Medical Hypotheses 85 (2015) 887–890

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Medical Hypotheses
journal homepage: www.elsevier.com/locate/mehy

The physiologic sclerotic dentin: A literature-based hypothesis

F. Kabartai a,⇑, T. Hoffmann a, C. Hannig b
a
Department of Periodontology, Medical Faculty Carl Gustav Carus, TU Dresden, Dresden, Germany
b
Department of Operative and Pediatric Dentistry, Medical Faculty Carl Gustav Carus, TU Dresden, Dresden, Germany

a r t i c l e i n f o a b s t r a c t

Article history: Despite the many hypotheses trying to explain how the physiologic sclerotic dentin is formed, there has
Received 19 June 2015 been so far no convincing explanation for all of its observations. In this review, we tried to make a
Accepted 11 September 2015 hypothesis based on the facts published to date. We found that the apoptosis of odontoblasts, which takes
place after the formation of the apical constriction, may be the key-factor for the development of phys-
iologic sclerotic dentin, because the resulting apoptotic bodies cannot be eliminated through phagocyto-
sis and become trapped within the dentinal tubules due to the continuous formation of secondary dentin.
The apoptotic bodies suffer later from a secondary or apoptotic necrosis leading to the release of the
internal contents of pyrophosphate and hydrogen phosphate. Pyrophosphate can dehydrate the dentin
and hydrogen phosphate can demineralize it, leading to the release of Ca2+ ions which then contribute
to the intratubular mineralization.
Ó 2015 Elsevier Ltd. All rights reserved.

Introduction
The physiologic sclerotic dentin is identified through the accu-
mulation of mineral deposits within the lumen of the dentinal
tubules. It begins after 3–4 years from the complete eruption of
teeth, first at the apical part of the root then moves coronally,
and at the external end of the tubules near the cementum then
moves toward the pulp. Although it increases with age, it is not
the result of aging process itself because the tubules where the
physiologic sclerotic dentin starts to accumulate (i.e. near the apex
of the teeth) are the youngest [1].
The characteristic feature of sclerotic dentin is that it reduces
the amount of scattered light. Therefore, it has a transparent
appearance to transmitted light [1,2]. Since the physiologic scle-
rotic dentin is located more at the mesial and distal areas of the
roots than at the buccal or lingual areas, it appears on the horizon-
tal sections as a butterfly shape (Fig. 1a and b). Moreover, the line
where the sclerotic dentin meets the normal dentin looks serrated
on the vertical sections (Fig. 2a and b) [1].
When transmission electron microscopy was used, the absence
of odontoblasts and predentin was evident where the sclerotic
dentin was formed [3–5]. Therefore, it was concluded that the
odontoblasts, despite their role in forming the peritubular dentin,
⇑ Corresponding author at: Department of Periodontology, Medical Faculty Carl
Gustav Carus, TU Dresden, Fetscherstr. 74, 01307 Dresden, Germany. Tel.: +49 351
458 2712; fax: +49 351 458 5341.
E-mail address: Firas.Kabartai@uniklinikum-dresden.de (F. Kabartai).
do not secret the sclerotic dentin [6]. This conclusion was also sup-
ported by the following facts:
– The difference in the appositional manner between the per-
itubular dentin (clear forming front) and the sclerotic dentin
(diffused deposits) [7].
– One of the adaptive changes in dental pulp with age is the
reduction of the cellular content including the odontoblasts
[8]. Nevertheless, the physiologic sclerotic dentin continues to
form even in an increasing rate [1].
Moreover, the role of pulpal extracellular fluid in the mineral-
ization process of sclerotic dentin remains a matter of question.
Despite the fact that the extracellular fluid has a concentration of
calcium ions that can reach 3 mM [9], which is considered suffi-
cient to induce the mineralization of predentin and demineralized
dentin [10], it cannot passively pass through the dentinal tubules,
because the odontoblast with its process fills the tubule lumen
completely at least in the predentin and the adjacent dentinal layer
[6]. Even if there is a discontinuation in this seal of the dentinal
tubule in such a way that allows the movement of pulpal fluid,
the mineralization will take place first at the pulpal side of the
tubule and will be a self-limiting process (i.e. as the calcification
at the pulpal side of the tubule increases, it hinders the later flow
of the pulpal fluid so that the intratubular mineralization will stop
at a certain depth in the tubule). Considering all of the above, the
question that may now arise is: which factor is responsible for
forming the physiologic sclerotic dentin?

http://dx.doi.org/10.1016/j.mehy.2015.09.016
0306-9877/Ó 2015 Elsevier Ltd. All rights reserved.
888 F. Kabartai et al. / Medical Hypotheses 85 (2015) 887–890

Fig. 1. (a) and (b) The distribution of physiologic sclerotic dentin on the horizontal root section (butterfly shape).

Fig. 2. (a) and (b) The distribution of physiologic sclerotic dentin on the vertical root section (serrated line).

The pulp has relatively high normal tissue pressure and low tis-
sue compliance. Moreover, it is located within the rigid dentinal
walls of the tooth, so that any increase in pulpal tissue volume will
increase the tissue pressure [11]. 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 [12,13].
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 com-
pression of the pulp by the continuous formation of secondary
dentin).
The increase in pulpal tissue pressure due to the physiologic
compression can be given as follows [14]:
DP ¼ B ðDV=ViÞ
where DP, the increase in pulpal tissue pressure; B, the bulk modu-
lus for pulpal tissue; Vi, the initial volume of pulpal tissue; DV, the
difference in pulpal tissue volume due to the physiologic compres-
sion (The new volume – The initial volume). It is equal to the vol-
ume of the formed secondary dentin but it is in this case a
negative value. For this reason it was modified by adding a minus.
Considering the fact that the regular secondary dentin forms at
a daily rate of 0.8 lm [15], the pulpal tissue pressure will increase
the most where the pulp has the smallest volume (i.e. at the apical
 F. Kabartai et al. / Medical Hypotheses 85 (2015) 887–890
constriction) and then will weaken in a coronal direction as the
pulpal volume increases.
Since the normal pulpal pressure (10.4 mm Hg) is close to the
capillary pressure [16], any increase in tissue pressure, even if
small, may compromise the blood flow in the capillaries and lead
to the development of hypoxia [11,17], especially that the blood
vessels in the pulp have thin walls compared to those with the
same diameter existing in other tissues [18,19].
Seelig, in his study in 1965 [8], had noticed the death of odon-
toblasts in groups after two years from the complete eruption of
teeth, first at the level of root apex then advanced coronally,
regardless 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
[20]. It was then concluded that the death of odontoblasts in this
context represents a genetically programmed stage in the tooth
development [6] but in fact it can be the result of the developing
hypoxia in the apical part of the root, as the pulp tries to survive
the lack of blood flow by reducing its cellular content.
The odontoblasts, that suffer from hypoxia the most, are the
ones in crowding, because they are in a competition with the
neighboring cells for the limited blood supply. Since the odonto-
blasts are crowded more on the mesial and distal walls of the root
canal, their death due to hypoxia will be more remarkably there,
leading to the formation of irregular secondary dentin on the
mesial and distal walls compared to the regular secondary dentin
on the buccal and lingual walls [21].
Altogether, the death of odontoblasts after root development is
completed and the apical constriction is formed (which takes place
within 2–4 years after complete tooth eruption) and its gradually
expansion in a coronal direction with more odontoblasts dying
on the mesial and distal dentinal walls is compatible with the
observations related to the physiologic sclerotic dentin, but the
question is: how does the death of odontoblasts contribute to the
formation of the physiologic sclerotic dentin?
The former mentioned death of odontoblasts seen with age is
regulated by apoptosis (programmed cell death) [22] which
includes several changes at the level of the nucleus, the cytoplasm
and the membrane ending in separating the original cell into sev-
eral small parts named the apoptotic bodies which get phagosi-
tozed by the macrophages or the neighboring cells without
electing an immune response [22–24].
The macrophages can eliminate the apoptotic bodies resulted
from the body of the odontoblast, but the apoptotic bodies resulted
from the its process, which lay all the way of the dentinal tubule
[25,26], will remain out of reach due to the following reasons:
– The absence of blood supply in the dentin.
– The smallest diameter of a macrophage (8.7 lm) [27] is bigger
than the diameter of the dentinal tubule at the pulpal side
(3 lm) [28].
– The continuous formation of the secondary dentin from the
intact odontoblasts near the dead one will rapidly seal the open
dentinal tubule especially in the presence of crowding, so that
the apoptotic bodies become trapped inside the lumen of the
dentinal tubule. However, the formed secondary dentin,
although being irregular because it contains less dentinal
tubules, is not accompanied by an inflammatory response (com-
pared to the irregular secondary dentin formed in the presence
of caries), thus it may be formed at a daily rate resembling that
of the regular secondary dentin (0.8 lm) [15].
This situation is similar to the apoptosis of the chondrocytes in
the articular cartilage with age since the resulting apoptotic bodies
are trapped within the articular cartilage which is avascular tissue
so they stay out of reach of macrophages and contribute later to
889
the development of the pathological calcification of articular carti-
lage with age [29].
All the cells that can form mineral tissue (osteoblasts–chondro
cytes–odontoblasts) are capable to produce the pyrophosphate
P2O4
7 (short form PPi) to use it as a regulator for mineralization
process due to its function as mineralization-inhibitor [30]. In
addition, they have alkaline phosphatase activity that can hydro-
lyze the pyrophosphate into hydrogen phosphate HPO2 4 (short
form Pi) according to the following chemical equation [31–35]:
P2 O4 2
7 þ H2 O ! 2HPO4
PPi þ H2 O ! 2Pi
Therefore, both of the matrix vehicles resulting from the func-
tional cells and the apoptotic bodies resulting after their death
can also have pyrophosphate and hydrogen phosphate inside
[29,30,36].
After sealing the dentinal tubule from its pulpal end by the
irregular secondary dentin, the apoptotic bodies within the tubule
lumen become isolated from the pulpal extracellular fluid and thus
without a constant source of Ca2+ ions, so they finally suffer from a
secondary or apoptotic necrosis [37,38] which affects the integrity
of their membrane and releases the internal content of (Pi and PPi)
into the tubule lumen. Dehydrating the surface of the peritubular
dentin by the released pyrophosphate will not only facilitate the
adsorption of the hydrogen phosphate but it will also increase its
production. Hydrogen phosphate can exchange ions with hydrox-
yapatite crystals leading to the release of Ca2+ ions which then con-
tribute to the intratubular mineralization [39,40].
The Pi/PPi molar ratio plays an important role in determining
the type of the crystals formed. The formation of hydroxyapatite
(HA) increases when the Pi/PPi molar ratio is above 140, but is
completely inhibited when the ratio is below 70. On the other
hand, the formation of calcium pyrophosphate dihydrate (CPPD)
increases when the ratio is below 6, but it is inhibited when the
ratio is above 25 [41].
Considering all the facts mentioned above, it seems likely that
the source of Ca2+ ions, which contribute to the formation of the
physiologic sclerotic dentin, is the peritubular dentin and there-
after the intertubular dentin. This is in agreement with the disso-
lution & re-precipitation theory which is supported by the
following observations:
– The absence of the peritubular dentine in some regions where
the sclerotic dentin is formed [42].
– With age, the intertubular crystals dissolve uniformly, thereby
decreasing in size, while the intratubular crystals grow and
increase in size [2].
– The similar chemical composition of minerals in the intertubu-
lar and intratubular dentin [43].
Because the odontoblast process lies all the way along the
dentinal tubule [25,26], the resulting apoptotic bodies will be dis-
tributed at the whole length of the tubule, this will guarantee the
ongoing formation of sclerotic dentin without being a self-limiting
process.
Since the tubule diameter decreases in a pulpo-cemental direc-
tion [44], the formed crystals will completely fill the tubule first at
its smallest diameter near the cementum. Therefore, the formation
of physiologic sclerotic dentin begins at the external end of the
dentinal tubule near the cementum then advances in a pulpal
direction.
Linking the time at which the physiologic sclerotic dentin
begins to accumulate with the time of complete tooth eruption is
a common mistake that should be avoided, because the physiologic
sclerotic dentin was seen in both the fully erupted and unerupted
890 F. Kabartai et al. / Medical Hypotheses 85 (2015) 887–890
teeth [40]. A reliable time point will be the time at which the apical
constriction forms, which is in accordance with the beginning in
secondary dentin formation.
Conclusion
We could hypothesize that the apoptosis of odontoblasts, which
takes place after the formation of the apical constriction, may be
the key-factor for the development of the physiologic sclerotic
dentin, because the resulting apoptotic bodies cannot be elimi-
nated through phagocytosis and thus become trapped within the
dentinal tubules due to the continuous formation of secondary
dentin from the surviving odontoblasts. The apoptotic bodies suffer
later from a secondary or apoptotic necrosis which releases the
internal contents of pyrophosphate and hydrogen phosphate.
Pyrophosphate can dehydrate the dentin and hydrogen phosphate
can demineralize it, leading to the release of Ca2+ ions into the
tubule lumen. Thus, the intratubular mineralization can begin
and continue without being a self-limiting process.
Conflict of interest statement
None declared.
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