res 70:90–94. Pellat BP, Grand M (1986). Inorganic pyrophosphatase activity in a plaque calcifying microorganism: Bacterionema matruchotii. J Biol Buccale 14:223–228. Peterson S, Woodhead J, Crall J (1985). Caries resistance in children with chronic renal failure: plaque pH, salivary pH, and salivary composition. Paediatric Res 19:796–799. Poff AM, Pearce EI, Larsen MJ, Cutress TW (1997). Human supragingival in vivo calculus formation in relation to saturation of saliva with respect to calcium phosphates. Arch Oral Biol 42:93–99. Poirier TP, Holt SC (1983). Acid and alkaline phosphatases of Capnocytophaga species. Isolation, purification and characterization of the enzymes from Capnocytophaga ochracea. Can J Microbiol 29:1361–1368. Pratt LA, Kolter R (1998). Genetic analysis of Escherichia coli biofilm formation: roles of flagella, motility, chemotaxis and type I pili. Mol Microbiol 30:285–293. Pulcini E (2001). Biofilms: sensing and signalling. CA Dent Assoc J 29:351–353. Quirynen M, Listgarten M (1990). The distribution of bacterial morphotypes around natural teeth and titanium implants ad modum Brånemark. Clin Oral Implant Res 1:8–12. Raj PA, Johnsson M, Levine MA, Nancollas GH (1992). Salivary statherin. Dependence on sequence, charge, hydrogen bonding potency, and helical conformation for adsorption to hydroxyapatite and inhibition of mineralization. J Biol Chem 267:5968–5976. Regos J, Hitz HR (1974). Investigations on the model of action of triclosan, a broad spectrum antibacterial agent. Zbl Bakt Hyg 226:390–401. Rice A, Hamilton MA, Camper AK (2000). Apparent surface associated lag time in growth of primary biofilm cells. Microb Ecol 40:8–15. Robinson C, Shore RC, Bonassn A, Brooks SJ, Boteva E, Kirkham J (1998). Identification of human serum albumin in human caries lesions of enamel. The role of putative inhibitors of remineralization. Caries Res 32:193–199. Rølla G, Melsen B (1975). Desorption of proteins and bacteria from hydroxyapatite by fluoride and monofluorophosphate. Caries Res 9:66–73. Rølla G, Gaare D, Langmyhr FJ, Helgeland K (1989). Silicon in calculus and its potential role in calculus formation. In: Recent advances in the study of dental calculus. Oxford: IRL Press at Oxford University Press, pp. 97-104. Rowles SL (1964). Biophysical studies on dental calculus in relation to periodontal disease. Dent Pract Dent Rec 15:2–7. Salako NO, Kleinberg I (1989). Incidence of selected ureolytic bacteria in human dental plaque from sites with differing salivary access. Arch Oral Biol 34:787–791. Saxton CA, Harrap G, Lloyd A (1986). The effect of dentifrices containing zinc citrate on plaque growth and oral zinc level. J Clin Periodontol 13:301–306. Scheie AA (1994). Mechanisms of dental plaque formation. Adv Dent Res 8:246–253. Schenk R, Merz WA, Mühlbauer R, Russell RGG, Fleisch H (1973). Effect of ethane-1-hydroxy-1-diphosphonate (EHDP) and dichloromethylene diphosphonate on the calcification and resorption of cartilage and bone in the tibial epiphysis and metaphysis of rats. Calcif Tissue Res 11:196–214. Schiff TG (1987). Comparative clinical study of two anticalculus dentifrices. Compend Suppl 8:275–277. Scruggs RR, Stewart PW, Samuels MS, Stamm JW (1991). Clinical evaluation of seven anticalculus dentifrice formulations. Clin Prev Dent 12:23–27. Segreto VA, Collins EM, D’Agostino R, Cancro LP, Pfeifer HJ, Gilbert RJ (1991). Anticalculus effect of a dentifrice containing 0.5% zinc citrate trihydrate. Community Dent Oral Epidemiol 19:29–31. Shannon IL, Prigmore JR (1960). Parotid gland flow rate and parotid fluid urea concentration. Oral Surg Oral Med Oral Pathol 13:1013–1018. Sidaway DA (1980). A microbiological study of dental calculus. IV. An electron microscopic study of in vitro calcified microorganisms. J Periodontal Res 15:240–254. Simmonds R, Tompkins GR, George RJ (2000). Dental caries and the microbial ecology of dental plaque: a review of recent advances. NZ Dent J 96:44–49. Sissons CH, Cutress TW, Pearce EI (1985). Kinetics and product stoichiometry ureolysis by human salivary bacteria and artificial-mouth plaque. Arch Oral Biol 30:781–790. Sissons CH, Cutress TW, Hoffman MP, Wakefield JS (1991). A multi-station dental plaque microcosm (artificial mouth) for the study of plaque growth, metabolism, pH, and mineralization. J Dent Res 70:1409–1416. Slomiany A, Slomiany BL, Mandel ID (1981). Lipid composition of human parotid saliva from light and heavy dental calculus formers. Arch Oral Biol 26:151–152. Stookey GK, Jackson RD, Beiswanger BB, Stookey KR (1989). Clinical efficacy of chemicals for calculus prevention. In: Recent advances in the study of dental calculus. Oxford: IRL Press at Oxford University Press, pp. 235-258. Swain LD, Boyan BD (1989). Ion-transport properties of membrane proteins associated with microbial calcification. In: Recent advances in the study of dental calculus. Oxford: IRL Press at Oxford University Press, pp. 37-46. Theilade J, Fitzgerald RJ, Scott DB, Nylen MU (1964). Electron microscopic observations of dental calculus in germ-free rats and conventional rats. Arch Oral Biol 9:97–100. Triratana T, Rustogi KN, Lindhe J, Volpe AR (1991). The effect of an anticalculus dentifrice on supragingival calculus formation and gingival recession in Thai adults: one-year study. J Clin Dent 3:22–26. van Dijk S, Dean DD, Liu Y, Zhao Y, Chirgwin JM, Schwartz Z, et al. (1998). Purification, amino acid sequence, and cDNA sequence of a novel calcium-precipitation proteolipid involved in calcification of Corynebacterium matruchotii. Calcif Tissue Int 62:350–358. van Loosdrecht MCM, Lyklema J, Norde W, Zehnder AJ (1990). Influence of interfaces on microbial activity. Microbiol Res 4:75–87. Vogel JJ, Boyan-Salyers BD (1976). Acidic lipids associated with the local mechanism of calcification. Clin Orthop Rel Res 118:230–241. Volpe AR, Schiff TJ, Cohen S, Petrone ME, Petrone D (1992). Clinical comparison of the anticalculus efficacy of two triclosan-containing dentifrices. J Clin Dent 3:93–95. Watanabe T, Toda K, Morishita M, Iwamoto Y (1982). Correlations between salivary protease and supragingival or subgingival calculus index. J Dent Res 61:1048–1051. Weinstein E, Mandel ID (1964). The present status of anticalculus agents. J Oral Ther Pharm 1:327–334. White DJ, Bowman WD, Nancollas GH (1989). Physical-chemical aspects of dental calculus formation and inhibition: in vitro and in vivo studies. In: Recent advances in the study of dental calculus. Oxford: IRL Press at Oxford University Press, pp. 175-188. Wuthier RE, Cummins JW (1974). In vitro incorporation of (3H) since phospholipid of proliferating and calcifying epiphyseal cartilage and liver. Biochim Biophys Acta 337:50–59. Zacherl WA, Pfeiffer HJ, Swancar JR (1985). The effect of soluble pyrophosphates on dental calculus in adults. J Am Dent Assoc 110:737–738. 【未完待续】

*** 618 那一波购物潮， 无妨顺势买一下家用的必须品

三氯生已经在消费品中利用了数十年，颠末全球监管机构的普遍审查并允许停止利用。 数年来多项科学研究，为抗菌成分的平安和效果停止了佐证。 2016 年 9 月，美国食物药品办理局 (FDA) 颁布了一条新规，暗示含有特定 成分（包罗三氯生）的非处方消费类抗菌洗涤产物（抗菌皂）不得继续销售，因为 消费商并没有证明那些成分在那种产物中的效果。该规定仅适用于做为洗手液或 洗澡露的消费类抗菌洗涤产物/肥皂，其实不影响消费类洗手液或医疗保健及食物处置情况中利用的抗菌产物。 FDA 还对三氯生可能有助于构成抗药性细菌而感应担忧。

** 备注： 能否利用含有“三氯生”等成分的药物牙膏，敬请征询您本身的牙医， 若是您罹患牙周疾病。本文不合错误药物牙膏做任何保举。