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 Table of Contents  
REVIEW ARTICLE
Year : 2022  |  Volume : 17  |  Issue : 1  |  Page : 166-169

Possible link between acidic interstitial fluid and various mineralization disorders of teeth: Evidence-based hypothesis


Department of Oral and Maxillofacial Pathology and Microbiology, School Of Dentistry, D. Y. Patil University, Navi Mumbai, Maharashtra, India

Date of Submission18-Dec-2021
Date of Decision16-Feb-2022
Date of Acceptance18-Mar-2022
Date of Web Publication25-Jul-2022

Correspondence Address:
Dr. Sandhya Tamgadge
Department of Oral and Maxillofacial Pathology and Microbiology, School of Dentistry, D. Y. Patil University, Sector 7, Nerul, Navi Mumbai - 400 706, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdmimsu.jdmimsu_468_21

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  Abstract 


Effects of pH fluctuation of blood and interstitial fluid have a tremendous effect on bone which leads to osteoporosis. This evidence has been widely mentioned in dental and medical literature. However, the same interstitial fluid enters teeth too through the apical foramen and periodontal space. Thus, it will have a similar effect in teeth too. This article is about the effect of interstitial fluid and its effect on teeth on the basis of evidence mentioned in the literature. Various databases have been researched such as PubMed, MEDLINE, and Google for literature search.

Keywords: Acidic pH, demineralization, dentinal tubules, hypothesis, interstitial fluid, teeth


How to cite this article:
Tamgadge S, Tamgadge A. Possible link between acidic interstitial fluid and various mineralization disorders of teeth: Evidence-based hypothesis. J Datta Meghe Inst Med Sci Univ 2022;17:166-9

How to cite this URL:
Tamgadge S, Tamgadge A. Possible link between acidic interstitial fluid and various mineralization disorders of teeth: Evidence-based hypothesis. J Datta Meghe Inst Med Sci Univ [serial online] 2022 [cited 2022 Aug 16];17:166-9. Available from: http://www.journaldmims.com/text.asp?2022/17/1/166/352246




  Introduction Top


Each cell is bathed by interstitial fluid, which plays a critical role in the exchange of metabolites. Thus, responsible for the health of all cells and ultimately all systems of the body.[1]

The normal pH of interstitial fluid is 7.4, which is crucial for the health of every cell. Therefore, when it drops below normal, the body tries buffering it by borrowing calcium ions from hard tissues (bones and teeth) resulting in demineralization and porosities in them.[2] Even a 0.05 dip is considered acidic for bone and leads to osteoporosis. There is a plethora of literature on acidic pH of interstitial fluid and osteoporosis.[3]

This fluid flows through intercellular spaces in bone. It enters teeth too through the apical foramen and periodontal space (PDL) through the bloodstream. Pulpal interstitial fluid forms due to the transudation process enter the dentinal tubules as dental lymph and then through dentin-enamel junction (DEJ) enters enamel too. It gains entry through PDL into the cementum ad cementodentinal junction and ultimately into the enamel. All these routes have been proved in animal experiments.[4],[5],[6]

Dr. Steinman proved in his experiment to explore the theory. He developed an ingenious technique involving injecting a fluorescent dye (radioactive acriflavine hydrochloride) into the abdomen of experimental rats and observing the pathway the marker took in their body. What he found, was astonishing: the dye took just 6 min to show up in the dentinal tubules and an hour to reach the enamel. This discovery was tantamount to prove that teeth are active structures possessing a fluid in dentin. This fluid is derived from inside the body, reaches the pulp chamber, and then enters dentin–pulp interface through the dentin tubules and enamel and eventually into the mouth.[4]

This fluid also enters through an external route through PDL and gains entry within cementum through Sharpey's fibers; cement dentinal junction then goes up to DEJ.[7],[8] Therefore, it affects teeth through both routes.

However, the association between acidic interstitial fluid and demineralization of teeth has not been much explored yet and is rarely mentioned. There is evidence of such nonbacterial and nonerosive tooth demineralization due to acidic interstitial fluid causing microporosities. The body tries preventing these porosities by blocking or preventing the flow of this fluid within the teeth and thus prevents internal demineralization. This article is about the explanation of the association between acidic pH of interstitial fluid and its effect on teeth leading to various lesions through evidence mentioned in the literature.

Various databases have been researched such as PubMed, MEDLINE, and Google for literature search.

This acidic interstitial fluid interacts with teeth in several ways and the body manifests in several ways as follows:

1. The acidic pH of interstitial fluid and tooth demineralization: Acidic interstitial fluid enters tooth pulp through the apical foramen in the form of blood initially. The transudate of blood now becomes interstitial fluid, leaves the pulp chamber, and enters the dentinal tubules in the form of dental lymph. The body tries buffering it by borrowing minerals initially from peritubular dentin leading to internal porosities and weak dentin and enamel too.[4],[9]

2. Acidic pH of interstitial fluid and pulp stones and linear calcification: Pulp stones and linear calcification are considered an aging phenomenon, seen only in older individuals and never seen in children. The acidic pH of interstitial fluid too found in older individuals. Therefore, it could be a protective mechanism to block the entry of acidic fluid inside the pulp chamber.[10] Some authors say it cannot be due to aging as calcifications are mostly seen in radicular pulp and odontoblasts are younger in this region compared to crown odontoblasts. Thus, calcification occurs to block the entry of acidic interstitial fluid and is not due to aging.

3. Acidic pH of interstitial fluid and sclerosis of dentin: Sclerosis of dentinal tubules means deposition of minerals within the tubules seen in older individuals. It is predominantly observed at the pulpal end and terminal end of the radicular portion of dentinal tubules because interstitial fluid gains entry from both sides of dentinal walls, which has been proven in animal experiments.[4],[5],[6],[11]

L. S. Fosdick also mentioned that the crystals within the rods and interrod substances consist of apatite contaminated by some of the nonapatite ions present in the interstitial fluid from which the crystals were derived from,[11] which support the hypothesis.

The tubules are normal in the middle region in most of the teeth in ground sections and sclerosed at pulpal and terminal branches most of the time to block the entry of acidic interstitial fluid from both ends. Thus, transparency can be seen only at the ends, and mostly, the central part is seen as normal tubules.[12],[13],[14],[15],[16] If the entire length of the tubule is transparent, then the body can be considered under the continuous attack of interstitial fluid.

4. Acidic pH of interstitial fluid and zones of caries: Incipient lesion is considered the initial event in caries and shows various histopathological zones in dentin and enamel.[17] Both zones start from the inner surface to the outer surface. Thus, dentin zones start from the pulpal end to DEJ and enamel zones too start from DEJ to the surface of tooth, but caries-producing bacteria are present on the surface. How is this possible? Etiological factors are present on the surface causing demineralization first on the deepest portion of the tooth. As mentioned by Fosdick LS et al., there could be initial demineralization of the inner surface of teeth due to the acidic pH of interstitial fluid which leads to zones of sclerosis and fatty degeneration and nonmicrobial demineralization. When this demineralization progresses from the pulpal end and occupies full thickness of dentin first, followed by enamel, in focal areas of teeth, it can be clinically seen as incipient lesion. Such porous teeth are then prone to bacterial attack from oral route which is called as dental caries. Thus, teeth have to be porous before caries attack as mentioned by Sandhya et al.[4],[18] Therefore, some lesions appear to begin below the surface, leaving a thin layer of undecalcified enamel at the surface called as an intact surface zone.[11]

M. Larmas in 2003[9] stated that the connection between osteoblasts and osteoporosis has been widely analyzed in medicine. A search of PubMed (December 10, 2002) with these two keywords revealed a total of 792 articles, whereas the keywords “odontoblasts” and “caries” identified only 99 articles, about 10% of which had been published by his research group. A search with the keywords “osteoblast” and “fluoride” revealed 166 articles, whereas “odontoblasts” and “fluoride” identified only 26 articles.

Research on chronic bone disease, osteoporosis has been ten times more abundant than research on other chronic diseases such as caries, in dentin. In contrast, there are one hundred times as many doctors treating dental caries clinically worldwide compared with those treating osteoporosis.

Dental caries research has successfully solved the chemistry and crystallography of apatite destruction (in both bones and teeth), and even the submolecular changes are known. What we need now is knowledge of the pathobiology of this important and common disease in dentin–pulp that is the inside–out process.[9]

Larmas also suggested that it is difficult for oral biologists to join the research family interested in dental caries, to broaden the approach from pure chemistry to applied biology of dentin, so that pulpal responses are included in it, as they should be.[9]

Acidic pH of interstitial fluid and critical pH of dentin and bone-bone demineralization caused by acidic interstitial fluid have been correlated enough in dental and medical literature. When this fluid flows in dentinal tubules in the form of dental lymph, it should cause porosity and demineralization there too which has been mentioned by Steinman. It has also been mentioned in the literature that the critical pH of bone and dentin is same that is 6.9 which is a strong evidence to suggest that if nonbacterial bone demineralization (internal porosities) is happening, then tooth demineralization is also happening simultaneously causing microporosities in teeth making them weak and prone to caries attack through external route.[19]

Thus, the effect of pH fluctuation of acidic interstitial fluid will be seen, internally in teeth too similar to bone.[4],[5],[6]

5. Acidic pH of interstitial fluid dental erosion and dental erosion occurs due to ingestion of acidic food. Etiological factors acting through systemic routes have been mentioned much in the literature. Thus, acidic pH of interstitial fluid when causes internal demineralization in patients with good oral hygiene, then caries occurrence is very rare, but due to internal microporosities and demineralization, such weak teeth undergo occlusal and labial and lingual wear and become smooth leads to erosion.[20],[21]

6. Dentinogenesis imperfecta – Few studies have compared bone demineralization with tooth demineralization.[22],[23] Tuula Bäckman in 1999 mentioned that there are numerous similarities between the osteoblasts and the odontoblasts.[21]


  Discussion Top


The odontoblasts are partly under the same metabolic regulation as the osteoblasts, and therefore, the formation of the bone and the dentin is probably regulated by similar factors. Thus, there is a reason to assume that the changes in acid–base balance have effects on dentin metabolism as they do on the bone. Indeed, in previous studies, it was found that chronic metabolic acidosis slowed down the rate of dentin formation and general body growth in young rats. In humans, several congenital chronic diseases, causing acid–base disturbances, result in changes in dental health and development and the structure of the teeth.[24]

Acid–base imbalance of the body has the same kind of systemic effects on caries and on the odontoblasts in the dentin as they have on the osteoclasts, osteoblasts, and osteocytes in the bone.[24]

A simple method to evaluate interstitial fluid is through blood samples for the measurement of pH.[24] It has been broadly accepted that capillary blood is a clinically acceptable sample alternative to arterial blood if only acid–base parameters (pH and pCO2) are of interest.[26]

There is an online information promoting an alkaline diet for bone health and cancer therapy, and thus, it should also be considered for the health of dentition as a part of holistic dentistry.[1],[27]

Charles F. Bodecker in 1933 stated that we know almost nothing. Dental physiology, as applied to the metabolism of the dental tissues, is in fact an almost nonexistent science. With this in mind, it is comprehensible that, as yet, little definite information can be given as to the relation of specific systemic disturbances to dental diseases. There appears to be a protective mechanism in each tooth (the dental pulp), which increases the resistance of the dental tissues to attack.[28]

Maxwell Karshax 1941 mentioned that additional protective influences reside within the tooth itself; that is, variations in the chemical composition of teeth determine whether they will or will not decay. This question has been studied in many ways, such as chemical analysis of blood for some constituents, such as calcium and phosphorus, which might affect the composition of the teeth, and second, by analysis of teeth themselves.[28]

Nobuhiro Takahashi a Bente Nyvad 2016 raised a query that the contribution made by bacteria to the initial degradation of tooth organic materials remains questionable. Host-derived proteases (then) or might be our hypothesis (now) seem to be the main contributors to this process. It is possible that these host-derived enzymes (now, interstitial fluid), with microbial proteases, promote the degradation of dentin matrix in deep caries lesions.[30] Usha and Sathyanarayanan stated that “We, “operative surgeons,” logically adopted the surgical model of treatment for such a cavity, only to make a bigger, more geometrically perfect cavity, and fill it with the most compatible, artificial materials. This surgical model of “drill and fill” resulted in more “drills and fills” and the tooth land from the socket into the bucket.”[24]

It is found that when a white spot area increases, its depth also increases. If the surface diameter of white spots is up to 3 mm, the changes affect ½ of the enamel thickness; in case it exceeds 5 mm at diameter, the spot reaches the enamel–dentin border.[25],[29]


  Conclusion Top


Thus, teeth too undergo demineralization through an internal systemic route caused due to acidic interstitial fluid which has not been explored much yet. This unexplored area of research might answer still existing drawback of etiopathogenesis of theories of dental caries.

Clinical relevance

All hypotheses related to interstitial fluid might answer many diseases of disturbances of mineralization of teeth and would help to solve the mystery of many disorders of teeth in future.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Schwalfenberg GK. The alkaline diet: Is there evidence that an alkaline pH diet benefits health? J Environ Public Health 2012;2012:727630.  Back to cited text no. 1
    
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Larmas M. Dental caries seen from the pulpal side: A non-traditional approach. J Dent Res 2003;82:253-6.  Back to cited text no. 9
    
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Manuela P, Igreja N. Biochemical Basis of Dental Aging (Integrated Master Dentistry). New York: Porto University; 2012. p. 758-70.  Back to cited text no. 10
    
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Fosdick LS, Hutchinson AC. The mechanism of caries of dental enamel. Ann N Y Acad Sci 1965;131:758-70.  Back to cited text no. 11
    
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Fish EW. Dead tracts in dentine. Proc R Soc Med 1928;22:227-36.  Back to cited text no. 13
    
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Porter AE, Nalla RK, Minor A, Jinschek JR, Kisielowski C, Radmilovic V, et al. A transmission electron microscopy study of mineralization in age-induced transparent dentin. Biomaterials 2005;26:7650-60.  Back to cited text no. 14
    
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Manly RS, Brooks EJ. Transparency and light scattering of dental hard tissues. J Dent Res 1947;26:427-34.  Back to cited text no. 15
    
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Shafer WG, Hine MK, Levy BM. Dental caries. In: Shafer's Textbook of Oral Pathology. 5th ed. Amsterdam: Elsevier; 2006.  Back to cited text no. 17
    
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Tamgadge S, Tamgadge A. Is systemic (interstitial fluid) acidosis an initial event in the etiopathogenesis of dental caries? A hypothesis. Dent Hypotheses 2018;9:96-100.  Back to cited text no. 18
  [Full text]  
19.
Delgado AJ, Olafsson VG. Acidic oral moisturizers with pH below 6.7 may be harmful to teeth depending on formulation: A short report. Clin Cosmet Investig Dent 2017;9:81-3.  Back to cited text no. 19
    
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Kapoor N, Cherian KE, Pramanik BK, Govind S, Winford ME, Shetty S, et al. Association between dental health and osteoporosis: A study in South Indian postmenopausal women. Mid Life Health 2017;8:159-62.  Back to cited text no. 21
    
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Fabiani L, Mosca G, Giannini D, Giuliani AR, Farello G, Marci MC, et al. Dental caries and bone mineral density: A cross sectional study. Eur J Paediatr Dent 2006;7:67-72.  Back to cited text no. 22
    
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Usha C, Sathyanarayanan R. Dental caries – A complete changeover (Part I). J Conserv Dent 2009;12:46-54.  Back to cited text no. 24
[PUBMED]  [Full text]  
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Kunin AA, Evdokimova AY, Moiseeva NS. Age-related differences of tooth enamel morphochemistry in health and dental caries. EPMA J 2015;6:3.  Back to cited text no. 25
    
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Hugar SM. Holistic dentistry: “Your body hears what your mind says”. Acta Sci Dent Sci 2019;3:49-52.  Back to cited text no. 27
    
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Bödecker CF. Metabolic disturbances in relation to the teeth. Bull N Y Acad Med 1934;10:553-73.  Back to cited text no. 28
    
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Karshan M. Biochemical studies of dental caries. Am J Orthod Oral Surg 1942;28:B469-73.  Back to cited text no. 29
    
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Takahashi N, Nyvad B. Ecological hypothesis of dentin and root caries. Caries Res 2016;50:422-31.  Back to cited text no. 30
    




 

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