Rate of accumulation (Plaque Formation Rate Index)
The quantity of plaque that forms on clean tooth surfaces during a given time represents the net result of interactions among etiologic factors, many internal and external risk indicators and risk factors, and protective factors:
· The total oral bacterial population
· The quality of the oral bacterial flora
· The anatomy and surface morphology of the dentition
· The wettability and surface tension of the tooth surfaces
· The salivary secretion rate and other properties of saliva
· The intake of fermentable carbohydrates
· The mobility of the tongue and lips
· The exposure to chewing forces and abrasion from foods
· The eruption stage of the teeth
· The degree of gingival inflammation and volume of gingival exudate
· The individual oral hygiene habits
· The use of fluorides and other preventive products, such as chemical plaque control agents
This observation has been the rationale for the development of the Plaque Formation Rate Index (PFRI) by Axelsson (1989, 1991). The index includes all but the occlusal tooth surfaces and is based on the amount of disclosed plaque freely accumulated (de novo) in the 24 hours following professional mechanical toothcleaning (PMTC), during which period subjects refrain from all oral hygiene practices. In a pilot study on 50 adult subjects, adherent plaque was disclosed on 5% to 65 % of the total number of tooth surfaces (for details on materials and methods, see Axelsson, 1989, 1991). On the basis of this study, the following five-point scale was constructed for the PFRI.
· Score 1 = 1% to 10% of surfaces affected: very low
· Score 2 = 11% to 20% of surfaces affected: low
· Score 3 = 21% to 30% of surfaces affected: moderate
· Score 4 = 31% to 40% of surfaces affected: high
· Score 5 = More than 40% of surfaces affected: very high
The PFRI was evaluated in a large-scale cross-sectional study of 14-year-old schoolchildren (n = 667) in the city of Karlstad, Sweden, in 1984. The subjects were followed over a 5-year period, up to the age of 19 years (Axelsson, 1989, 1991).
Many indicators and factors possibly related to PFRI were also evaluated, including (1) caries prevalence and caries incidence; (2) gingival inflammation; (3) Plaque Index; (4) dietary intake during the 24 hours of free plaque accumulation; (5) salivary levels of Streptococcus mutans and glucosyl transferase; (6) agglutinin levels in resting saliva; and (7) oral hygiene, dietary, and fluoride habits.
Figure 12 shows the frequency distribution of PFRI scores 1 to 5 among the 14-yearold schoolchildren. The majority were low (score 2 = 48%) or moderate (score 3 = 27%) plaque formers. However, the standard of oral hygiene is very high among schoolchildren in Karlstad, and, as a consequence, the caries prevalence is low.
The relationship between caries prevalence (the mean number of decayed or filled surfaces) and different scores is presented in Fig 13. These results indicated a threshold for caries risk between PFRI scores 2 and 3, and this was subsequently confirmed in the longitudinal part of the study over 5 years (Axelsson, 1989, 1991).
Among other observations from the study were:
1. Individuals with a PFRI score of 4 or 5 had considerably higher scores for gingival bleeding than did individuals with a PFRI score of 1 or 2.
2. An initially high Plaque Index usually correlated with PFRI scores 3 to 5.
3. There was no significant correlation between different salivary S mutans levels and PFRI scores.
4. The level of salivary glucosyl transferase was lower in individuals with a PFRI score of 4 or 5 than in those with a score of 1 or 2, probably because glucosyl transferase had already accumulated in the matrix of the plaque in the high and very high plaque formers.
5. The scores for individuals with a very low and low PFRI (scores 1 and 2, respectively) tended to remain constant over the 5-year period, while the scores of some individuals with PFRI scores of 3 to 5 tended to vary, increasing or decreasing by 1 unit.
This final observation indicates that plaque formation rates in individuals with a PFRI score of 4 or 5 can be reduced; such individuals should, therefore, be thoroughly evaluated to identify the factors that contribute to their rapid plaque formation. Needsrelated preventive measures could then be introduced.
For example, there is a strong correlation among plaque formation rate, the severity of gingival inflammation, and the volume of gingival exudate (Axelsson, 1989; Quirynen et al, 1986a; Ramberg et al, 1994a,b, 1995; Saxton 1973, 1975). Initially intensive and frequent mechanical and chemical plaque control, both self-care and professional, is indicated in individuals with PFRI scores of 4 and 5 and high gingival index scores to heal all inflamed sites as quickly as possible and thereby reduce the plaque formation rate.
If the high plaque formation rate is associated with inadequate salivary secretion, frequent plaque control measures (before every meal) should be supplemented with salivary stimulation, provided by the use of fluoridated chewing gum immediately after every meal.
A high intake of fermentable carbohydrates¾particularly sucrose ¾ will result in sticky plaque, rich in polysaccharides, and an increased plaque formation rate (Carlsson and Egelberg, 1965). Needs-related prevention for individuals with a PFRI score of 4 or 5 and a frequent intake of sugar-containing products should, therefore, emphasize not only frequent plaque control but also a reduction in the frequency of sugar intake. In the above study, it was observed that some individuals with a PFRI score of 5 had consumed several bananas during the 24-hour period of free plaque
accumulation.
Many other factors are also related to plaque formation rate. For example, antimicrobial proteins of human whole saliva may influence plaque formation rate.
The PFRI has recently been applied in studies on different populations and age groups. From more than 1,000 17 to 19 year olds in the city of Karlstad, Sweden, 30% with the highest gingival index score were selected to participate in a 4-month doubleblind mouthrinse study. At baseline, most of the subjects had PFRI scores of 3 (more than 40%) or 4 (about 25%) (Axelsson et al, 1994). Subjects with the highest gingival index scores also had the highest PFRI scores. In addition, sites with gingival inflammation had significantly higher plaque formation rates than healthy gingival sites (Rahmberg et al, 1995).
Brazil has the highest caries prevalence in the world. In Sao Paulo, a 3-year cariespreventive study based on self-diagnosis and self-care was carried out in 12- to 15- year-old schoolchildren; the PFRI was used as a tool for self-diagnosis and establishment of needs-related oral hygiene habits. At baseline, almost 100% of the 12-year-old schoolchildren had a PFRI score of 5. The mean percentage of surfaces with reaccumulated plaque was more than 70%, probably because of the extremely high caries prevalence, a high gingival index, and the presence of erupting permanent teeth. At reexamination of the subjects 3 years later, the PFRI had dropped significantly: most of the 15 year olds had scores of 3 or 4. The main contributing factors were an improvement in oral hygiene habits and gingival health and the fact that all teeth were now fully erupted (Albander et al, 1995; Axelsson et al, 1994; Buischi et al, 1994).
In Duisburg, Germany, the PFRI was evaluated in different age groups of children; preschool children, children with mixed dentitions and erupting permanent teeth, and children with fully erupted teeth. Children with erupting teeth had the highest PFRI scores (Fig 14). However, the German children generally had higher PFRI scores than did Swedish children of comparable age with very low caries prevalence, excellent gingival conditions, and good oral hygiene habits (Fig 15) (Axelsson, 1991; Cunea and Axelsson, 1997). According to the World Health Organization’s Data Bank
(1993), caries prevalence is high among 12-year-old German children.
Pattern of plaque reaccumulation
As discussed earlier, plaque formation rate is influenced by such factors as (1) the anatomy and surface morphology of the teeth; (2) the stage of eruption and functional status of the teeth; (3) the wettability and surface tension of the tooth surfaces (both intact and restored surfaces); and (4) gingival health and volume of gingival exudate.
The pattern of plaque reaccumulation will also be influenced by these factors, but may differ somewhat between, on the one hand, tooth surfaces exposed to chewing forces, abrasion from foods, and friction from the dorsum of the tongue, the lips, and the cheeks, and, on the other hand, less accessible areas, such as approximal sites, along the gingival margin, and in irregularities such as occlusal fissures. These less accessible areas are often designated “stagnation areas” for plaque.
In a 6-week study by Lang et al (1973), plaque reaccumulation was registered in four groups of dental students who carried out oral hygiene procedures (mechanical toothcleaning by self-care) with different frequencies: twice daily or every second, third, or fourth day. Figure 16 shows the pattern of reaccumulated plaque according to the Silness and Loe (1964) Plaque Index (scores 0 to 3) on the distal, mesial, facial, and lingual surfaces of the maxillary and mandibular teeth. After only 12 hours of free plaque reaccumulation, there was visible plaque on some of the approximal surfaces of the molars and the lingual surfaces of the mandibular molars (score 2). After 48 hours, almost 100% of these surfaces and most of the remaining approximal surfaces had scores of 2 or 3. The pattern of visible plaque after 2 and 3 days seems to be similar, except on the facial surfaces.
According to Listgarten (1976), freely accumulated plaque is about five times thicker after 3 days than after 2 days (see Fig 6). This explains why gingivitis developed in the group of students cleaning only every third or fourth day but not in those who cleaned at least every second day. It also explains the striking difference in response to rinsing with 10% sucrose solution shown by Imfeld (1978): a dramatic fall in pH on approximal surfaces covered by 3-day-old plaque compared to the pH on lingual surfaces covered by immature (12-hour) plaque.
Figure 17 presents the percentage of freely reaccumulated (de novo) plaque, 24 hours after PMTC, in 667 14-year-old children in the city of Karlstad (Axelsson, 1989, 1991). Plaque reaccumulation was greatest on the mesiolingual and distolingual mandibular surfaces (33%), particularly on the molars, followed by the mesiobuccal and distobuccal surfaces of both maxillary and mandibular teeth, particularly on the molars. There was almost no plaque reaccumulation (3%) on the palatal surfaces of the maxillary teeth, mainly because of friction from the rough dorsum of the tongue.
Figures 18 and 19 illustrate the percentage of de novo plaque on maxillary and mandibular tooth surfaces, respectively, 24 hours after PMTC, in young German subjects (Cunea and Axelsson, 1997). The highest percentages are found in 6 to 14 year olds with many erupting teeth on distobuccal and mesiobuccal surfaces of molars, and on distolingual and mesiolingual surfaces of mandibular molars.
Carvalho et al (1989) studied the pattern and amount of de novo plaque, 48 hours after PMTC, on the occlusal surfaces of partly and fully erupted first molars. Figure 20 illustrates the heavy plaque reaccumulation, particularly in the distal and central fossae, in the eruptin maxillary and mandibular molars, in contrast to the reaccumulation in the fully erupted molars, which are subjected to normal chewing friction. Abrasion from normal mastication significantly limits plaque formation; this explains why almost 100% of occlusal caries in molars begins in the distal and central
fossae during the eruption period of 14 to 18 months.
It is important to differentiate between plaque indices and plaque reaccumulation rate (PFRI). For successful primary and secondary prevention of dental caries and periodontal diseases, an understanding of plaque formation rates and patterns is essential. Mechanical removal of dental plaque according to the nonspecific plaque hypothesis is a rational method for prevention and control of periodontal diseases as well as dental caries, because it is directed toward the cause (etiology) of these diseases. However, for cost-effectiveness, the program should be related to the pattern of plaque reaccumulation, PFRI, and predicted risk. (For reviews on plaque formation rate and the role of needs-related plaque control see Axelsson 1994, 1998.)
