PLAQUE CONTROL

  Plaque Control

Research has indicated that dental caries does not develop in 

experimental animals fed their entire diet by stomach tube. How￾ever, Bowen (1969a) has shown that plaque still forms on tooth 

surfaces of monkeys in spite of receiving their diet in this manner. 

Bowen (1969a) further showed that the capacity of plaque to 

produce acid was influenced by the experimental regimen. When a 

normal cariogenic diet was fed by stomach tube for two weeks, 

almost no acid was formed in the plaque. Plaque formed in the 

presence of glucose had a "much less acidogenic capacity than that 

formed from sucrose. Plaque formed three months after the ani￾mals had been returned to their normal diet had approximately the 

same acidogenic potential as that formed before the experiment. 

Periodontal disease is the major cause oftooth loss after 35 years 

of age. In common with dental caries, periodontal disease is wide￾spread. In one study 99 per cent of secondary schoolchildren were 

found to have some form of the disease and, by 17 years of age, 36 

per cent had one or more true periodontal pocket (Sheiham 1969). 

From 35 to 39 years of age, 46 per cent of adults in the UK exhibit 

the terminal stages of periodontal disease and are about to lose 

teeth because of the disease. In those between 55 and 59 years of 

age, the percentage has increased to 95 per cent (Sheiham 1971). It 

has been shown (Loe et al. 1965) that clinical gingival inflam￾mation can be eliminated by thorough toothbrushing. In addition, 

most periodontal disease can be controlled or prevented by oral 

hygiene practice aimed at the removal of plaque (Greene and 

Vermillion 1971). 

It is now well accepted that dental plaque is a major aetiological 

factor in the two main dental diseases-caries and periodontal 

disease. Plaque consists essentially of microcolonies of bacteria 

held in a gel-like matrix. The matrix is derived from the bacteria 

themselves, from saliva and, in areas adjacent to gingival tissue, 

from gingival fluid and inflammatory exudate. The mechanism of 

plaque formation has been mentioned in Chapter 1. Shortly after a 

polished tooth surface is exposed to saliva, a structure less organic 

pellicle forms. The first micro-organisms start to colonize it and a 

thin layer of bacterial plaque is formed within hours. After 24 

hours without tooth cleansing, a clinically observable soft deposit is 

seen at the tooth-gingival margin interface. Plaque formation at 

the cervical margins is relatively independent of the passage of 

food orally. Hence, the concept of 'self-cleansing' on an ordinary 

diet does not exist in man. Tube-feeding is associated with as much 

plaque formation as chewing and swallowing. Excessive chewing of 

fibrous foods between meals cannot prevent the formation of 

plaque. Even if the bacteria which cause caries and periodontal 

disease are present in the mouth, they cannot initiate either disease 

process until they are able to attach themselves to the teeth in the

L. M. Silverstone, Preventive Dentistry

© Update Books Ltd and Leon M. Silverstone 197

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