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1. Introduction
Particulate matter (PM) refers to solid particles and liquid droplets found in air. Many manmade and natural sources produce PM directly, or produce pollutants that react in the atmosphere to form PM. The resultant solid and liquid particles come in a wide range of sizes, and particles that are 10 micrometers or less in diameter (PM10) can be inhaled into and accumulate in the respiratory system and are believed to pose health risks (Environmental Protection Agency, 2010). Particulate matter is one of the six primary air pollutants the Environmental Protection Agency (EPA) regulates, due to exposure to high outdoor PM10 concentrations causes increased disease and death (Environmental Protection Agency, 2010). Therefore, PM10 concentrations, amongst many other air pollutants, are sampled and measured in various places in California, United States.
The general trend of PM air pollutant concentrations in the air in California are on the decrease, but it continues to be monitored and observed. The California standards for annual PM10 concentrations is that the annual arithmetic mean is 20 µg/m3, and the national standard is 50 µg/m3 before 2006 (California Environmental Protection Agency Air Resources Board, 2010, Environmental Protection Agency, 2010). The State of California sets very high standards for their air quality, and air pollutants are carefully monitored.
However, in reality, it is too costly in terms of time, finance, and manpower to keep all the 213 sites to be monitoring and recording. In Fig. 1, a complete map of all 213 sample locations for PM10 are shown. However, one must note that these sample sites are never all used at any given year, PM10 samples are taken at different locations each year. At best, a maximum of 102 PM10 samples are collected during some years, and at worst, 61 PM10 samples are collected at that year. Therefore comparisons of PM10 between years are difficult, due to missing data at sample sites. It is difficult to construct kriging maps in terms of actual observations annually since the air pollutants were measured in different locations each year although the site design originally planned was quite delicate statistically.
Each year, approximately 40% of the 213 sites were actually observed. We call a site that does not have a recorded PM10 value as "missing value", and since there are no patterns so that serious problems would twist the kriging map constructions. In Fig. 2, this is clearly demonstrated. In 1989, there are 61 PM10 samples collected (29% of 213 locations), and in 2000, there are 94 PM10 samples collected (44%).
Figure 1.
Complete 213 Observational Sites in the California State
Figure 2.
PM10 Samples Collected in California in 1989 (61 sites) and 2000 (94 sites)
The data scarcity brings in a series of (five) fundamental issues into the spatial-temporal modelling and prediction practices for California PM10 data, namely:
The necessity to recognize the impreciseness in analyzing the spatial-temporal pattern in terms of California PM10 records, which inevitably acts the solidness of a geo-statistical analysis;
Which theoretical foundations are appropriate for modelling impreciseness uncertainty;
How to fill up the "missing value" sites so that the "complete" records are available, which is either an original annual average from the original observations (40%) recorded on the site or a or predicted value by "neighbourhood sites" (60%), i.e., to facilitate spatial-temporal imprecise PM10 value by interpolations and extrapolations;
How to estimate the parameters of uncertain processes (temporal patterns), particularly the rate of change parameterαi,i=1,2,⋯,213;
Create annual kiging maps (19 maps) under spatially isotropy and stationarity assumptions so that the changes between annual maps can be analyzed by kriging map difference between 2007 and 1989 and kriging map of location rate of change.
These issues will be addressed in the remaining sections sequentially.
2. The necessity of modelling impreciseness in California PM10 spatial-temporal analysis
Impreciseness is a fundamental and intrinsic feature in the PM10 spatial-temporal modelling, due to the observational data shortage and incompleteness. Spatially, there are 213 sites involved, and temporally, PM10 observations were collected from 1989 to 2007, over a 19-year period. During the 19-year period, there are only two sites (Site 2125 and Site 2804) having complete 19 year records. There are 16 sites having only 1 record (8%) and 70 sites having 10 or above records. To have a statistically significant time-series analysis, 50 data points are minimal requirement for each site, so classical time-series analysis (probabilistic analysis) cannot be performed. In order to have a quick overall evaluation of PM10 records on each site, we borrow the statistical quality control idea here (Electric, 1956, Montgomery, 2001). But we do not carry on traditional 6-sigma rule, rather, classify the PM10 records into four groups: 1-(5,20], 2-(20,35], 3-(35,50], 4-(50,160]. These four-group limits in Table 1 reflect the national standard, (50 µg/m3) and California state standard (20 µg/m3) respectively. For example, 1 -(5,20]is for a location whose PM10 fall in 5 to 20 (µg/m3).
County name
1-(5,20]
2-(20,35]
3-(35,50]
4-(50,160]
No. of Sites
Los Angeles
3
7
10
Kern
1
2
1
5
9
Riverside
3
3
3
9
San Diego
5
3
8
Imperial
3
4
7
Lake
3
3
Inyo
2
2
4
8
Table 1.
PM10 Hazard level evaluation over selected 7 counties
One must be aware that the classification is not in absolute sense, rather, additional rules are adding (similar to quality control chart pattern analysis (Electric, 1956):
(1) if a single point, then, classify the site hazard level according to which group it falls in; (2) if a sequence of records, some of them, particularly early points may fall in higher (or lower) hazard level, but if last three points fall in a lower (or higher) hazard level, the later level would be chosen for the site.
The additional rule 1 can attribute to expert\'s knowledge confirmation, while the additional rule 2 can be regarded as an expert\'s decision based on trend pattern.
Figure 3.
The 7 sites from the selected 7 counties with original PM10 data plots and the hazard level classifications
Fig. 3 shows the classifications of a seven sites from the selected 7 counties in Table 1, each county one site is picked up for illustration purpose. The red coloured plot means the hazard level 1(5,20]; the green coloured plot means the hazard level 2(20,35]; the purple coloured plot means the hazard level 3(35,50]; and the black coloured plot means the hazard level 4(50,160].
It is evident that facing the impreciseness caused by incomplete data recording, one has to rely on expert\'s knowledge to compensate the inadequacy and accuracy in collected observational data. Impreciseness is referred to a term with a connotation specified by an uncertain measure or an uncertainty distribution for each of the actual or hypothetical members of an uncertainty population (i.e., collection of expert\'s knowledge). An uncertain process is a repeating process whose outcomes follow no describable deterministic pattern, but follow an uncertainty distribution, such that the uncertain measure of the occurrence of each outcome can be only approximated or calculated.
The uncertainty modelling without a measure specification will not have an rigorous mathematical foundations and consequently the modelling exercise is baseless and blindness. In other words, measure specification is the prerequisite to spatial-temporal data collection and analysis. For example, without Kolmogrov\'s (1950) three axioms of probability measure, randomness is not defined and thus statistical data analysis and inference has no foundation at all.
Definition 2.1: Impreciseness is an intrinsic property of a variable or an expert\'s knowledge being specified by an uncertain measure.
It is therefore inevitably to seek appropriate form of uncertainty theory to meet the impreciseness challenges. In the theoretical basket, interval uncertainty theory (Moore, 1966), fuzzy theory (Zadeh, 1965, 1978), grey theory (Deng, 1984), rough set theory (1982), upper and lower provisions (or expectations) (Walley, 1991), or Liu’s uncertainty theory (2007, 2010) may be chosen.
While imprecise probability theory (Utikin and Gurov, 1998) may be a typical answer to address the observational data inaccuracy and inadequacy. However the imprecise probability based spatial modelling requires too heavy assumptions. Just as Utikin and Gurov (2000) commented, “the probabilistic uncertainty model makes sense if the following three premises are satisfied: (i) an event is defined precisely; (ii) a large amount of statistical samples is available; (iii) probabilistic repetitiveness is embedded in the collected samples. This implies that the probabilistic assumption may be unreasonable in a wide scope of cases.” Guo et al. (2007) and Guo (2010) did attempt to address the spatial uncertainty from the fuzzy logic and later Liu\'s (2007) credibility theory view of point.
Nevertheless, Liu’s (2007, 2010) uncertainty theory is the only one built on an axiomatic uncertain measure foundation and fully justified with mathematical rigor. Therefore it is logical to engage Liu’s (2007, 2010, 2011) uncertainty theory for guiding us to understand the intrinsic character of imprecise uncertainty and facilitate an accurate mathematical definition of impreciseness in order to establish the foundations for uncertainty spatial modelling under imprecise uncertainty environments.
3. Uncertain measure and uncertain calculus foundations
Uncertainty theory was founded by Liu in 2007 and refined in 2010, 2011. Nowadays uncertainty theory has become a branch of mathematics.
A key concept in uncertainty theory is the uncertain measure, which is a set function defined on a sigma-algebra generated from a non-empty set. Formally, let Ξ be a nonempty set (space), and A(Ξ) the σ-algebra onΞ. Each element, let us say,A⊂Ξ ,A∈A(Ξ) is called an uncertain event. A number denoted asƛ{A}, 0≤ƛ{A}≤1, is assigned to eventA∈A(Ξ), which indicates the uncertain measuring grade with which event A∈A(Ξ) occurs. The normal set functionƛ{A}satisfies following axioms given by Liu (2011):
Axiom 1: (Normality)ƛ{Ξ}=1.
Axiom 2: (Self-Duality) ƛ{⋅}is self-dual, i.e., for anyA∈A(Ξ),ƛ{A}+ƛ{Ac}=1.
Axiom 3: (σ-Subadditivity) ƛ{∪i=1∞Ai}≤∑i=1∞ƛ{Ai}for any countable event sequence{Ai}.
Axiom 4: (Product Measure) Let (Ξk,AΞk,ƛk)be the kthuncertain space,k=1,2,⋯,n. Then product uncertain measure ƛon the product measurable space(Ξ,AΞ)is defined by
ƛ=ƛ1∧ƛ2∧⋯∧ƛn=min1≤k≤n{ƛk}E1
where
Ξ=Ξ1×Ξ2×⋯×Ξn=∏k=1nΞkE2
and
AΞ=AΞ1×AΞ2×⋯×AΞn=∏k=1nAΞkE3
That is, for each product uncertain event Λ∈AΞ (i.e,Λ=Λ1×Λ2×⋯×Λn∈AΞ1×AΞ2×⋯×AΞn=AΞ), the uncertain measure of the event Λis
ƛ{Λ}={supA1×⋯×An⊂Λmin1≤k≤nƛ{Λk} if supA1×⋯×An⊂Λmin1≤k≤nƛ{Λk}>0.51−supA1×⋯×An⊂Λcmin1≤k≤nƛ{Λk}if supA1×⋯×An⊂Λcmin1≤k≤nƛ{Λk}>0.50.5 otherwiseE4
Definition 3.1: (Liu, 2007, 2010, 2011) A set function ƛ:A(Ξ)→[0,1] satisfies Axioms 1-3 is called an uncertain measure. The triple (Ξ,A(Ξ),ƛ) is called an uncertainty space.
Definition 3.2: (Liu, 2007, 2010, 2011) An uncertainty variable is a measurable function ξfrom an uncertainty space (Ξ,A(Ξ),ƛ)to the set of real numbers, i.e., for any Borel set B of real numbers, the set{τ∈Ξ:ξ(τ)⊂B∈B(ℝ)}∈A(Ξ), i.e., the pre-image of B is an event.
Remark 3.3: Parallel to revelation of the connotation of randomness in geostatistics, impreciseness occupies an fundamental position in geospatial-temporal uncertainty statistical analysis. In California PM10 spatial-temporal study, nearly 60% sites do not have "complete" temporal sequences so that in order to fill the "missing" observations, we have to engage expert\'s knowledge to pursue "complete sequences" (i.e., to have 19 PM10 values at each individual site), which is inevitably imprecise and incomplete. Impreciseness is referred to a term here with an intrinsic property governed by an uncertainty measure or an uncertainty distribution for each of the actual or hypothetical members of an uncertainty population (i.e., collection of expert\'s knowledge). An uncertainty process is a repeating process whose outcomes follow no describable deterministic pattern, but follow an uncertainty distribution, such that the uncertain measure of the occurrence of each outcome can be only approximated or calculated.
Remark 3.4: Impreciseness exists in engineering, business and research practices due to measurement imperfections, or due to more fundamental reasons, such as insufficient available information,..., or due to a linguistic nature, because it is an unarguable fact that impreciseness exists intrinsically in expert’s knowledge on the real world.
Definition 3.5: Letξbe a uncertainty quantity of impreciseness on an uncertainty measure space(Ξ,A(Ξ),ƛ). The uncertainty distribution of ξ is
Ψξ(x)=ƛ{τ∈Ξ|ξ(τ)≤x}E5
An imprecise variable ξ is an uncertainty variable and thus is a measurable mapping, i.e.,ξ:D→ℝ,D⊆ℝ. An observation of an imprecise variable is a real number, (or more broadly, a symbol, or an interval, or a real-valued vector, a statement, etc), which is a representative of the population or equivalently of an uncertainty distributionΨξ(⋅) under a given scheme comprising set and σ-algebra. The single value of a variable with impreciseness should not be understood as an isolated real number rather a representative or a realization from the uncertain population.
Definition 3.6: (Lipschitz condition) Let f(x)be a real-valued function,f:ℝ→ℝ. If for anyx,y∈ℝn, there exists a positive constantM>0, such that
|f(x)−f(y)|<M|x−y|E6
Definition 3.7: (Lipschitz continuity) Let f:ℝm→ℝm
∀B⊂ℝmBfB∃M>0
‖f(x)−f(y)‖<M‖x−y‖,∀x,y∈BE7
where ‖⋅‖is some metric (for example, Euclidean distance inℝm), such
d(f(x),f(y))<Md(x,y),∀x,y∈BE8
for eachz∈ℝm, fis Lipschitz continuous locally on the open ballBof center zradius M>0 such
BM(z)={y∈ℝm|d(y,z)<M}E9
fℝm
Remark 3.8: For continuity requirements, Lipschitz continuous function is stronger than that of the continuous function in Newton calculus but it is weaker than the differentiable function in Newton differentiability sense. In other words, Lipschitz-continuity does not warrant the first -order differentiability everywhere but it does mean nowhere differentiability. Lipschitz-continuity does not guarantee the existence of the first-order derivative everywhere, however, if exists somewhere, the value of the derivative is bounded since
|f(x)−f(y)||x−y|<ME10
by recalling the definition of the Newton derivative
limy→xf(x)−f(y)x−y=f\'(x)E11
Similar to the concept of stochastic process in probability theory, an uncertain process {ξt,t≥0}is a family of uncertainty variables indexed by tand taking values in the state spaceS⊆ℝ.
Definition 3.9: (Liu 2010, 2011) Let {Ct,t≥0}be an uncertain process.
C0=0
{Ct,t≥0}
every increment Ct+s−Csis a normal uncertainty variableb with expected value 0 and variancet2, i.e., the uncertainty distribution of Ct+s−Csis
ΨCt+s−Cs(z)=(1+exp(−xz3t))−1E12
Then {Ct,t≥0}is called a canonical process.
Remark 3.10: Comparing to Brownian motion process {Bt,t≥0}in probability theory, which is continuous almost everywhere and nowhere is differentiable, while Liu\'s canonical process {Ct,t≥0}is Lipschitz-continuous and if{Ct,t≥0}is differentiable somewhere, the derivative is bounded. Therefore{Ct,t≥0}is smoother than{Bt,t≥0}.
Definition 3.11: (Liu, 2010, 2011) Suppose {Ct,t≥0}is a canonical process, and fand gare some given functions, then
dξt=f(t,ξt)dt+g(t,ξt)dCtE13
is called an uncertain differential equation. A solution to the uncertain differential equation is the uncertain process{ξt,t≥0}satisfying it for any t>0.
Remark 3.12: Since dCt and dξt are only meaningful under the umbrella of uncertain integral, i.e., the an uncertain differential equation is an alternative representation of
ξt=ξ0+∫0tf(s,ξs)ds+∫0tg(s,ξs)dCsE14
Definition 3.13: The geometric canonical process {Gt,t≥0}satisfies the uncertain differential equation
dGt=αGtdt+σGtdCtE15
has a solution
Gt=exp(αt+σCt)E16
where αcan be called the drift coefficient and σ>0can be called the diffusion coefficient of the geometric canonical process {Gt,t≥0}due to the roles played respectively.
4. Spatial interpolation and extrapolation via inverse distance approach
Statistically, spatial interpolation and extrapolation modeling is actually a kind of linear regression modeling exercises, say, kriging methodology. Considering the shortage of California PM10 data records, we will utilize a weighted linear combination approach, which was first proposed by Shepard (1968). The weights are the inverse distances between the missing value cell to the actual observed PM10 value cells. The weight construction is a deterministic method, which is neutral and does not link to any specific measure theory. It is widely used in spatial predictions and map constructions in geostatistics, but is not probability oriented, rather, molecular mechanics stimulated. A unique aspect of geostatistics is the use of regionalized variables which are variables that fall between random variables and completely deterministic variables. The weight of an observed PM10 value is inversely proportional to its distance from the estimated value.
Cij=wij∑i=1213wijzijE17
Figure 4.
The 7 sites from the selected 7 counties with completed 19 year observations of PM10
We wrote a VBA Macro to facilitate the interpolations and the extrapolations to "fill" up the 2048 missing value cells in terms of the 1639 cells with PM10 values. With the interpolations and the extrapolations, every site has 19 PM10 values now. As to whether the inverse distance approach can facilitate highly accurate predictions for each cell without a observed PM10 value, we performed a re-interpolation and re- extrapolation scheme (by deleting a true PM10 record, then fill it by the remaining records one by one) to evaluate the mean square value for error evaluation, the calculated mean of sum of error squares is 59.885, which is statistically significant (asymptotically).
We plotted sites 2045, 2744, 2199, 2263, 2297, 2914, and 2248 (appeared in Fig. 3) respectively in Fig. 4. By comparing Fig. 3 and 4, it is obvious that only Site 2744 the hazard level changed (moving up to next higher hazard level), while the hazard level of other six sites are unchanged. This may give an justification of the inverse distance approach. Keep in mind, the aim of this article is investigate whether the PM10 level is changed over 1989 to 2007 19-year period. The change is not necessarily be accurate but reasonably calculated because of the impreciseness features of PM10 complete records.
5. Uncertain analysis of site temporal pattern
Once the interpolations and the extrapolations in terms of the inverse distance approach is completed, a "complete" data set is available, containing 4047 data records of 213 sites over 19 years. The next task is for a given site, how to model the uncertain temporal pattern. It is obvious that the "complete" data set contains impreciseness uncertainty due to the interpolations and the extrapolations. We are unsure that the impreciseness uncertainty is of random uncertainty, so that we still use uncertain measure theory to pursue the temporal uncertainty modelling.
Recall that the Definition 3.13 in Section 3 facilitates a uncertain geometric canonical process,{Gt,t≥0}. Notice that G0=0may not fit the data reality so that we propose a modified uncertain geometric canonical process, {Gt*,t≥0}withG0>0:
Gt*=G0Gt=G0exp(αt+σCt)E18
Note that
lnGt*=lnG0+αt+σCtE19
Letyt=lnGt*, α0=lnG0, then we have
yt=α0+αt+σCtE20
Recall the relevant definitions in Section 3, we have
since if ξ1and ξ2are independent uncertain variables with uncertainty distributions Ψξ1and ϒξ2 respectively, then the joint uncertainty distribution of (ξ1,ξ2) isΦξ1,ξ2(z1,z2)=min{Ψξ1(z1),ϒξ2(z2)}. Hence we obtain the expression ofσs,t:
in terms of numerical integration, Then an estimate for Γimatrix is obtained:
Γ^i=σ^i2(σj,ki)19×19E33
Finally, we use the approximated objective function
J^i(αi0,αi)=(Y¯i−Xβ¯i)\'Γ^i−1(Y¯i−Xβ¯i)E34
to obtain a pair of estimates(α˜i0,α˜i). Repeat this estimation process until all the 213 weighted least square estimate (α˜i0,α˜i)are obtained.
Recall the definition of coefficient αi so that the sign and the absolute value of αi indicates the geometric change over the 19 years. Since the estimation procedure of αi involves all the spatial-temporal information, it is reasonable to have them plotted in a kriging map to reveal the overall changes over 19-year period.
6. Kriging maps and time-change maps based on completed PM10 data
Kriging map presentation is vital for a geostatistian\'s visualization, and maps reveal hidden information or the whole picture. A sample statistic is typically condensing the wide-spread information into a numerical point. While, a kringing map is actually a map statistic (or a statistical map) which contains infinitely many information aggregated from limited "sample" information (i.e., observations). Kriging itself is not specifically probability oriented, it is another weighted linear combination prediction, but requires more mathematical assumptions. In fuzzy geostatistics, the fuzzy kriging scheme has also been developed (Bardossy et al., 1990).
Ordinary kriging (abbreviated as OK) is a linear predictor, see Cressie (1991) and Mase (2011). The formula is
Z(s0)=∑j=1NλjZ(sj)E35
where sj are spatial locations with observation Z(sj)available and the coefficients λj satisfy the OK linear equation system
The OK system is generated under the assumptions of an additive spatial model
Z(s)=μ(s)+ε(s)E37
where µ(s) is the basic (expected) spatial trend and ε(s) is a Gaussian errorN(0,σ2(s)), i.e., Gaussian variable with mean and variance
Ε[ε(s)]=0,V[ε(s)]=σ2(s)E38
respectively. Accordingly, the variogram 2γ of the random error function ε(⋅) is just defined by
2γ(h)=Ε[(ε(s+h)−ε(h))2]E39
where h is the separate vector between two spatial point s+h and sunder the isotropy assumption.
Figure 5.
Kriging Prediction Maps for PM10 in California 1989-2007.
The 213 observation sites now have 19-year PM10 values, a "complete" data set is now available, containing 4047 data records of 213 sites over 19 years, and then the 19 ordinary kriging pred4iction maps are generated for comparisons. In Fig. 5, all 19 years of PM10 concentration in California State are shown. It is very interesting to examine the change in PM10 concentrations through the 19 years, based upon the modelled complete 213 site data. In particular, 1998 shows to have an extremely low PM10 concentration. Although air quality is varied over the years, but in general, the PM10 concentration is decreasing, showing an improvement of air quality trend.
Figure 6.
Changes in PM10 values and the rate of change of PM10 in California between 1989 and 2007.
As one can clearly see from Fig. 6, that PM10 concentration has clearly decreased over the 19 years, and air quality has improved remarkably over the years. The blue and green colours show negative changes, and red shows positive changes or near positive changes. Counties such as San Diego, Inyo, Santa Barbara, Imperial, still show an increase in PM10 concentration in the air, and indicate bad air quality. While Kern, Modoc, Siskiyou counties show the most improvement in air quality. The left map in Fig. 6 is PM10 record difference between 2007 and 1989 at each location, in total 231 values, and then a difference map is constructed. It is obvious that the difference map only utilizes 1989 and 2007 two-year PM10 records, 1990, 1991,..., 2006 seventeen years\' information do not participate the change map construction. The right map in Fig. 6 show completedα˜i,i=1,2,⋯,213, the rate of change over 1989 to 2007 19-year period.
Note that the calculations of α˜i,i=1,2,⋯,213involve all nineteen years by temporal regression, the dependent variable yare estimated form the actual PM10 observations cross over all the available locations. Therefore, the rate of change parameter αiat each individual location contains all spatial-temporal information. It is reasonable to say the rate of change parameter α˜iis an aggregate statistic for revealing the 19-year changes over 213 locations. α˜ikriging map is thus different from 2007-1989 kriging maps. The positive sign of α˜i indicates the increasing trend in PM10 concentration, while the negative sign f α˜i indicates the decreasing trend in PM10 concentration. The absolute value of α˜ireveals the magnitude of change of PM10 concentration. It is worth to report, among 213 locations, 193 locations have negativeα˜i, while the negative α˜ilocations are 20 (9% approximately).
7. Discussion
Air quality and health is always a central issue to public concern on the quality of life. In this chapter, we examined PM10 levels over 19 years, from 1989 to 2007, in the California State. Facing the difficult task of a lack of "complete" PM10 observational data, we utilised the inverse distance weight methodology to "fill" in the locations with missing values. By doing so, the impreciseness uncertainty is introduced, which is not necessarily explained by probability measure foundation. We noted the character of a regionalized variable in geostatistics and therefore engage Liu\'s (2010, 2011) uncertainty theory to address the impreciseness uncertainty. In this case, we developed a series of uncertain measure theory founded spatial-temporal methodology, including the inverse distance scheme, the kriging scheme, and the geometric canonical process based weighted regression analysis in order to extract the change information from the incomplete 1989-2007 PM10 records. The use of the rate of change parameter alpha is a new idea and it is an aggregate change index utilized all spatial-temporal data information available. It is far better than classical change treatments. However, due to the limitations of our ability, we are unable to demonstrate the detailed uncertain measure based spatial analysis model. In the future research, we plan to develop a more solid uncertain spatial prediction methodology.
Acknowledgments
I would like to thank the California Air Resources Board for providing the air quality data used in this paper. This study is supported financially by the National Research Foundation of South Africa (Ref. No. IFR2009090800013) and (Ref. No. IFR2011040400096).
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Introduction",level:"1"},{id:"sec_2",title:"2. The necessity of modelling impreciseness in California PM10 spatial-temporal analysis",level:"1"},{id:"sec_3",title:"3. Uncertain measure and uncertain calculus foundations",level:"1"},{id:"sec_4",title:"4. Spatial interpolation and extrapolation via inverse distance approach",level:"1"},{id:"sec_5",title:"5. Uncertain analysis of site temporal pattern",level:"1"},{id:"sec_6",title:"6. Kriging maps and time-change maps based on completed PM10 data",level:"1"},{id:"sec_7",title:"7. Discussion",level:"1"},{id:"sec_8",title:"Acknowledgments",level:"1"}],chapterReferences:[{id:"B1",body:'BardossyA.BogardiI.KellyE.1990Kriging with imprecise (fuzzy) variograms, I: Theory. Mathematical Geology, 226379'},{id:"B2",body:'California Environmental Protection Agency Air Resources Board.2010Ambient Air Quality Standards (AAQS) for Particulate Matter. (www.arb.ca.gov)'},{id:"B3",body:'CressieN.1991Statistics for Spatial Data. 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Department of Statistical Sciences, University of Cape Town, Cape Town, South Africa
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1. Introduction
From the ancient time, dental caries has existed, even from the time when the only way to eat and drink was hunting and gathering. According to the World Health Organization, 60–90% of schoolchildren worldwide have experienced caries, with the disease being most prevalent in Asian and Latin American countries (WHO, 2008). Dental caries is a multifactor disease which appears when demineralization of the hard tissues of the teeth occurs by organic acids formed by bacteria in dental plaque through the anaerobic metabolism of sugars derived from the diet.
Calcium is lost from the tooth surface, and demineralization occurs only when sugars or other fermentable carbohydrates are ingested in which results fall in dental plaque pH caused by organic acids that increase the solubility of calcium hydroxyapatite in the dental hard tissues.
Lifestyle or dental health habits are the factors that should be connected to dental diseases. Dietary and daily habits, familial and physiological well-being, socioeconomic status and lifestyle, awareness and education, and area where they live are the factors that should be taken into consideration when discussing oral health. The higher the socioeconomic status is, the more the people are exposed to the availability of junk foods and susceptible to its frequent consumption. Those from lower economic group and rural area are not as much exposed to such food habits, and they do not buy them because they are expensive for their pocket. Many adolescents fail to brush their teeth effectively and tend to consume cariogenic foods even though they have basic knowledge of dental health. Children who have caries eat snacks between meals, more than those children without dental caries do. The basic means of avoiding these primary public health measures are compiled with the use of topical fluorides and fluoridated water. When it comes to nutrition perspective, one of the main things is to have balanced diet and adherence to the dietary guidelines and the dietary reference intakes.
1.1 The dental caries process
Dental caries occurs due to the demineralization of enamel and dentin (the hard tissues of the teeth) by organic acids formed by bacteria in dental plaque through the anaerobic metabolism of sugars and other fermentable carbohydrates derived from the diet [1]. Organic acids increase the solubility of calcium hydroxyapatite in dental hard tissues, and demineralization process of the tooth surface occurs due to calcium loss.
Teeth are most susceptible to dental caries soon after they erupt, and therefore the peak ages for dental caries are 2–5 years for the deciduous dentition and early adolescence for the permanent dentition [2]. The age of adolescences is when permanent teeth begin to grow and get their full position in the dental arch. This is a crucial age for the development of several oral diseases. Dental caries, periodontal disease, and orthodontic problems such as overcrowding of the teeth or malocclusions are bringing changes and altering the facial profile and esthetic appearance.
Certain psychological factors like self-confidence and social outlook of the individuals can also be affected, and they can leave permanent effect on the psychology of the child if not appropriately treated.
Neglecting the general problems, the lack of awareness and expertise is one of the reasons that most of the children at this age face these problems. Since the treatment of dental disease is very expensive especially in low-income countries, it would exceed the available resources for health care. The large financial benefits of preventing dental diseases should be emphasized to countries where current disease levels are high [3].
1.2 Effects of dental caries
It is undisputable that the development of dental caries is a result of poor diet, and it has been observed in humans and animals that frequent and prolonged exposure to carbohydrates and sugars results in an appearance of dental caries. Important bacteria in the development of dental caries are Streptococcus mutans and Streptococcus sobrinus. These bacteria produce organic acids from food sugars and help bacterial colonization of the tooth surface. The bacteria attached to teeth in dental plaque, found as a thin film on the surface of the enamel, utilize mono- and disaccharides (e.g., glucose, fructose, and sucrose) to produce energy, and acid is the by-product of this metabolism.
Consequently, the acidity of dental plaque may decrease to a point where the demineralization of the tooth begins. Demineralization occurs at a low pH when the oral environment is undersaturated with mineral ions, relative to a tooth’s mineral content. The enamel crystal, which consists of carbonated apatite, is dissolved by organic acids (lactic and acetic) that are produced by the cellular action of plaque bacteria in the presence of dietary carbohydrates. The “white spot lesion” is the initial stage that occurs just below the enamel surface and produces a visual whitening of the tooth. At this stage of mineral loss, the lesion may not progress any further or could even regain minerals (i.e., remineralize) if the cariogenic environment diminishes. The prevention measures that can remineralize the initial carious lesion are as follows: decreasing the carbohydrate source to the bacteria, treating the tooth with fluoride, reducing the levels of cariogenic bacteria, or reducing the bacterial ability to produce acid.
The initial lesion will continue to lose mineral if the procedure of disease suppression is not initiated and the acidic challenge is unabated. The progressive dissolution of enamel and loss of enamel surface structure eventually give rise to a frank carious lesion [4]. Sugary food products and their everyday consumptions exert our teeth. The reasons behind dental caries are the exposure to junk foods, colas, sweets, and other dietary products which are easy to access and abundantly available for children to consume. That is why dental caries is like a sort of non-transmittable and nonfatal sickness [5].
1.3 Dietary factors in the initiation and progression of dental caries
Some authors emphasize the importance of the dental biofilm and dietary sugars as essential primary etiological factors causing the appearance of the caries; moreover, one of them cannot cause caries in the absence of the other.
The main direct impact of the diet is mediated through its effect on the pH of the dental biofilm. Foods high in fermentable carbohydrates (mainly sugars) cause a low biofilm pH, while foods high in proteins and fats favor a more neutral biofilm pH. High-protein foods increase the urea concentration of saliva, which can be converted by ureolytic bacteria to ammonia; this raises the biofilm pH and is associated with decreased caries risk. Dietary factors can have an indirect effect by modifying the composition and metabolic activity of dental biofilm.
The major dietary factor affecting dental caries prevalence and progression is sucrose [6]. A low consumption example is from a study of the Hopewood House in Australia, conducted between 1947 and 1952. As a matter of fact, children living in this closely supervised environment consumed food that was virtually free of sugar and white flour products. Data collected from these children revealed an extremely low dental caries prevalence, compared to children attending other Australian schools [7].
High sugar consumption’s effect is best revealed from the report of the classic Vipeholm study [8]. This study examined three factors leading to these stages as follows: the timing of sugar ingestion, the effects of the frequency of sugar consumption, and finally the consistency of the sugar on dental caries rates. According to the results, the degree of the sugar’s consistency was more important than the addition of sugar to the diet and especially if it was consumed between meals, or products, which are sticky, in a form that stayed longer in the mouth such as toffees. These products have a bigger cariogenicity impact than foods that are eliminated quickly from the oral cavity. Therefore, frequent ingestion of foods such as hard candies and throat lozenges that contain fermentable carbohydrates can be extremely harmful to the teeth. The conclusions from this study, conducted a half century ago, are still well regarded today:
If sugar is taken with meals, then only a small caries increase is noted.
A marked increase in caries increment is shown if sugar is consumed as snacks between meals.
If you consume sticky candies containing sugar, then the caries activity will be at the highest form.
Caries activity may vary greatly among individuals.
By eliminating sugar-rich foods, caries activity will be declined.
The detrimental effects of sugar in causing tooth decay are shown in the two major studies of public health importance, and those are the classic Vipeholm study in Sweden and Hopewood House study in Australia. Children generally consume diets which are rich in sugar like sweets, candies, cakes, colas, etc. That is why a lot of awareness has been raised since this food has a negative effect on oral health, and that is the appearance of dental caries. Nowadays, the household food that we generally eat contains certain amounts of sugar. That is why these two studies are of huge public health importance when conducting preventive dental health programs especially in schools where the drawbacks of consuming such diet containing sugars can be addressed.
1.4 Food products that play a main role in the development of dental caries
A direct relationship between dental caries incidence and sugar (carbohydrates) intake is indisputed. The caries will not be developed if there are no fermentable carbohydrates in the food [9].
Free sugars as defined by the World Health Organization present as monosaccharides and disaccharides added to food, and sugars are naturally present in honey, syrups, and fruit juices. Fermentable carbohydrates are free sugars, glucose polymers (syrups and maltodextrins), fermentable oligosaccharides, and highly refined starches. They are added to food in industrialized countries and are as acidogenic as sucrose. However, sucrose and starches today present as the main carbohydrates in modern society diet. Sucrose is the most cariogenic sugar which is a highly soluble substrate transformed into intracellular (IPS) and extracellular polysaccharides (EPS). It diffuses easily into the dental plaque accumulation and induces a lower pH [10]. Starch is a carbohydrate that can cause very small amounts of caries, unlike real sugar. It is found in fruits and vegetables and can be consumed raw or cooked. Starchy foods such as rice, potatoes, pasta, and bread have very low cariogenicity, and this is why they can cause less caries than sucrose. Starch can be sorted out to mono- and disaccharides and metabolized by bacteria, so it is retained on the teeth long enough to be hydrolyzed by salivary amylase.
Since the original Miller’s study, Stephan in both of his researches (1940, 1944) about the relationship between caries and sugar showed that fermentable carbohydrates can transform into acid in dental plaque. A direct relationship between caries incidence and the frequency of consumption of sweets was also presented [11], and these findings supported those of the Vipeholm study [12].
Sucrose is freely diffusible in dental biofilm and metabolized by oral bacteria Streptococcus mutans [13]. Bacteria metabolize sucrose to soluble and insoluble extracellular polysaccharide glucan by enzyme glucosyltransferases (GTFs). Few mechanisms are involved in the role of extracellular glucans as the major caries associated factor. Glucan enables the bacteria to adhere firmly to the teeth [14], and in dental plaque, they contribute to the structural integrity of dental biofilms [15].
Several studies showed that the presence of insoluble glucan enhanced the demineralization potential of S. mutans. Glucan altered the diffusion properties of plaque and allowed deeper penetration of dietary carbohydrates [16, 17].
There are several important and critical cariogenic factors to be considered when evaluating starch and caries relationship. They are the size and frequency of tooth exposure, the bioavailability of the starches, the microbial flora of dental plaque, the pH-lowering capacity of dental plaque, and the flow rate of saliva. Starchy foods with higher amounts of sucrose are as cariogenic as а sucrose. Some cooked and processed starches are dissolved by salivary amylase, and they release glucose and maltose metabolized by oral bacteria to acids. In Rugg-Gunn [18] study, the relationship between starches and dental caries was proved, and several conclusions were made. Rice, potatoes, bread, and cooked staple starchy foods have low cariogenicity in humans. Uncooked starch has low cariogenicity, while heat-treated starch induces lesser caries than sugars. Foods with cooked starch and higher amounts of sucrose are as cariogenic as similar quantities of sucrose.
Fresh fruits contain various sugars and may be capable of causing caries under some conditions. They have low cariogenicity, while citrus fruits have not been associated with dental caries. Increased consumption of fresh fruit in the diet is decreasing the level of dental caries in a population [19]. Although excessive exposure to fructose may produce dental caries, fresh fruits are likely to be much less cariogenic than most sucrose-rich snack foods consumed by children. One hundred percent fruit juice has also been associated with caries, but the relationship is less clear. Children consuming more than 17 oz. 100% juice are more likely to have caries, than children consuming water or milk [20]. Conversely, in a cohort of low-income African-American children, 100% fruit juice was found to be protective of caries. The fact that 100% fruit juice contains about the same amount of sugar as the average sugar-sweetened beverages made it important to understand its role in caries [21]. Animal studies revealed that all fruits cause less caries than sucrose but dried fruits may potentially be more cariogenic since the drying process breaks down the cellular structure, releasing free sugars that tend to have a longer oral clearance.
Flavored drinks, especially aerated beverages like cola, have a much greater cariogenic potential due to high sugar content and regular consumption. Children are frequently offered with these drinks because of their high acceptance, low cost, and parent’s belief of being very nutritious [22]. Different campaigns and various forms of advertising by the media changed public health knowledge, and people started to become aware and understand about the bad effect of this kind of food.
Milk is most frequently consumed by schoolchildren. In milk а sugar named lactose is not fermented as the other sugars, so it is less cariogenic because the phosphor proteins inhibit enamel dissolution and the milk antibacterial factors may interfere with the oral microbial flora.
Cheese can lead to protection against creating caries as it stimulates salivary flow and raises the calcium, phosphorus, and protein content of plaque.
The sugar alcohols like sorbitol, mannitol, and xylitol are kind of sweeteners that are metabolized by bacteria at much slower rate than glucose or sucrose, which is not metabolized at all. According to certain clinical studies, xylitol chewing gum has the ability to reverse initial white spot lesions on teeth.
When dental decay happens there is high probability of losing a tooth. That leads to a reduced ability to eat a varied diet. It is in particular associated with a low consumption of fruits, vegetables and non-starch polysaccharides (NSP) in the persons diet [23]. NSP intakes of less than 10 g/day and fruits and vegetable intakes of less than 160 g/day have been reported in edentulous subjects. Therefore, tooth loss may impede the achievement of dietary goals related to the consumption of fruits, vegetables, and NSP. Tooth loss has also been associated with loss of enjoyment of food and confidence to socialize. So, basically, it is clear that dental diseases have a detrimental effect on the quality of life both in childhood and older age [24].
1.5 Eating between meals
An important issue for the appearance of dental caries in older children as well as infants is not only the total quantity but also the form of the carbohydrate as well as the frequency of consumption since the refined carbohydrates exert their effect in the appearance of dental caries by serving as a substrate for caries-producing streptococci, which as a small piece of it adheres to the teeth for almost an hour. In the case of sugars that are not in sticky form, a specified amount consumed at one time is likely to be less conducive to the formation of dental caries than the same amount consumed in small portions throughout the day. There is considerable evidence that between-meal snacks cause the development of dental caries. Foods that must be avoided between meals are the following: sugar, honey, corn syrup, candies, jellies, jams, sugared breakfast cereals, cookies, cakes, chewing gum, and sweetened beverages, including flavored kind of milks, carbonated drinks, sweetened fruit juices, and fruit or fruit-flavored drinks. Finally, eating frequency, particularly constant grazing or sipping of foods and beverages, is also caries promoting. In a recent study in a diverse sample of children aged 2 to 6 years, eating frequency was associated with severe early childhood caries [25].
1.6 Dietary fluoride and water fluoridation
Reduction of dental caries can be achieved with the help of fluoride or in other words dietary fluoride drinking water, which also has rich sources. The ingested fluoride becomes incorporated into enamel during tooth formation and increases the resistance of the tooth to decay. However, the main protection from dietary fluoride is the localized intraoral effect. Fluoride promotes the remineralization of damaged enamel with resistant fluorapatite and also inhibits bacterial metabolism of sugars. As we can see, the benefits to the exposure of teeth to fluoride are therefore beneficial lifelong. It may be added to an optimum concentration of 1 mg/L as a caries preventive measure if natural water supplies are low in fluoride; Murray et al. [26] have reviewed the published data on the effect of water fluoridation on caries and have concluded that on average water fluoridation reduces dental caries by 50%. In a study of 5-year-old children, Carmichael et al. have demonstrated that water fluoridation is effective in reducing dental caries across social classes and, in terms of the number of teeth saved per child, the benefits are greatest in the lower social classes [27].
According to UK national surveys, it has been indicated that those from lower social classes have higher levels of dental diseases and poorer oral hygiene practice and are less likely to visit the dentist [28]. In these cases, dental caries is not eliminated even though the benefit of fluoride is reducing caries. Fluoride repairs the damage caused by acids produced by plaque bacteria but does not remove the cause of caries, i.e., dietary sugars. The process of prevention requires both a reduction in sugar intake as well as optimum exposure to fluoride. Very extensive and comprehensive research by the National Health Survey concluded that a preventive dentistry program is water fluoridation.
1.7 Dietary advice
Dietary advice by dental health professionals should be consistent and not conflict with the advices from other health professionals, based on the evidence in the various professional fields and based on the national dietary guidelines. The advices may be more readily accepted from the people when the oral healthcare professionals can make unequivocally clear that the advice benefits caries prevention. If not, the person may not understand why the dental professional interferes with his diet and not accept the advices. However, this does not dismiss the dental professional from also explaining the benefits for general health on limiting or reducing the intake of sugars. Under the premise that it benefits oral health, the dental health professional can make stronger restrictions than the general guidelines as long as they do not harm general health. Generally speaking a diet that is beneficial to both general and dental health is one that is low in free sugars, saturated fat, and salts, as well as high in fresh fruits, vegetables, nuts and seeds, and wholegrain carbohydrates with modest amounts of legumes, fish, poultry, and lean meat and plenty of fluids preferably water and milk and, thus, modest with sugar sweetened beverages [29].
2. Saliva and oral health
The teeth and oral mucosa are cleaned with the help of saliva, which is a mixed glandular secretion. Saliva by itself is consisted of three glands, and they are as follows: submandibular, sublingual, and finally the parotid. It also has hundreds of small glands inside the oral mucosa and submucosa as well as gingival cervical fluid.
The maintenance of healthy teeth and oral tissues could be achieved only with the help of saliva’s presence. If there were a severe reduction of the saliva’s production, then there would be a very fast deterioration of oral health as well as the patient’s life. The results from such a condition could lead to eating difficulties like: swallowing difficulties, bad oral hygiene, dental caries that progresses very fast, mucosa’s burning sensation, difficulty in talking, wearing denture, oral infections like Candida, and ulceration of oral mucosa.
Dry mouth is a problem, which appears in huge proportions. Xerostomia or in other words dry mouth is very common for people with Sjogren’s syndrome, as a result of radiotherapy in the head and neck in cancer treating and especially in the case of older generations when they are prescribed with drugs. The saliva’s role in oral health is huge especially taking into consideration the sicknesses that appear because of decreased quantity or quality of saliva. That is why it is very important to early diagnose and prevent this condition.
Saliva is considered as the most easily available diagnostic fluid for noninvasive collection and analysis because through it we can diagnose caries susceptibility, systemic, physiological, and pathological, and we can monitor the level of hormones, drugs, antibodies, microorganisms, and ions.
In this research, we will try to present the main functions of saliva, the anatomy and histology of salivary glands, the physiology of saliva formation, the constituents of saliva, and the use of saliva as a diagnostic fluid, including its role in caries risk assessment.
2.1 Saliva’s functions
Saliva has several functions which are very protective, but it has also other functions presented in Figure 1. Salivary function can be organized into five major categories that serve to maintain oral health and create an appropriate ecologic balance: (1) lubrication and protection, (2) buffering action and clearance, (3) maintenance of tooth integrity, (4) antibacterial activity, and (5) taste and digestion [30].
Figure 1.
Functions of saliva.
Figure 2 presents the changes in plaque pH following as a result of sucrose rinse. The graphs are named as Stephan’s curve according to the name of the scientist who was the first one who described it in 1944. By using antimony probe microelectrodes in a series of experiments, he also measured changes in plaque pH.
Figure 2.
Stephan’s curve illustrating the changes in plague pH over time following a sucrose rinse.
The unstimulated plaque pH in Figure 2 is approximately 6.7. After the process of sucrose rinse, the plaque pH within a few minutes is reduced to less than 5.0. When the enamel is below the critical pH 5.5, then there is demineralization of the enamel. For about 15–20 min, plaque pH stays below the critical pH and does return to normal for about 40 min. In the presence of saliva and other fluids that are supersaturated with the help of hydroxyapatite and fluorapatite, the enamel itself could be remineralized only when the plaque pH recovers to a level above the critical pH.
The buffering capacity, the degree of access to saliva, the velocity of the salivary film, and the saliva’s urea content are the ones that determine the variation of the shape of Stephan’s curve among individuals and the rate of recovery of the pH plaque.
The major buffer in stimulated saliva is the carbonic acid/bicarbonate system. As the bicarbonate ion concentration gets higher, also the buffering capacity of saliva increases.
2.2 Saliva as a diagnostic fluid
2.2.1 General diagnostics
Nowadays for the study of bacteria, proteins, and genes, there are very high-level techniques where they apply saliva in order to spread out the field of oral diagnostics in the process of learning and understanding the oral diseases, systemic diseases, as well as metabolism. Saliva by itself presents an opportunity for the identification of biomarkers for the diseases like dental caries, periodontal diseases, and oral diseases, but all this should be easily done with careful collection and handling.
2.3 Caries risk assessment
There have been developed a series of caries risk assessment tests based on saliva’s measurements. These tests measure the capacity of salivary buffering and salivary mutans streptococci and lactobacilli. The increased risk of developing caries comes because of high levels of mutans streptococci, i.e., >105 colony-forming units (CFUs) per mL of saliva. Individuals with high levels of lactobacilli (>105 CFUs per mL saliva) are the ones who consume frequently carbohydrates, and because of that they have an increased risk of caries.
As an answer to the question what is buffering capacity, one could answer that it is the host’s capability to neutralize reduction pH’s plaque constructed by acidogenic organisms. Useful caries indicators for monitoring, preventive measures, and profiling patient’s disease are the salivary tests.
Table 1 lists some salivary variables measured for caries risk assessment in dentistry, which are more used for measurement than the other types.
Fluid/lubricant
It coats hard and soft tissue. Helps to protect against mechanical, thermal, and chemical irritation and tooth wear. Assists smooth air flow, speech, and swallowing.
Ion reservoir
Solution supersaturated with respect to tooth mineral facilitates remineralization of the teeth. Acidic proline-rich proteins and statherin in saliva inhibit spontaneous precipitation of calcium phosphate salts.
Buffering action and clearance
Helps to neutralize plaque pH after eating, thus reducing time for demineralization.
Mechanical function of cleaning the tooth surface
Clears food and aids swallowing.
Antimicrobial activity
Specific (e.g., sIgA) and non-specific (e.g. lysozyme, lactoferrin, and myeloperoxidase) anti-microbial mechanisms help to control the oral microflora.
Digestion
The enzyme α-amylase is the most abundant salivary enzyme; it splits starchy foods into maltose, maltotriose, and dextrins.
Protective remineralization (promoted by fluoride)
Saliva also inhibits caries by protective remineralization. This is promoted by fluoride ions in saliva.
Table 1.
Salivary variables measured for caries risk assessment.
While either measuring unstimulated or stimulated saliva’s flow rates, we should bear in mind the conditions of saliva’s collection process. When measuring unstimulated flow, which is usually at rest, repeated measurements should be assessed during the same day as a result of circadian rhythm and also because chewing (mechanical) and citric acid (gustatory) produce different results.
The best way of measuring unstimulated or stimulated saliva is using commercial kit. When it comes to buffering capacity of unstimulated saliva which is lower or stimulated saliva, they are very easily measured at the chairside. In order to do bacteriological tests as chewing dislodges the flora into the saliva, then the best way is to use paraffin wax-stimulated saliva samples. From stimulated saliva samples, you can culture mutans streptococci and lactobacilli. Their measurements could also be facilitated with the help of commercially available chairside tests. However, when it comes to fluoride, calcium, and phosphate biochemical measurement, then these must be done with the help of special laboratory facilities that are not available to practitioners.
2.4 Unstimulated saliva
As an answer to the question what is unstimulated whole saliva, one could answer that it is the mouth’s secretion mixture with tastants or chewing in the absence of exogenous stimuli. It is composed of parotid, submandibular, and sublingual secretions as well as the minor mucous glands, but it also contains desquamated epithelial cells, gingival crevicular fluid, leucocytes (mainly from the gingival crevice), bacteria, and possibly food residues, blood, and viruses.
The collection of saliva from the patient is done in that way that the patient spits out saliva in regular intervals of time without swallowing it, and there is another way when the patient keeps his or her head down and mouth just a bit open so that saliva can drip down from the mouth into a beaker during a time interval. However, one should bear in mind that when saliva is spit down, the number of desquamated epithelial cells as well as bacteria are increased. The difference between the secreted amount by the different salivary glands and the evaporated volumes is the measured flow rate. The unstimulated salivary flow rates in healthy individuals and the average value for whole saliva is about 0.3–0.4 mL/min. Patients say that they have dry mouth (xerostomia) only when saliva is almost completely absent. Objective evidence of hyposalivation is considered a flow rate of <0.1 mL/min.
Dentists should also measure salivary flow as part of their regular examination so that when patients complain of dry mouth, they will have the tests. The usual problems are related to swallowing difficulty that often leads to individuals with very little saliva but without discomfort and others with saliva flow rates within the normal range who feel that their mouth is drowning in saliva.
2.5 Stimulated saliva
Stimulated saliva is produced in response to a mechanical, gustatory, olfactory, or pharmacological stimulus, contributing to around 40–50% of daily salivary production. Several studies of stimulated salivary flow rates have been done in healthy populations and show a wide variation among individuals. The salivary flow (SF) index is a parameter allowing stimulated and unstimulated saliva flow to be classified as normal, low, or very low (hyposalivation). In adults, normal total stimulated SF ranges 1–3 mL/min, and low ranges 0.7–1.0 mL/min, while hyposalivation is characterized by a stimulated SF <0.7 mL/min. Many factors influence the stimulated salivary flow rate which, for whole saliva, has an average maximum value of about 7 mL/min.
2.5.1 Mechanical stimuli
Eating is a strong stimulus for the secretion of saliva by the major salivary glands. Large volumes of saliva are secreted before, during, and after eating via the gustatory-salivary reflex, masticatory-salivary reflex, olfactory-salivary reflex, and esophageal-salivary reflex. The action of chewing, in the absence of any taste, will stimulate salivation to a smaller degree than maximum gustatory stimulation with citric acid. Mastication also serves to mix the contents of the mouth, thus increasing slightly the distribution of the different types of saliva around the mouth. Mechanical stimulation of the fauces (the gag reflex) leads to increased salivation.
2.5.2 Gustatory and olfactory stimuli
Acid is the most potent of the five basic taste stimuli, the other four being salty, bitter, sweet, and umami. A study performed with different concentrations of citric acid revealed that 5% citric acid stimulated an average maximum salivary flow rate of about 7 mL/min. The citric acid was continuously infused into the mouth, and the teeth were covered with a paraffin film to protect them against the acid. For a clinical evaluation of the residual secretory capacity in patients with hyposalivation, a 3% citric acid solution can be applied to the patient’s tongue at regular intervals so that the degree of stimulation is relatively standardized. If a gustatory stimulus is held in the mouth without movement, salivary flow decreases to nature of stimulus gland size, mechanical unilateral stimulation, gustatory vomiting, pharmacological olfaction, food intake smoking, and gag reflex.
Dawes [31] has stimulated the flow of saliva alters its composition and noted that the rate of salivary flow increases the concentration of protein, sodium, chloride, and bicarbonate and decreases the concentration of magnesium and phosphorus. Perhaps of greatest importance is the increase in the concentration of bicarbonate, which increases progressively with the duration of stimulation. The increased concentration of bicarbonate diffuses into the plaque, neutralizes plaque acids, increases the pH of the plaque, and favors the remineralization of damaged enamel and dentin.
2.6 Saliva’s buffering ability
Buffer solutions are solutions that maintain an approximately constant pH when small amounts of either acid or base are added or when the solution is diluted. These solutions own the capacity of resisting changes of pH when either acids or alkalis are added to them. There are three possible buffer systems in saliva—the carbonic acid/bicarbonate system, the phosphate system, and the proteins.
2.6.1 Bicarbonate
Bicarbonate is one of the most important systems in saliva, which is produced by dental plaque, and its concentration could be from less than 1 mmol/L in unstimulated parotid saliva to a very high flow rate of 60 mmol/L which is elicited by chewing gum thus having a bicarbonate concentration of about 15 mmol/L. The level of bicarbonate ions in unstimulated saliva is too low to be an effective buffer. For those who suffer from the gastroesophageal reflux disease, the bicarbonate in saliva will help them in the clearance process of acid from the esophagus.
The carbonic acid/bicarbonate system is one of the components of the saliva that modifies the creation of caries. It does this by changing the environmental pH and possibly the virulence of bacteria that cause decay. Tanzer et al. [32] tasted the efficacy of a sodium bicarbonate-based dental power and paste with the addition of fluoride on dental caries and on Streptococcus sobrinus or Streptococcus mutans recoveries in rats. These authors observed that the caries reductions in these studies ranged from 42 to 50% in the rats treated with bicarbonate dentifrices when compared with rats treated with water [33, 34].
2.6.2 Phosphate
The concentration of phosphate in non-stimulated saliva is about 5–6 mmol/L, compared to a level of about 1 mmol/L in plasma; there is still too little phosphate in saliva to act as a significant buffer. The pH of unstimulated saliva is less than the pK2 value of 7.2 for phosphate so that most of the phosphate is present as H2PO4− and cannot accept another hydrogen ion until the pH is close to 2.1, the pK1 for phosphate.
2.6.3 Proteins
In saliva’s plasma there is about one-thirtieth protein concentration as well as few amino acids with acidic or basic side chains which present an important buffering effect at the usual pH of the oral cavity.
2.6.4 pH
When the bicarbonate concentration increases, the salivary pH increases too. Henderson and Hasselbalch give the equation of the relationship between the pH and the bicarbonate concentration, which is pH = pK + log[HCO3−]/[H2CO3], in which the pK (about 6.1) and [H2CO3] (about 1.2 mmol/L) are virtually independent of the flow rate. The latter is in equilibrium with the pCO2 which, in saliva, is about the same as that in the venous blood. If we try to measure the pH of saliva, then it is very obligative to avoid exposure of the saliva to the atmosphere because the pH will be artificially elevated and CO2 will be released. At very low flow rates, the pH of parotid saliva can be as low as 5.3, rising to 7.8 at very high flow rates. Because of the low bicarbonate concentration, patients with hyposalivation will have a low salivary buffering capacity and a low salivary pH (Figure 3).
Figure 3.
The effects of flow rate on the concentrations of some components of saliva.
2.6.5 Urea
The importance of salivary urea was acknowledged early in dental literature [35, 36]. The pH-raising effect of intraoral urea application was first described by Stefan [37]. This author found that in both in vivo and in vitro, urea could raise plaque pH up to pH 9 and that the addition of 40–50% urea to carbohydrates largely overcame the pH-lowering effect for up to 24 h. The value of salivary urea ranges from 2 to 6 mmol/L.
Urea possesses the capability to inhibit the metabolism and multiplication of bacteria in the saliva, which indirectly neutralizе the acids in the oral environment and maintain the salivary acidobasic balance due to its buffer capacity [37, 38].
Less aciduric oral bacteria (Streptococcus sanguinis and Streptococcus gordonii) associated with dental health have the ability for alkali generation by hydrolyzing urea or arginine to ammonia. Production of ammonia is a mechanism that influences the balance remineralization-demineralization of the tooth, maintains neutral pH in oral cavity, and prevents the appearance of a cariogenic microflora [39, 40].
Urea can be used as a constituent of chewing gums for neutralized acids. Imfeld [41] explored the effect of sugar-free chewing gums containing various amounts of urea on the pH recovery in dental plaque.
After rinsing the mouth with 10 or 50% (w/v) sucrose solution, the respondents chewed the gum with different content of urea (10, 20, 30 mg) for 10 min. Increased value of salivary or plaque pH was found in the first minutes of chewing, and the effect of urea continued and lasted over 10 min. The higher concentrations of urea in chewing gum resulted in a faster leveling of the pH. As a result, the highest values of pH in the examined groups were observed in cases where they were treated with chewing gum containing 30 mg urea. With the use of such chewing gum, the salivary pH value does not fall below the level which is risky for the occurrence of dental caries, and there is a positive effect of chewing on the salivary flow that also affects neutralizing the acids in saliva or plaque [42, 43]. For the purpose of demonstrating the effect it can have on unstimulated saliva, a mathematical model of the influence of salivary urea on dental plaque was constructed. Data from study indicated that urea present in unstimulated saliva has a significant effect on plaque pH by elevating and counteracting the fall of plaque pH in the fasting state. The correlation of higher salivary urea concentrations and low salivary caries activity was registered in patients with chronic renal disease. These patients, who have elevated salivary urea concentration, have a reduced incidence of dental caries [44].
2.6.6 Calcium and phosphate concentrations
Saliva contains a supersaturated solution of calcium and phosphate, which neutralizes acids. Some epidemiological studies have revealed that humans with relatively high Ca and P in their plaque experience correspondingly lower caries. Higher Ca concentration of plaque is associated with low caries incidence. The process of undersaturation of the saliva with respect to tooth mineral content is a result of decreasing total phosphate concentration at high flow rates which would be bad for the teeth.
However, if the flow rate increases, then the saliva’s pH increases together with the bicarbonate concentration, and therefore high pH is altered. In the proportions of four different phosphate species (H3PO4, H2PO4−, HPO42−, and PO43) together with the fall in total phosphate concentration, there is a fall in H2PO4− and a slight increase in HPO42− but a dramatic increase in PO43−, all as a result high pH. It is the PO43− that is an important ionic species with respect to the solubility of tooth mineral. So, although the total level of phosphate falls with increasing flow rate, the concentration of PO43− actually increases as much as 40-fold when flow rate increases from the unstimulated level to high flow rates. The three components (Ca2+, PO43−, and OH−) increase with salivary flow if taking into consideration the components of the ion product determining the solubility of tooth mineral in saliva. The saliva is more effective in reducing demineralization and promoting remineralization of the teeth if the flow rate is higher as well as the potential for calculus formation.
3. Conclusion
It can be concluded that tooth decay is a disease of great importance for general health. As a result, strategies to reduce the risk for dental caries are extremely important. The strategies may involve decreasing the growth or activity of bacteria especially S. mutans. To do so, people need to change their daily diet. Parents should advise children to avoid eating between meals, especially food containing carbohydrate.
Diet and oral microflora are connected to caries along with host factors such as salivary composition and flow.
Diet rich in fermentable carbohydrates is responsible for causing caries. Sucrose is one of the most cariogenic sugars, and glucose and fructose have also been shown to be less cariogenic. The cariogenic potential of carbohydrate-containing foods depends on their stickiness characteristics, frequency, and amount.
The saliva with its components plays an important role in maintaining oral, especially dental, health. Saliva is a natural factor that protects against demineralization. Apart from the activity of human saliva in diluting, clearing, neutralizing, and buffering acids, it also reduces demineralization and enhances the remineralization process.
Saliva performs its mechanical cleaning and protective functions though several physical and biochemical mechanisms. Saliva has buffer capacity which neutralizes acids in the mouth. The carbonic acid/bicarbonate system is the most important buffer in stimulated saliva.
The urea contributes to maintaining the acidobasic balance of saliva and thus affects the incidence of caries.
\n',keywords:"dental caries, diet, sucrose, saliva, salivary buffer",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/72145.pdf",chapterXML:"https://mts.intechopen.com/source/xml/72145.xml",downloadPdfUrl:"/chapter/pdf-download/72145",previewPdfUrl:"/chapter/pdf-preview/72145",totalDownloads:679,totalViews:0,totalCrossrefCites:1,dateSubmitted:"January 17th 2020",dateReviewed:"April 6th 2020",datePrePublished:"May 12th 2020",datePublished:"May 5th 2021",dateFinished:"May 12th 2020",readingETA:"0",abstract:"Diet and oral microflora are connected to caries along with host factors such as salivary composition and flow. The only component of the food with potentially cariogenic effect is fermentable carbohydratе sucrose. Sucrose is generally accepted as the most cariogenic dietary factor, and consumption of sucrose is associated with the frequency of dental caries in humans. Saliva is a biological environment, important for the physiology of the mouth. It achieves its mechanical functions of cleaning and protection through various physical and biochemical mechanisms. Bicarbonates, phosphates, and proteins have a buffer role in the saliva environment. Other compounds or enzymes in this group acting as prophylactic buffers are urea, salivary amylases, and fluorides.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/72145",risUrl:"/chapter/ris/72145",signatures:"Efka Zabokova Bilbilova",book:{id:"10126",type:"book",title:"Dental Caries",subtitle:null,fullTitle:"Dental Caries",slug:"dental-caries",publishedDate:"May 5th 2021",bookSignature:"Efka Zabokova Bilbilova",coverURL:"https://cdn.intechopen.com/books/images_new/10126.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",isbn:"978-1-83968-115-8",printIsbn:"978-1-83968-114-1",pdfIsbn:"978-1-83968-116-5",isAvailableForWebshopOrdering:!0,editors:[{id:"275097",title:"Associate Prof.",name:"Efka",middleName:null,surname:"Zabokova Bilbilova",slug:"efka-zabokova-bilbilova",fullName:"Efka Zabokova Bilbilova"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"275097",title:"Associate Prof.",name:"Efka",middleName:null,surname:"Zabokova Bilbilova",fullName:"Efka Zabokova Bilbilova",slug:"efka-zabokova-bilbilova",email:"efka_zabokova@hotmail.com",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/275097/images/system/275097.png",institution:{name:"University of Ss. Cyril and Methodius",institutionURL:null,country:{name:"Slovakia"}}}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_1_2",title:"1.1 The dental caries process",level:"2"},{id:"sec_2_2",title:"1.2 Effects of dental caries",level:"2"},{id:"sec_3_2",title:"1.3 Dietary factors in the initiation and progression of dental caries",level:"2"},{id:"sec_4_2",title:"1.4 Food products that play a main role in the development of dental caries",level:"2"},{id:"sec_5_2",title:"1.5 Eating between meals",level:"2"},{id:"sec_6_2",title:"1.6 Dietary fluoride and water fluoridation",level:"2"},{id:"sec_7_2",title:"1.7 Dietary advice",level:"2"},{id:"sec_9",title:"2. Saliva and oral health",level:"1"},{id:"sec_9_2",title:"2.1 Saliva’s functions",level:"2"},{id:"sec_10_2",title:"2.2 Saliva as a diagnostic fluid",level:"2"},{id:"sec_10_3",title:"2.2.1 General diagnostics",level:"3"},{id:"sec_12_2",title:"2.3 Caries risk assessment",level:"2"},{id:"sec_13_2",title:"2.4 Unstimulated saliva",level:"2"},{id:"sec_14_2",title:"2.5 Stimulated saliva",level:"2"},{id:"sec_14_3",title:"2.5.1 Mechanical stimuli",level:"3"},{id:"sec_15_3",title:"2.5.2 Gustatory and olfactory stimuli",level:"3"},{id:"sec_17_2",title:"2.6 Saliva’s buffering ability",level:"2"},{id:"sec_17_3",title:"2.6.1 Bicarbonate",level:"3"},{id:"sec_18_3",title:"2.6.2 Phosphate",level:"3"},{id:"sec_19_3",title:"2.6.3 Proteins",level:"3"},{id:"sec_20_3",title:"2.6.4 pH",level:"3"},{id:"sec_21_3",title:"2.6.5 Urea",level:"3"},{id:"sec_22_3",title:"2.6.6 Calcium and phosphate concentrations",level:"3"},{id:"sec_25",title:"3. Conclusion",level:"1"}],chapterReferences:[{id:"B1",body:'Arens U. 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Sugar restriction for caries prevention: Amount and frequency. Which is more important? Caries Research. 2019;53:168-175. DOI: 10.1159/000489571'},{id:"B29",body:'Moynihan P, Makino Y, Petersen PE, Ogawa H. Implications of WHO guideline on sugars for dental health professionals. Community Dentistry and Oral Epidemiology. 2018;46:1-7'},{id:"B30",body:'Leone WC, Oppenheim GF. Physical and chemical aspects of saliva as indicators of risk for dental caries in humans. Journal of Dental Education. 2001;65(10):1054-1062'},{id:"B31",body:'Dawes C, Dong C. The flow rate and electrolyte composition of whole saliva elicited by the use of sucrose-containing and sugar-free chewing-gums. Archives of Oral Biology. 1995;40:699-705'},{id:"B32",body:'Tanzer J, Grant L, McMahon T. Bicarbonate-based dental powder, fluoride and saccharin inhibition of dental caries associated with S. mutans infection of rats. Journal of Dental Research. 1988;67:969-972'},{id:"B33",body:'Bardow A, Moe D, Nyvad B, Nauntofte B. The buffer capacity and buffer systems of human whole saliva measured without loss of CO2. Archives of Oral Biology. 2000;45:1-12'},{id:"B34",body:'Bardow A, Hofer E, Nyvad B, Cate JM, Kirkeby S, Moe D, et al. Effect of saliva composition on experimental root caries. Caries Research. 2005;39:71-77'},{id:"B35",body:'Nauntofte B, Tenovuo JO, Lagerlöf F. Secretion and composition of saliva. In: Fejerskov O, EAM K, editors. Dental Caries The Disease and its Clinical Management. Oxford: Blackwell, Munksgaard; 2003. pp. 7-27'},{id:"B36",body:'Arends J, Jongebloed WL, Goldberg M, Schuthof J. Interaction of urea and human enamel. Caries Research. 1984;18:17-24'},{id:"B37",body:'Macpherson LMD, Dawes C. Urea concentration in minor mucous gland secretions and the effect of salivary film velocity on urea metabolism by streptococcus vestibularis in an artificial plaque. Journal of Periodontal Research. 1991;26:395-401'},{id:"B38",body:'Sjögren K, Ruben J, Lingstrom P, Lundberg AB, Birkhed D. Fluoride and urea chewing gums in an intra-oral experimental caries model. Caries Research. 2002;36:64-69'},{id:"B39",body:'Dawes C, Dibdin GH. Salivary concentrations of urea released from a chewing gum containing urea and how these affect the urea content of gel-stabilized plaques and their pH after exposure to sucrose. Caries Research. 2001;35:344-353'},{id:"B40",body:'Leone CW, Oppenheim FG. Physical and chemical aspects of saliva as indicators of risk for dental caries in human. Journal of Dental Education. 2001;65:1054-1064'},{id:"B41",body:'Imfeld T, Birkhed D, Lingstrom P. Effect of urea in sugar – Free chewing gums on pH recovery in human dental plaque evaluated with three different methods. Caries Research. 1995;29:172-180'},{id:"B42",body:'Raymond G, Schipper A, Erika Silletti A, Vingerhoeds MH. Saliva as research material: Biochemical, physiochemical, and practical aspects. Archives of Oral Biology. 2007;52:1114-1135'},{id:"B43",body:'Zabokova-Bibilova E, Sotirovska-Ivkovska A, Ambarkova V. Correlation between salivary urea level and dental caries. Contributions. 2012;33(1):289-302'},{id:"B44",body:'Dibdin GH, Dawes C. A mathematical model of the influence of salivary urea on the pH of fasted dental plaque and on the changes occurring during a cariogenic challenge. Caries Research. 1998;32:70-74'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Efka Zabokova Bilbilova",address:"efka_zabokova@hotmail.com",affiliation:'
Faculty of Dentistry, Department of Pediatric and Preventive Dentistry, “Ss. Cyril and Methodius” University, University Dental Clinic Center “St. Panteleimon”, Skopje, Republic of North Macedonia
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Samim Al Azad and Slimane Ed-dafali",coverURL:"https://cdn.intechopen.com/books/images_new/11392.jpg",editedByType:"Edited by",publishedDate:"May 11th 2022",editors:[{id:"418514",title:"Dr.",name:"Muhammad",middleName:null,surname:"Mohiuddin",slug:"muhammad-mohiuddin",fullName:"Muhammad Mohiuddin"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10400",title:"The Application of Ant Colony Optimization",subtitle:null,isOpenForSubmission:!1,hash:"f4fdfd07ee1ab99fb7c740d6d0c144c6",slug:"the-application-of-ant-colony-optimization",bookSignature:"Ali Soofastaei",coverURL:"https://cdn.intechopen.com/books/images_new/10400.jpg",editedByType:"Edited by",publishedDate:"May 11th 2022",editors:[{id:"257455",title:"Dr.",name:"Ali",middleName:null,surname:"Soofastaei",slug:"ali-soofastaei",fullName:"Ali Soofastaei"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10915",title:"Leadership",subtitle:"New Insights",isOpenForSubmission:!1,hash:"0d72e79892f2a020cee66a52d09de5a4",slug:"leadership-new-insights",bookSignature:"Mário Franco",coverURL:"https://cdn.intechopen.com/books/images_new/10915.jpg",editedByType:"Edited by",publishedDate:"May 11th 2022",editors:[{id:"105529",title:"Dr.",name:"Mário",middleName:null,surname:"Franco",slug:"mario-franco",fullName:"Mário Franco"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10683",title:"Technological Innovations and Advances in Hydropower Engineering",subtitle:null,isOpenForSubmission:!1,hash:"7ce7ad8768bd2cad155470fe1fd883f4",slug:"technological-innovations-and-advances-in-hydropower-engineering",bookSignature:"Yizi Shang, Ling Shang and Xiaofei Li",coverURL:"https://cdn.intechopen.com/books/images_new/10683.jpg",editedByType:"Edited by",publishedDate:"May 11th 2022",editors:[{id:"349630",title:"Dr.",name:"Yizi",middleName:null,surname:"Shang",slug:"yizi-shang",fullName:"Yizi Shang"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"7102",title:"Pneumonia",subtitle:null,isOpenForSubmission:!1,hash:"9fd70142814192dcec58a176749f1b60",slug:"pneumonia",bookSignature:"Nima Rezaei",coverURL:"https://cdn.intechopen.com/books/images_new/7102.jpg",editedByType:"Edited by",publishedDate:"May 11th 2022",editors:[{id:"116250",title:"Dr.",name:"Nima",middleName:null,surname:"Rezaei",slug:"nima-rezaei",fullName:"Nima Rezaei"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"9670",title:"Current Trends in Wheat Research",subtitle:null,isOpenForSubmission:!1,hash:"89d795987f1747a76eee532700d2093d",slug:"current-trends-in-wheat-research",bookSignature:"Mahmood-ur-Rahman Ansari",coverURL:"https://cdn.intechopen.com/books/images_new/9670.jpg",editedByType:"Edited by",publishedDate:"May 11th 2022",editors:[{id:"185476",title:"Dr.",name:"Mahmood-ur-Rahman",middleName:null,surname:"Ansari",slug:"mahmood-ur-rahman-ansari",fullName:"Mahmood-ur-Rahman Ansari"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},subject:{topic:{id:"1165",title:"Urologic Oncology",slug:"urologic-oncology",parent:{id:"204",title:"Urology",slug:"urology"},numberOfBooks:4,numberOfSeries:0,numberOfAuthorsAndEditors:93,numberOfWosCitations:10,numberOfCrossrefCitations:3,numberOfDimensionsCitations:8,videoUrl:null,fallbackUrl:null,description:null},booksByTopicFilter:{topicId:"1165",sort:"-publishedDate",limit:12,offset:0},booksByTopicCollection:[{type:"book",id:"10339",title:"Modern Approach to Diagnosis and Treatment of Bladder Cancer",subtitle:null,isOpenForSubmission:!1,hash:"d1fdae263fb8a59eef2795dc748a1155",slug:"modern-approach-to-diagnosis-and-treatment-of-bladder-cancer",bookSignature:"Francesco Ziglioli and Umberto Maestroni",coverURL:"https://cdn.intechopen.com/books/images_new/10339.jpg",editedByType:"Edited by",editors:[{id:"62240",title:"Dr.",name:"Francesco",middleName:null,surname:"Ziglioli",slug:"francesco-ziglioli",fullName:"Francesco Ziglioli"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6424",title:"Evolving Trends in Kidney Cancer",subtitle:null,isOpenForSubmission:!1,hash:"e9305ef1c5e6ad63407fd9262a27cf31",slug:"evolving-trends-in-kidney-cancer",bookSignature:"Sashi S. Kommu and Inderbir S. Gill",coverURL:"https://cdn.intechopen.com/books/images_new/6424.jpg",editedByType:"Edited by",editors:[{id:"9902",title:"Dr.",name:"Sashi S.",middleName:"S",surname:"Kommu",slug:"sashi-s.-kommu",fullName:"Sashi S. Kommu"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6423",title:"Prostate Cancer",subtitle:null,isOpenForSubmission:!1,hash:"d072a079624084c12169a118fdbbfa87",slug:"prostate-cancer",bookSignature:"Cem Onal",coverURL:"https://cdn.intechopen.com/books/images_new/6423.jpg",editedByType:"Edited by",editors:[{id:"43940",title:"Dr.",name:"Cem",middleName:null,surname:"Onal",slug:"cem-onal",fullName:"Cem Onal"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"5516",title:"Bladder Cancer",subtitle:"Management of NMI and Muscle-Invasive Cancer",isOpenForSubmission:!1,hash:"fa255c022acc85f2bd2c12ce4cd9a67b",slug:"bladder-cancer-management-of-nmi-and-muscle-invasive-cancer",bookSignature:"M. Hammad Ather",coverURL:"https://cdn.intechopen.com/books/images_new/5516.jpg",editedByType:"Edited by",editors:[{id:"88868",title:"Prof.",name:"M Hammad",middleName:null,surname:"Ather",slug:"m-hammad-ather",fullName:"M Hammad Ather"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}],booksByTopicTotal:4,seriesByTopicCollection:[],seriesByTopicTotal:0,mostCitedChapters:[{id:"54132",doi:"10.5772/67473",title:"Cross-Polarization OCT for In Vivo Diagnostics and Prediction of Bladder Cancer",slug:"cross-polarization-oct-for-in-vivo-diagnostics-and-prediction-of-bladder-cancer",totalDownloads:1079,totalCrossrefCites:1,totalDimensionsCites:3,abstract:"This chapter contains three parts covering recent efforts to increase the accuracy of optical coherence tomography (OCT) differential diagnostics of bladder pathologies. The first part compares the diagnostic efficacy of traditional OCT and cross-polarization OCT (CP OCT); CP OCT and fluorescence cystoscopy (FC) for detecting flat lesions in the bladder at the early stages of cancer. The second part contains a report on achievements in application of CP OCT for detection of recurrent carcinoma in the scar area that is a hardly distinguishable form of bladder cancer using an optimized CP OCT image analysis. The third part of the chapter reviews the results on CP OCT usage for in vivo diagnosis of the bladder cancer after radiation therapy of cervical cancer.",book:{id:"5516",slug:"bladder-cancer-management-of-nmi-and-muscle-invasive-cancer",title:"Bladder Cancer",fullTitle:"Bladder Cancer - Management of NMI and Muscle-Invasive Cancer"},signatures:"Elena Kiseleva, Gladkova Natalia, Streltzova Olga, Kirillin Mikhail,\nMaslennikova Anna, Dudenkova Varvara, Yunusova Katerina and\nSergeeva Ekaterina",authors:[{id:"68196",title:"Prof.",name:"Natalia",middleName:null,surname:"Gladkova",slug:"natalia-gladkova",fullName:"Natalia Gladkova"},{id:"191970",title:"Dr.",name:"Elena",middleName:null,surname:"Kiseleva",slug:"elena-kiseleva",fullName:"Elena Kiseleva"},{id:"191990",title:"Dr.",name:"Olga",middleName:null,surname:"Streltzova",slug:"olga-streltzova",fullName:"Olga Streltzova"},{id:"191992",title:"Mrs.",name:"Varvara",middleName:null,surname:"Dudenkova",slug:"varvara-dudenkova",fullName:"Varvara Dudenkova"},{id:"191993",title:"Prof.",name:"Anna",middleName:null,surname:"Maslennikova",slug:"anna-maslennikova",fullName:"Anna Maslennikova"},{id:"191994",title:"Dr.",name:"Katerina",middleName:null,surname:"Yunusova",slug:"katerina-yunusova",fullName:"Katerina Yunusova"},{id:"191995",title:"Dr.",name:"Mikhail",middleName:null,surname:"Kirillin",slug:"mikhail-kirillin",fullName:"Mikhail Kirillin"},{id:"193422",title:"Dr.",name:"Ekaterina",middleName:null,surname:"Sergeeva",slug:"ekaterina-sergeeva",fullName:"Ekaterina Sergeeva"}]},{id:"54019",doi:"10.5772/67309",title:"Bladder Cancer Markers and Recent Innovations",slug:"bladder-cancer-markers-and-recent-innovations",totalDownloads:1669,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"Bladder cancer (urothelial carcinoma) is the most common tumor of the urinary tract. It occurs more frequently among men about 65 years old on average. Two forms of the tumor are known: a non–muscle-invasive one and a muscle-invasive one. The latter turns out to be very aggressive with a survival of 5 years average. The non–muscle-invasive form frequently recurs (60–70%) and in 15% of cases, it progresses into the invasive form. The diagnosis is made mainly by cystoscopy and urine cytology. A high number of researches were dedicated in order to find a simple test using voided urine to frequently monitor possible tumor recurrence. During the last 10 years, many tests were proposed concerning either special proteins of which the most common are the bladder tumor antigen (BTA) and the nuclear matrix protein 22 (NMP22) or the presence of genetic mutations [most frequently, fibroblasts growth factor receptor 3 (FGFR3) and TP53], alteration of DNA methylation, chromatin structure and, more recently, the presence of specific micro-RNA. Recently the analysis of lipids present in voided urine showed a difference in fatty acids between healthy individuals and those affected by non-invasive forms. These markers appear to have a high specificity and sensitivity: a deepening of these results could lead to the development of a test that avoids invasive treatment and the cost of cystoscopy.",book:{id:"5516",slug:"bladder-cancer-management-of-nmi-and-muscle-invasive-cancer",title:"Bladder Cancer",fullTitle:"Bladder Cancer - Management of NMI and Muscle-Invasive Cancer"},signatures:"Mariapia Viola-Magni, Samuela Cataldi and Daniela Marocco",authors:[{id:"192375",title:"Prof.",name:"Mariapia",middleName:null,surname:"Viola-Magni",slug:"mariapia-viola-magni",fullName:"Mariapia Viola-Magni"},{id:"197851",title:"BSc.",name:"Samuela",middleName:null,surname:"Cataldi",slug:"samuela-cataldi",fullName:"Samuela Cataldi"},{id:"197852",title:"Dr.",name:"Daniela",middleName:null,surname:"Marocco",slug:"daniela-marocco",fullName:"Daniela Marocco"}]},{id:"54063",doi:"10.5772/67280",title:"Intravesical Chemohyperthermia for NMIBC: Rationale and Results of This Developing Treatment",slug:"intravesical-chemohyperthermia-for-nmibc-rationale-and-results-of-this-developing-treatment",totalDownloads:1368,totalCrossrefCites:0,totalDimensionsCites:1,abstract:"Bladder cancer is the fourth most common cancer in men, and the lifetime risk of getting bladder cancer is 2.4%. Approximately 75% of newly diagnosed cases of bladder cancer are non-muscle-invasive bladder cancer (NMIBC), and half of them will show recurrence and/or progression after transurethral resection. Therefore, after transurethral resection, in high-risk patients, intravesical therapy is mandatory. However, bacillus Calmette-Guérin (BCG) is associated with important side effects such as systemic tuberculosis and bladder retraction. Chemohyperthermia (CHT) has shown a 60% lower recurrence rate than standard mitomycin C (MMC). However, its effectiveness in high-risk patients, especially CIS and BCG refractory patients, is even more important. CHT will probably be an option for patients unsuitable for radical cystectomy or those on whom BCG can’t be used. Two main technologies are currently available for intravesical CHT: microwaves and recirculating heated fluids. Both of them have pros and cons that should be known and evaluated by a urologist. In this chapter, we will speak about rationale, technical options, clinical results, ongoing studies, and future perspective for this interesting treatment option for intermediate and high-risk patients with NMIBC.",book:{id:"5516",slug:"bladder-cancer-management-of-nmi-and-muscle-invasive-cancer",title:"Bladder Cancer",fullTitle:"Bladder Cancer - Management of NMI and Muscle-Invasive Cancer"},signatures:"Sousa-Escandón Manuel Alejandro, Flores Carbajal Javier, Sousa-\nGonzález Daniel and Rodriguez Gómez Silvia",authors:[{id:"191356",title:"Dr.",name:"Alejandro",middleName:null,surname:"Sousa-Escandón",slug:"alejandro-sousa-escandon",fullName:"Alejandro Sousa-Escandón"}]},{id:"54147",doi:"10.5772/67443",title:"Lymphadenectomy in Muscle Invasive Bladder Cancer",slug:"lymphadenectomy-in-muscle-invasive-bladder-cancer",totalDownloads:1234,totalCrossrefCites:0,totalDimensionsCites:1,abstract:"Bladder cancer is the second most common genitourinary malignancy with urothelial cancer comprising nearly 90% of primary bladder tumors. Urothelial carcinoma of the urinary bladder is the fifth most common malignancy in the United States, with an estimated 76,960 new cases and 163,900 deaths in 2016. Radical cystectomy with lymph node dissection remains the standard treatment for patients with muscle-invasive urothelial carcinoma of the bladder, and also for nonmuscle-invasive disease, refractory to intravesical therapy. The current approaches to pelvic lymph node dissections are based on the removal of lymph nodes most commonly harboring metastatic disease, notably the external iliac, obturator, and hypogastric lymph nodes. The boundaries for a standard pelvic lymph node dissection generally include the bifurcation of the common iliac vessels superiorly and the genitofemoral nerve laterally. Extended pelvic lymph node includes the removal of lymph nodes between the bifurcation of the common iliac vessels and the level of the aortic bifurcation, sometimes including distal aortic and caval nodes up to the level of the inferior mesenteric artery, as well as presacral nodes. Extended and superextended dissection has been reported to be associated with superior survival outcome.",book:{id:"5516",slug:"bladder-cancer-management-of-nmi-and-muscle-invasive-cancer",title:"Bladder Cancer",fullTitle:"Bladder Cancer - Management of NMI and Muscle-Invasive Cancer"},signatures:"Mustafa Ozan Horsanali and Kutan Ozer",authors:[{id:"59702",title:"Dr.",name:"Mustafa Ozan",middleName:null,surname:"Horsanali",slug:"mustafa-ozan-horsanali",fullName:"Mustafa Ozan Horsanali"},{id:"192699",title:"Dr.",name:"Kutan",middleName:null,surname:"Ozer",slug:"kutan-ozer",fullName:"Kutan Ozer"}]},{id:"59222",doi:"10.5772/intechopen.73515",title:"Development of Oncolytic Adenoviruses for the Management of Prostate Cancer",slug:"development-of-oncolytic-adenoviruses-for-the-management-of-prostate-cancer",totalDownloads:1079,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"Prostate cancer (PCa) is the fifth most common cause of cancer-related deaths in men globally. Androgen receptor (AR) signalling plays a vital role in initiation and progression and antiandrogens are standard of care first-line therapeutics. However, resistance frequently develops resulting in metastatic castration-resistant prostate cancer (mCRPC). Management of CRPC is currently chemotherapy and/or radiotherapy but is mostly palliative due to rapid development of resistance. The need for novel approaches to eliminate mCRPC is compelling; a promising option is replication-selective (oncolytic) adenoviruses with demonstrated efficacy in preclinical models of multidrug-resistant PCa. The safety of various viral mutants has been confirmed in numerous clinical trials with minimal toxicity in patients. Importantly, oncolytic adenoviruses synergise with the current standard of care for mCRPC even in treatment-resistant cells. In early phase I–II clinical trials, promising efficacy in patients with localised PCa was reported after intratumoural administration, and phase III trials are underway. To enable systemic delivery, for targeting of mCRPC, further developments are necessary because of the short half-life of the adenoviral mutants in human blood. Current progress in preventing the high-affinity binding of adenovirus to erythrocytes, hepatocyte uptake, and elimination by hepatic Kupffer cells will be described.",book:{id:"6423",slug:"prostate-cancer",title:"Prostate Cancer",fullTitle:"Prostate Cancer"},signatures:"Ahmed A. Ali and Gunnel Halldén",authors:[{id:"80427",title:"Dr.",name:"Gunnel",middleName:null,surname:"Hallden",slug:"gunnel-hallden",fullName:"Gunnel Hallden"},{id:"232386",title:"MSc.",name:"Ahmed",middleName:null,surname:"Ali",slug:"ahmed-ali",fullName:"Ahmed Ali"}]}],mostDownloadedChaptersLast30Days:[{id:"70881",title:"Robot-Assisted Partial Nephrectomy: Evolving Techniques",slug:"robot-assisted-partial-nephrectomy-evolving-techniques",totalDownloads:474,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Robotic-assisted partial nephrectomy is now embraced in urology as a recommended treatment option for small localised renal tumours. There is an increasing trend towards setting up robotic-assisted services in urological centres across the world. Our aim is to review the available published common robotic-assisted partial nephrectomy techniques. We present our institutions’ established step-by-step technique for performing robotic-assisted partial nephrectomy, in order to guide aspiring urologists interested in performing robotic-assisted partial nephrectomies. The importance of pre-operative review of imaging in a multi-disciplinary approach is critical. We emphasise certain tips inperforming a safer procedure.",book:{id:"6424",slug:"evolving-trends-in-kidney-cancer",title:"Evolving Trends in Kidney Cancer",fullTitle:"Evolving Trends in Kidney Cancer"},signatures:"Mohammed Kamil Quraishi, Edward Ramez Latif, Milan Thomas, Ben Eddy, Elio Mazzone and Alexandre Mottrie",authors:[{id:"277566",title:"Dr.",name:"Mohammed Kamil",middleName:null,surname:"Quraishi",slug:"mohammed-kamil-quraishi",fullName:"Mohammed Kamil Quraishi"},{id:"277570",title:"Dr.",name:"Milan",middleName:null,surname:"Thomas",slug:"milan-thomas",fullName:"Milan Thomas"},{id:"277571",title:"Dr.",name:"Ben",middleName:null,surname:"Eddy",slug:"ben-eddy",fullName:"Ben Eddy"}]},{id:"54132",title:"Cross-Polarization OCT for In Vivo Diagnostics and Prediction of Bladder Cancer",slug:"cross-polarization-oct-for-in-vivo-diagnostics-and-prediction-of-bladder-cancer",totalDownloads:1082,totalCrossrefCites:1,totalDimensionsCites:3,abstract:"This chapter contains three parts covering recent efforts to increase the accuracy of optical coherence tomography (OCT) differential diagnostics of bladder pathologies. The first part compares the diagnostic efficacy of traditional OCT and cross-polarization OCT (CP OCT); CP OCT and fluorescence cystoscopy (FC) for detecting flat lesions in the bladder at the early stages of cancer. The second part contains a report on achievements in application of CP OCT for detection of recurrent carcinoma in the scar area that is a hardly distinguishable form of bladder cancer using an optimized CP OCT image analysis. The third part of the chapter reviews the results on CP OCT usage for in vivo diagnosis of the bladder cancer after radiation therapy of cervical cancer.",book:{id:"5516",slug:"bladder-cancer-management-of-nmi-and-muscle-invasive-cancer",title:"Bladder Cancer",fullTitle:"Bladder Cancer - Management of NMI and Muscle-Invasive Cancer"},signatures:"Elena Kiseleva, Gladkova Natalia, Streltzova Olga, Kirillin Mikhail,\nMaslennikova Anna, Dudenkova Varvara, Yunusova Katerina and\nSergeeva Ekaterina",authors:[{id:"68196",title:"Prof.",name:"Natalia",middleName:null,surname:"Gladkova",slug:"natalia-gladkova",fullName:"Natalia Gladkova"},{id:"191970",title:"Dr.",name:"Elena",middleName:null,surname:"Kiseleva",slug:"elena-kiseleva",fullName:"Elena Kiseleva"},{id:"191990",title:"Dr.",name:"Olga",middleName:null,surname:"Streltzova",slug:"olga-streltzova",fullName:"Olga Streltzova"},{id:"191992",title:"Mrs.",name:"Varvara",middleName:null,surname:"Dudenkova",slug:"varvara-dudenkova",fullName:"Varvara Dudenkova"},{id:"191993",title:"Prof.",name:"Anna",middleName:null,surname:"Maslennikova",slug:"anna-maslennikova",fullName:"Anna Maslennikova"},{id:"191994",title:"Dr.",name:"Katerina",middleName:null,surname:"Yunusova",slug:"katerina-yunusova",fullName:"Katerina Yunusova"},{id:"191995",title:"Dr.",name:"Mikhail",middleName:null,surname:"Kirillin",slug:"mikhail-kirillin",fullName:"Mikhail Kirillin"},{id:"193422",title:"Dr.",name:"Ekaterina",middleName:null,surname:"Sergeeva",slug:"ekaterina-sergeeva",fullName:"Ekaterina Sergeeva"}]},{id:"61307",title:"Genetics in the Prostate Cancer",slug:"genetics-in-the-prostate-cancer",totalDownloads:1094,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Any disruption in the intracellular functions ranging from DNA transcription to protein ligand binding as well as intercellular communication may cause cellular transformation to malignant cell in the proper microenvironment when it could escape from the immune system. In this chapter, specifically, genetic alterations playing role in the prostate cancer are intended to be reviewed briefly under the subheadings of genomic instability and the hallmarks of cancer which are sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling the replicative immortality, inducing angiogenesis, activating invasion and progression to metastatic disease, reprogramming of the energy metabolism and evading immune destruction.",book:{id:"6423",slug:"prostate-cancer",title:"Prostate Cancer",fullTitle:"Prostate Cancer"},signatures:"Hikmet Köseoğlu",authors:[{id:"111496",title:"Dr.",name:"Hikmet",middleName:null,surname:"Köseoǧlu",slug:"hikmet-koseolu",fullName:"Hikmet Köseoǧlu"}]},{id:"54587",title:"Genital Organs‐Sparing Radical Cystectomy in Female Patients with Muscle Invasive Urothelial Carcinoma of the Bladder",slug:"genital-organs-sparing-radical-cystectomy-in-female-patients-with-muscle-invasive-urothelial-carcino",totalDownloads:1257,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"There has been considerable interest in urethral‐sparing cystectomy and preservation of the gynecological tract to maintain continence mechanism, sexual function, and reproductive function in young patients who undergo radical cystectomy for muscle‐invasive bladder cancer and this new technique gained acceptance in many centers. The issue of oncological safety of a urethra and anterior vaginal wall‐sparing cystectomy in selected patients has been addressed by several authors. The chapter will discuss the following items: (I) Technique of genital‐sparing radical cystectomy in female patients with muscle invasive transitional cell carcinoma of the bladder. (II) Definition and rationale of genital‐sparing radical cystectomy in female patients. (III) Rational and value of urethral preservation in genital‐sparing cystectomy in female patients with urothelial carcinoma. (IV) Previous reports about genital‐sparing cystectomy in patients with urothelial carcinoma. (V) Value of preservation of the internal genital organs in female patients undergoing radical cystectomy.",book:{id:"5516",slug:"bladder-cancer-management-of-nmi-and-muscle-invasive-cancer",title:"Bladder Cancer",fullTitle:"Bladder Cancer - Management of NMI and Muscle-Invasive Cancer"},signatures:"Hosni Khairy Salem",authors:[{id:"96052",title:"Prof.",name:"Hosni",middleName:"Khairy",surname:"Salem",slug:"hosni-salem",fullName:"Hosni Salem"}]},{id:"67209",title:"Robotic Surgery and Successful Set-Up: A Stepwise Approach",slug:"robotic-surgery-and-successful-set-up-a-stepwise-approach",totalDownloads:639,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Robot purchase, implementation, and sustainability require a number of key challenges to overcome. We provide our experience of managing a potentially daunting task, summarizing the key steps to help deliver such an exciting project. We will take you through team approach options for purchase and safe implementation in the current financial climate.",book:{id:"6424",slug:"evolving-trends-in-kidney-cancer",title:"Evolving Trends in Kidney Cancer",fullTitle:"Evolving Trends in Kidney Cancer"},signatures:"Christopher J. Anderson and Hiten R.H. 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Thus proteomics, an area of research that detects all protein forms expressed in an organism, including splice isoforms and post-translational modifications, is more suitable than genomics for a comprehensive understanding of the biochemical processes that govern life. The most common proteomics applications are currently in the clinical field for the identification, in a variety of biological matrices, of biomarkers for diagnosis and therapeutic intervention of disorders. From the comparison of proteomic profiles of control and disease or different physiological states, which may emerge, changes in protein expression can provide new insights into the roles played by some proteins in human pathologies. Understanding how proteins function and interact with each other is another goal of proteomics that makes this approach even more intriguing. Specialized technology and expertise are required to assess the proteome of any biological sample. Currently, proteomics relies mainly on mass spectrometry (MS) combined with electrophoretic (1 or 2-DE-MS) and/or chromatographic techniques (LC-MS/MS). MS is an excellent tool that has gained popularity in proteomics because of its ability to gather a complex body of information such as cataloging protein expression, identifying protein modification sites, and defining protein interactions. 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