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 Table of Contents  
ORIGINAL HYPOTHESIS
Year : 2017  |  Volume : 8  |  Issue : 2  |  Page : 42-45

Cellular reduction and pulp fibrosis can be related not only to aging process but also to a physiologic static compression


1 Department of Periodontology, Medical Faculty Carl Gustav Carus, TU Dresden, Dresden, Germany
2 Department of Operative and Pediatric Dentistry, Medical Faculty Carl Gustav Carus, TU Dresden, Dresden, Germany

Date of Web Publication11-May-2017

Correspondence Address:
Firas Kabartai
Department of Periodontology, Medical Faculty Carl Gustav Carus, TU Dresden, Fetscherstr. 74 / 01307 Dresden
Germany
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2155-8213.206105

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  Abstract 

Introduction: As the available space inside the tooth becomes smaller because of the continuous formation of secondary dentin, the pulp may suffer from a physiologic static compression. The hypothesis: The dental pulp is lifelong under a static compression because of the continuous formation of secondary dentin, so that both cellular reduction and pulp fibrosis can also represent adaptive changes caused by the compression. Evaluation of the Hypothesis: The physiologic compression of the dental pulp can lead not only to the development of a hypoxia followed by cell death but also to the development of excluded volume effect, which helps convert the procollagen into collagen and form a collagen fiber network.

Keywords: Dental pulp, excluded volume effect, hypoxia, physiologic compression, pulp fibrosis


How to cite this article:
Kabartai F, Hoffman T, Hannig C. Cellular reduction and pulp fibrosis can be related not only to aging process but also to a physiologic static compression. Dent Hypotheses 2017;8:42-5

How to cite this URL:
Kabartai F, Hoffman T, Hannig C. Cellular reduction and pulp fibrosis can be related not only to aging process but also to a physiologic static compression. Dent Hypotheses [serial online] 2017 [cited 2017 Dec 11];8:42-5. Available from: http://www.dentalhypotheses.com/text.asp?2017/8/2/42/206105


  Introduction Top


The physiologic compression of dental pulp is somewhat similar to the compression of the arm by a sphygmomanometer but with an important difference; the compression of the arm during blood pressure measurement causes rapid and considerable increase in tissue pressure,[1] while the compression of the pulp because of the continuous formation of secondary dentin causes slow and slight increase in tissue pressure (compatible with the daily formation rate which is about 0.8 µm).[2] Therefore, the pulp gets the chance to deal with the compression and make adaptive changes. Because no other organ is lifelong affected by a static compression, the physiologic compression of the dental pulp can be considered as a unique phenomenon.


  The Hypothesis Top


The dental pulp suffers from a static compression because of the continuous formation of secondary dentin. Therefore, both the reduction of the cellular content in the pulp and pulp fibrosis are not merely the results of aging process but also the consequences of compression.


  Evaluation of the Hypothesis Top


General facts/Simple physics

When external pressure is applied on a tissue (e.g., cartilage), tissue water moves toward the load. This movement of the water is directly related to the magnitude and duration of the applied pressure. Soon after the pressure is removed, the water moves back.[3] Based on these facts, the presence of Weil’s zone under the odontoblast layer can provide evidence that the pulp is suffering from a static compression caused by the continuous formation of secondary dentin, as the compression in this case will enhance the movement of tissue water toward the dentinal walls. Thus, a cell-free zone will be formed just beyond the odontoblast layer and become more intense with age because of the active formation of secondary dentin.[4]

The dental pulp has a relatively high tissue pressure and low tissue compliance. It is located within the rigid dentinal walls of the tooth so that any increase in pulpal tissue volume will increase the tissue pressure.[5] This increase in tissue pressure can remain located within the part of the pulp where it was raised without spreading to involve the whole pulpal tissue.[6],[7]

The increase in pulpal tissue volume can be either true (a direct increase in tissue volume due to increased blood flow and increased capillary filtration in case of pulp inflammation) or relative (an indirect increase in tissue volume due to the reduction in the available space inside the tooth and the physiologic compression).

The increase in pulpal tissue pressure due to the physiologic compression can be expressed as follows:[8]

ΔP = B × (−ΔV/Vi)

ΔP: The increase in pulpal tissue pressure due to the physiologic compression.

B: The bulk modulus for pulpal tissue.

Vi: The initial volume of pulpal tissue.

ΔV: The difference in pulpal tissue volume due to the physiologic compression (the new volume – the initial volume), which is equal to the volume of the formed secondary dentin.

Because the regular secondary dentin forms at a daily rate of 0.8 µm, the increase in pulpal tissue pressure due to compression will be the highest where the pulp has the smallest volume (i.e., at the apical constriction).

It is well known that the application of high external pressure on a tissue compromises the blood flow in it.[1],[9] However, it is significantly easier in the dental pulp because it has a relatively high tissue pressure (10.4 mmHg) close to the pressure in the capillaries,[4],[10] so even a small increase in tissue pressure may compromise the blood flow in the capillaries and lead to the development of hypoxia, especially that the blood vessels in the pulp have thin walls compared to those with the same diameter existing in other tissues.[11],[12] Some blood vessels may even become completely closed with age and constitute a part of pulp fibrosis.[13],[14]

Although the pulpal horn has the smallest diameter in the coronal pulp, it may be less affected by the physiologic compression and the subsequent hypoxia because the pulpal horn has the strongest capillary blood flow in the coronal pulp, which in turns has a capillary blood flow two times stronger than that in the radicular pulp.[14],[15]

Reduction of the cellular content in the pulp

Seelig, in his study in 1965,[16] noticed the death of odontoblasts in groups after two years from the complete eruption of teeth, first at the level of root apex which then advanced coronally, regardless of whether accompanied by external pathological factors or not and without being related to aging process itself because the odontoblasts in the apical region of the tooth are the youngest.[17] It was later concluded that the death of odontoblasts in this context may represent a genetically programmed stage in tooth development,[18] however, it can be the result of a developing hypoxia in the apical part of the root because the pulp will try to survive the lack of blood flow by reducing its cellular content. More interestingly, the death of odontoblasts can also be the activation key for the formation of physiologic sclerotic dentin.[19]

By comparing the number of cells in the pulp between the following two age groups (10–30 years old and 51–59 years old) it was found that the reduction in odontoblast number with age reached 15.6% in the coronal pulp and 40.6% in the radicular pulp, whereas the reduction in fibroblast number with age reached 26.9% in the coronal pulp and 41.3% in the radicular pulp.[20] Because the rate of cellular reduction with age was higher in the radicular pulp, despite that the cells in the radicular pulp are younger, it cannot be only the result of aging process but also a consequence of the physiologic compression and the resulting hypoxia, as they are significantly stronger in the radicular pulp.

Pulp fibrosis

With age, the pulp turns from a loose connective tissue into dense fibrous tissue. Pulp fibrosis was considered to be a response to previous irritation,[21] however,if it had been only so, it would have been more intense in the coronal pulp because it is more prone to external stimuli than the radicular pulp.

The ongoing reduction in the available pulpal space can lead to the development of excluded volume effect where the macromolecules (especially the proteins) get crowded, so that any reaction that can increase the available volume for the macromolecules will be enhanced, such as protein binding, folding, and aggregation.[22] The excluded volume effect can enhance the conversion of the water-soluble procollagen to the water-insoluble collagen through C and N proteinase, respectively. Moreover, it can increase the cross-linking of collagen through lysyl oxidase[23] and promotes bundling and alignment of extracellular matrix fibers.[24] It is worth mentioning that utilizing the excluded volume effect in vitro resulted in 20 to 30-fold faster collagen deposition.[25]

Because the physiologic compression is greater where the pulp has the smaller volume, the macromolecular crowding and thus the excluded volume effect will be greater in the radicular pulp. This can explain not only the increased pulp fibrosis in the radicular pulp but also the arrangement of collagen fibers as bundles in the radicular pulp and diffused depositions in the coronal pulp.[26]

Furthermore, the developing hypoxia may play a supplementary role in the fibrogenesis, as the hypoxia inducible factor-1 (HIF-1), which represents the cellular response to low oxygen, can enhance the fibrogenesis through the upregulation of connective tissue growth factor (CTGF), tissue inhibitor of matrix metalloproteinase 1 (TIMP-1), and plasminogen activator inhibitor 1 (PAI-1).[27]

The result will be a three-dimensional network of collagen fibers that provides a substantial tensile strength but makes little contribution to compressive resistance.[28] The compressive resistance is the main responsibility of proteoglycans (negatively charged molecules), which get trapped within the collagen fiber network. They become closer to each other as a result of macromolecular crowding, and thus provide high local concentration of negative charges, which interact with the mobile cations in tissue water. Because they occupy only a friction of their possible hydrodynamic domain, they also attract water and generate an osmotic swelling pressure, which is restrained by the stiffness and tensile strength of collagen fibers.[29],[30] This osmotic swelling pressure can counterbalance the compression and give the pulp finally its relatively high tissue pressure. [Figure 1] and [Figure 2] illustrate the main components involved in the physiologic compression of the dental pulp.
Figure 1: The main components of the dental pulp which are involved in the physiologic compression

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Figure 2: The physiologic compression of the dental pulp. The continuous formation of secondary dentin (1). The formation of a cell-free zone due to the movement of tissue water toward the pressure (2). The compression of the capillaries and development of hypoxia (3). The apoptosis of some odontoblasts due to hypoxia (4). The apoptosis of some fibroblasts due to hypoxia (5). The formation of a collagen fiber network as a result of excluded volume effect (6). The proteoglycans get crowded and trapped within the collagen fiber network and therefore generate an osmotic swelling pressure (7)

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  Conclusion Top


The physiologic compression of the dental pulp is a unique phenomenon that can result not only in a hypoxia followed by cell death but also in excluded volume effect and a subsequent fibrosis. Therefore, both cellular reduction and pulp fibrosis, which have been always attributed to the aging process, may also be considered as adaptive changes due to compression, especially that they are more intense in the radicular pulp where the compression is stronger, not in the coronal pulp where the pulp first develops.

Financial support and sponsorship

Nil.

Conflict of interest

There are no conflicts of interest.

 
  References Top

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Widmaier EP, Raff H, Strang KT. Vander’s human physiology: The mechanisms of body function. McGraw-Hill Higher Education;2008.  Back to cited text no. 1
    
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3.
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4.
Pashley DH, Walton RE, Slavkin HC. Histology and physiology of the dental pulp. In: Ingle JI, Bakland LK. Endodontics. Ontario, CA: PMPH-USA; 2002. pp. 25–61.  Back to cited text no. 4
    
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Tønder KJH, Kvinnsland I. Micropuncture measurements of interstitial fluid pressure in normal and inflamed dental pulp in cats. J Endod 1983;9:105-9.  Back to cited text no. 6
    
7.
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8.
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9.
Nielsen HV. Effects of externally applied compression on blood flow in subcutaneous and muscle tissue in the human supine leg. Clin Physiol 1982;2:447-57.  Back to cited text no. 9
    
10.
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11.
Dahl E, Mjor IA. The fine structure of the vessels in the human dental pulp. Acta Odontol Scand 1973;31:223-30.  Back to cited text no. 11
    
12.
Hals E, Tönder KJ. Elastic (pseudoelastic) tissue in arterioles of the human and dog dental pulp. Scand J Dent Res 1981;89:218-27.  Back to cited text no. 12
    
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15.
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16.
Seelig A. Dentin and pulp. N Y State Dent J 1965;31:54-69.  Back to cited text no. 16
    
17.
Schroff FR. Thoughts on the physiologic pathology of regressive and reparative changes in the dentine and dental pulp. Oral Surg Oral Med Oral Pathol 1952;5:51-8.  Back to cited text no. 17
    
18.
Vasiliadis L, Stavrianos C, Dagkalis P, Parisi K, Pantelidou O, Samara E. Root Dentine Translucency of Human Teeth: Factors Affecting Formation and Deposition. Res J Biol Sci 2011;6:82-8.  Back to cited text no. 18
    
19.
Kabartai F, Hoffmann T, Hannig C. The physiologic sclerotic dentin: A literature-based hypothesis. Med Hypotheses 2015;85:887-90.  Back to cited text no. 19
    
20.
Murray PE, Stanley HR, Matthews JB, Sloan AJ, Smith AJ. Age-related odontometric changes of human teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;93:474-82.  Back to cited text no. 20
    
21.
Stanley HR, Ranney RR. Age changes in the human dental pulp: I. The quantity of collagen. Oral Surg Oral Med Oral Pathol 1962;15:1396-404.  Back to cited text no. 21
    
22.
Perham M, Stagg L, Wittung-Stafshede P. Macromolecular crowding increases structural content of folded proteins. FEBS Lett 2007;581:5065-9.  Back to cited text no. 22
    
23.
Lareu RR, Arsianti I, Subramhanya HK, Yanxian P, Raghunath M. In vitro enhancement of collagen matrix formation and crosslinking for applications in tissue engineering: A preliminary study. Tissue Eng 2007;13:385-91.  Back to cited text no. 23
    
24.
Zeiger AS, Loe FC, Li R, Raghunath M, Van Vliet KJ. Macromolecular crowding directs extracellular matrix organization and mesenchymal stem cell behavior. PLoS One 2012;7:e37904.  Back to cited text no. 24
    
25.
Lareu RR, Subramhanya KH, Peng Y, Benny P, Chen C, Wang Z et al., Collagen matrix deposition is dramatically enhanced in vitro when crowded with charged macromolecules: The biological relevance of the excluded volume effect. FEBS Lett 2007;581:2709-14.  Back to cited text no. 25
    
26.
Chandra S. Textbook of dental and oral histology and embryology with MCQs. Jaypee Brothers Publishers; 2004.  Back to cited text no. 26
    
27.
Higgins DF, Kimura K, Bernhardt WM, Shrimanker N, Akai Y, Hohenstein B et al., Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition. J Clin Invest 2007;117:3810-20.  Back to cited text no. 27
    
28.
Lu Y, Parker KH, Wang W. Effects of osmotic pressure in the extracellular matrix on tissue deformation. Philos Trans A Math Phys Eng Sci 2006;364:1407-22.  Back to cited text no. 28
    
29.
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30.
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    Figures

  [Figure 1], [Figure 2]



 

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Introduction
The Hypothesis
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Conclusion
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