Toors F A
Rev Belge Med Dent (1984). 1992;47(3):67-92.
Clinical studies have demonstrated the caries promoting effects of sugar based gum when compared with non sugar chewing controls. Sucrose gum has been shown to stimulate plaque growth and increase its adhesivity. Acid produced in plaque and mixed saliva whilst chewing sugar gum is counteracted by the buffering action of mastication induced saliva. However the vast majority of studies measuring plaque pH has demonstrated acidification of plaque during use of sugar gum into the decalcifying zone (pH < or = 5.5), or after the gum is taken out. Sugar gum causes a more pronounced fall in plaque pH in individuals with an increased caries risk compared to the pH drop in more caries resistant individuals. Sorbitol, by itself or in combination with mannitol is slowly converted to acids by the plaque microorganisms. Chewing gums sweetened with these sugar alcohols do not cause a critical acidification of the plaque and appear not to promote caries in the clinical trial. Twelve weeks use of sorbitol chewing gum has been shown to induce a plaque more adapted to form acids from this sugar alcohol. This adaptation has been shown to persist for up to twelve weeks after cessation of the use of the sorbitol gum. Xylitol has generally been considered non-cariogenic because of its non-fermentability by most important plaque microorganisms. Plaque pH and pH of mixed saliva is increased during and following the use of xylitol based chewing gum. Prolonged use of xylitol or xylitol containing chewing gum reduces Streptococcus mutans counts in plaque and saliva, at the same time fostering remineralization of early caries lesions. Regular use of xylitol reduces the acidogenic potential of the plaque as well as its adhesiveness, at the same time increasing its mineral content. No adaptive changes in plaque metabolism resulting in the fermentation of xylitol have been reported, not even after long term, intense use. Xylitol chewing gum therefore is eminently suited to be used as part of a caries preventive regimen notably for high caries risk patients and those suffering from xerostomia. Adding mineral salts to sugar based chewing gum has been demonstrated to significantly inhibit caries development. Possible additional caries preventive benefits of mineral compounds added to sugar-free chewing gum have, so far not been reported. Sugar-free chewing gum has been shown to be an excellent vehicle for Fluoride. The plaque-growth retarding properties of Chlorhexidine-containing chewing gum have been shown to equal that of a Chlorhexidine mouthwash. Ureum added to a sugar-free chewing gum helps to neutralize plaque acids by liberating basic ammonia.
临床研究表明，与无糖咀嚼对照物相比，含糖口香糖具有促进龋齿形成的作用。已证实蔗糖口香糖会刺激牙菌斑生长并增加其黏附性。咀嚼含糖口香糖时，牙菌斑和混合唾液中产生的酸会被咀嚼诱导唾液的缓冲作用抵消。然而，绝大多数测量牙菌斑pH值的研究表明，在使用含糖口香糖期间或取出口香糖后，牙菌斑会酸化至脱矿区域（pH≤5.5）。与患龋风险较低的个体相比，含糖口香糖会使患龋风险增加的个体的牙菌斑pH值下降更为明显。山梨醇本身或与甘露醇结合，会被牙菌斑微生物缓慢转化为酸。在临床试验中，用这些糖醇类甜味剂调味的口香糖不会导致牙菌斑严重酸化，似乎也不会促进龋齿形成。已证实使用十二周山梨醇口香糖会诱导牙菌斑更适应从这种糖醇类形成酸。这种适应性在停止使用山梨醇口香糖后可持续长达十二周。木糖醇通常被认为是非致龋的，因为大多数重要的牙菌斑微生物都不能发酵它。在使用基于木糖醇的口香糖期间及之后，牙菌斑pH值和混合唾液的pH值会升高。长期使用木糖醇或含木糖醇的口香糖会减少牙菌斑和唾液中变形链球菌的数量，同时促进早期龋损的再矿化。经常使用木糖醇会降低牙菌斑的产酸能力及其黏附性，同时增加其矿物质含量。即使经过长期大量使用，也未报告牙菌斑代谢发生适应性变化从而导致木糖醇发酵。因此，木糖醇口香糖非常适合作为预防龋齿方案的一部分，尤其适用于患龋风险高的患者和患有口干症的患者。已证实向含糖口香糖中添加矿物盐可显著抑制龋齿发展。到目前为止，尚未报告向无糖口香糖中添加矿物化合物可能带来的额外防龋益处。无糖口香糖已被证明是氟化物的优良载体。含氯己定的口香糖抑制牙菌斑生长的特性已被证明与氯己定漱口水相当。添加到无糖口香糖中的尿素通过释放碱性氨来帮助中和牙菌斑酸。
