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Dental Caries Part 1 Dental Caries Part 2 Dental Caries Part 4
Is this an outrageous statement? Just think what a little pollen can do to you? If you are allergic to the pollen your body defenses can kill you. The fact that the host defense response may harm the host itself is recognized in pathology for quite some time. This fact is certainly not taken into account, or recognized in dental caries research.
For those who are not familiar with
what inflammatory cells can do, I quote a short paragraph from Baer and Benjamin:
"These cells are attracted to the site by the presence of bacteria and
bacterial byproducts, and conjugates of antigen-complement-antibody may not
only act beneficially by phagocytizing these elements, with subsequent intracellular
digestion, but may also liberate their cellular compliments of acid hydrolases,
as lysosomal membrane dissolved. These enzymes are multiphasic in their effects,
and serve to invoke collagen resorption, matrix dissolution, vascular dilation,
and permeability - the destructive facet of the inflammatory state. The inflammatory
cells with the greatest propensity for tissue destruction are neutrophil, and
monocyte." (Bear, et al,1974).
That females live longer than males and manifest stronger natural resistance to infection is well known, also to insurance companies.
Nicol and his group studied animals trying to elucidate the role of estrogens in body defenses. Some of their conclusions suggest that stimulation of the reticuloendothelial system (RES) leads to increased body defenses, raise serum globulin, and increased protection of experimental animal against virulent infections, The strongest RES stimulants according to Nicol appear to be oestrogens, both natural and synthetic (Nicol et al,1964).
Burger and Leonhardt observed in vitro that in human neutrophil leucocytes estradiol stimulated the ingestion of carmine or trypan blue stain (Burger et al,1952).
Sbarra, Paul, Strauss, and Mitchell in their review paper quoted studies which suggest that the leucocytes collected from pregnant women are more efficient phagocytes than those collected from non-pregnant women (Sbarra et al,1970).
Nilsson and his group also observed increased chemotaxis of neutrophil leucocytes under the influence of oestrogen/progestogen combinations (Nilsson et al,1980).
Therefore it can be concluded that females' stronger responses to infectious agents compared to that of man, will result in different pathology. I would like to mention that the NIH recognizes this and now initiated in the program special woman studies as well.
Shafer and Mahler demonstrated that diethylstilbestrol and estradiol are responsible for increased dental caries development on experimental rats. Their data showed that androgens are without effect on dental caries development in either male or female rats, while oestrogens increase dental caries significantly (Shafer et al,1954)(Muhler et al,1955). There are other data in the literature that support their findings (Liu et al,1973) but I could not find any data that would contradict their findings.
It is recognized that in almost any population group, higher frequencies of dental caries are found in girls than in boys (Legler et al,1980). Why? Some attribute this to a slightly earlier eruption of teeth in females.
Orosz and his group established a correlation between pregnancy and caries prevalence in a sample of 504 pregnant women.They observed that the DMF counts for nullipare were lower than of women who already had born children. The highest DMF counts were from women who had the largest number of deliveries and who were in the same age group as women who had the lowest number of children or none (Orosz et al,1977)In the past, in dental caries literature we could read that dental caries in pregnancy is only a myth perpetuated by the fallacious logic that because pregnant women develop dental caries, pregnancy causes caries. Today this is not even discussed in literature any more.
In under-privileged societies it has been shown that females have considerably higher dental caries scores than males. In rural Guatemala, for instance, dental caries experience was significantly greater in females in spite of the fact that males maintained poorer oral hygiene and consumed three times more sucrose than the females. The findings were laid to the nutrient drain on the women caused by frequent pregnancies, and long periods of lactation(Alfano MC,1980)
In the Pacific on the Tokelauan Islands observations were made that males had considerably lower dental caries frequency than females. The difference between the sexes was as high as 70% in the 20-24 year old age group (Beck et al,1966). Such a great difference cannot be explained solely by the earlier eruption of the teeth in females. The authors try to account for this by the difference in eating habits. Tokelauan males are fisherman and consume some of their catch raw while out fishing.
The difference in serum concentrations of estradiol between boys and girls is an established fact (Angsusingha K,et al,1974). Estradiol is significantly higher in girls, and girls have a higher incidence of dental caries (Legler et al,1980). It is common knowledge that the level of estrogens are higher in women than in men. During the pregnancy oestrogens are elevated even more. It can therfore be concluded that beside the Streptococcus mutans and sucrose (environmental factor) the main culprit in the above described cases of caries development are oestrogens (host factor).
Here I should also mention the experiment, where one group of Wistar rats were sensitized with horse serum and propolis stimulant. Another group of rats was not sensitized. Both groups received a cariogenic diet. The sensitized animals developed significantly more dental caries than nonsensitized animals (Ovrutsky et al,1971).This is an example where the stimulation of the immune system increased caries frequency.
Dental caries today is thought to be the result of specific bacterial action on the tooth surface in the presence of sugar. No other reason is accepted. But the acid theory alone cannot explain dental caries development!
Alfano,MC. (1980) Nutrition in Dental Caries. in Menaker,L.(ed) The Biologic Basis of Dental Caries. Harper & Row,.p356.
Angsusingha,K, Kenny,FM, Nankin,HR, and Taylor,FH.(1974) Unconjugated estrone, estradiol and FSH and LH in prepubertal males and females. J.of Clinical Endocrinology and Metabolism. 39,63-68.
Baer,PN, Benjamin,SD.(1974) Periodontal Disease in Children and Adolescents. Philadelphia, Toronto. Lippincott,p 21.
Beck,DJ, Ludwig,TG. (1966) Sex differences in dental disease in polynesian peoples. NZ.Dent.J. 62,279-291.
Burger,H, Leonhardt,K. (1952) Uber die Beeinflussung der Leukocytenphagocytose durch die weiblichen Sexual hormone in vitro. Arch. Gynacol, 181, 300-310.
Legler,DW, Menaker,L. (1980) Definition, Etiology, Epidemiology and Clinical Implications of Dental Caries. in Menaker,L. (ed) The Biological Basis of Dental Caries. Harper & Row, p.217.
Liu,FTY, Lin,HS. (1973) Effect of contraceptive steroids norethynodrel and menstranol on dental caries activity in young adult female rats. J.Dent.Res. 52,753-757.
Muhler,JD, Shafer,WG. (1955) Experimental Dental Caries .VII J.Dent.Res. 34,661-665.
Nicol,T, Bilbey,DLJ, Charles,LM, Cordingley,JL, Vernon-Roberts,B. (1964) Oestrogen: The Natural Stimulant of Body Defence. J.Endocrin. 30,277-291.
Nilsson,B, Damber,MG, von Schoultz,B. (1980) Effect of Oestrogen Progestogen combinations on Polymorphonuclear Leucocytes Chemotaxis. Acta Obstetrica et Gynecologica Scandinavica. 59(2),165-168.
Orosz,M, Rigo,O, Banoczy,J. (1975) Connection between Pregnancy and Caries Prevalence. Oral Res.Abstract.12(1) abstract 71.
Ovrutsky,GD, Gizatullin,RG. (1971) Experimental Dental Caries in Rats in Horse Serum Sensitization. Stomatologiia (Mosk.) 50(5),77.
Sbarra,AJ, Paul,B, Strauss,R, Mitchell,GW Jr.(1970) Metabolic and Bactericidal Activities of Phagocytizing Leucocytes. in Gordon,AS. ed. Regulation of Hematopoiesis. vol.2,1102-1103. Appleton Century Crofts, New York
Shafer,WG, Muhler,JD. (1954) Experimental Dental Caries. III. J.Dent.Res. 33,842-848.
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