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A Question for Scientists in Tissue Physiology
Stephen Foote*
Independent Researcher, UK
*Corresponding author: S Foote, Independent Researcher, UK, Tel: 07972537513; E-mail:
Received date: March 06, 2018; Accepted date: April 11, 2018; Published date: April 18, 2018
Copyright: © 2018 Foote S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,
distribution, and reproduction in any medium, provided the original author and source are credited.
is short informal article is intended to raise the issue of evidence
for a signicant oversight, in the published studies about a particular
tissue growth restriction. ese studies currently fail to consider a
in vivo
growth control that according to the accepted science
must play a central role. So here I would like to ask scientists if there is
any evidence that this particular tissue is a special case and so not
subject to this widely accepted fundamental
in vivo
growth control.
According to the accepted science, all normal (non-cancerous)
tissue growth in vivo, is ultimately restricted by the external resistance
based growth control [1].
According to this, external pressure based growth controls have an
overruling action upon all normal (non-cancerous) tissue growth
. It does not matter what is driving new tissue growth
in vivo
, a
certain degree of external resistance will switch this o.
As demonstrated in the study linked above, increased external
pressure restricts new growth, and reduced external pressure allows
increased new growth.
Hair follicles regularly go through a cycle of regression then re-
enlargement "within" the dermal tissue. Research in this eld seeks to
understand why the size of the hair follicles created by this process can
vary greatly and in particular why the new follicle growth is oen
severely restricted. Yet nowhere in the published studies is there any
consideration of the normal pressure based spatial growth controls that
according to the accepted science must apply in this situation (Figure
Figure 1: Hair growth stages.
Hair production is closely linked to the size enlarging anagen
follicles ultimately achieve, and the oen restricted growth of follicles
is known to be responsible for the common cases of hair loss (Figures 2
and 3).
Figure 2: Scalp hair types.
Figure 3: Time-lapse: Miniaturization of hair follicles in baldness.
Once the inuence of pressure based external growth controls are
considered in changes in follicle size and hair growth, a clear common
factor is identied in the recognised data in the eld. I discuss this and
its wider implications in my main article with further references [2].
To sum this up, the indication is that hair follicles have evolved in
mammals, to have their maximum size potential adjusted by small
pressure changes in the dermal tissue. is has important purpose in
evolution as I discuss in my article.
ISSN: 2157-7552
Journal of Tissue Science &
Engineering Foote, J Tissue Sci Eng 2018, 9:1
DOI: 10.4172/2157-7552.1000217
Perspective Open Access
J Tissue Sci Eng, an open access journal
Volume 9 • Issue 1 • 1000217
In the modern Human condition, all the factors known to increase
hair follicle size and hair production, all reduce external tissue pressure
by one action or another. is includes Minoxidil, anti-inammatories,
low level lasers and lately Latanoprost. is drug was actually
developed to reduce tissue pressure in cases of Glaucoma [3].
All the known changes in the surrounding dermal tissue in cases of
hair follicle miniaturisation are fully consistent with increased tissue
uid pressure, as in lymphedema. ese include signicant
inammatory changes, hypoxia, increased brotic tissue formation,
and signicantly increased sweating capacity [4-7].
is external inuence also explains why certain transplantation
procedures succeed, whilst others fail. In my opinion assumptions have
been made about the results of hair transplantation, as I argue with
references in my main article. Most of the current cell based research is
based upon one of these assumptions. It is thought that because large
so called androgen resistant follicles survive in bald areas when
transplanted, cells from these will also grow large new follicles in bald
e big dierence here is that in transplantation the follicles are
"already" large; they are not required to grow in the bald scalp
conditions. Any cell based treatment requires the follicles produced to
enlarge in the higher pressure conditions of the bald scalp, and these
follicles will not be immune to the normal pressure based spatial
Spatial growth controls are overruling. It does not matter if hair
follicles are created or modied to initiate growth, or increase their
internal growth potential, if external pressure conditions dictate
otherwise, the expected growth will not happen.
is factor impacts negatively upon all the current research
intended to create new hair follicles, initiate existing follicle
enlargement, or boost the amount of follicle enlargement in Humans.
is indicated scalp condition in humans, also explains why the results
in vitro
and mouse studies in this eld, and are just not relevant to
the Human condition.
In my opinion this currently overlooked dermal interaction, also
oers an important insight into mammalian and modern Human
evolution and disease. is includes the indication for a signicant role
of the male hormone Dihydrotestosterone (DHT), in lymphatic
function and Female susceptibility to autoimmune diseases. is
indication could be easily tested by those in the position to do so, as I
describe in my main article.
Scientists in tissue engineering are aware of the inuence of spatial
considerations in the development and guidance of new tissue growth
in vivo
. Hence the use of scaolds to inuence this process [8].
e indication here that hair follicles have evolved to use variable
spatial conditions in their growth cycle, suggests they may be
convenient as an
in vivo
model for further study in tissue engineering.
So given the important implications of this growth control in this
context, I would repeat my basic question to scientists. Is there any
evidence that hair follicle enlargement is not signicantly inuenced
by the normal pressure based spatial growth controls?
3. Blume-Peytavi U, Lönnfors S, Hillmann K, Garcia-Bartels N (2012) A
randomized double-blind placebo-controlled pilot study to assess the
ecacy of a 24 week topical treatment by latanoprost 0.1% on hair growth
and pigmentation in healthy volunteers with androgenetic alopecia. J Am
Acad Dermatol 66: 794-800.
4. Swezey L (2011) Lymphedema – Overview and etiology.
5. Zampell JC, Yan A, Elhadad S, Avraham T, Weitman E, et al. (2012)
CD4(+) cells regulate brosis and lymphangiogenesis in response to
lymphatic uid stasis. PLoS One 7: e49940.
6. Goldman BE, Fisher DM, Ringler SL (1996) Transcutaneous PO2 of the
scalp in male pattern baldness: A new piece to the puzzle. Plast Reconstr
Surg 97: 1109-1116.
7. Cabanac M, Brinnel H (1988) Beards, baldness and sweat secretion. Eur J
Appl Physiol Occup Physiol 58: 39-46.
8. Chan BP, Leong KW (2008) Scaolding in tissue engineering: General
approaches and tissue-specic considerations. Eur Spine J 17: 467-479.
Citation: Foote S (2018) A Question for Scientists in Tissue Physiology. J Tissue Sci Eng 9: 217. doi:10.4172/2157-7552.1000217
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Volume 9 • Issue 1 • 1000217
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Full-text available
Scaffolds represent important components for tissue engineering. However, researchers often encounter an enormous variety of choices when selecting scaffolds for tissue engineering. This paper aims to review the functions of scaffolds and the major scaffolding approaches as important guidelines for selecting scaffolds and discuss the tissue-specific considerations for scaffolding, using intervertebral disc as an example.
Latanoprost is a prostaglandin analogue used to treat glaucoma. It can cause adverse effects, such as iridial and periocular hyperpigmentation, and eyelash changes including pigmentation and increased thickness, length, and number. Latanoprost has been used to treat eyelash alopecia, but knowledge on its effects on human scalp hair growth is not available. The primary objectives were to assess the efficacy of latanoprost on hair growth and pigmentation. The secondary objectives were to assess the effect on scalp pigmentation; investigate the treatment duration needed to affect hair growth, hair pigmentation, and scalp pigmentation; and assess safety of latanoprost. Sixteen men with mild androgenetic alopecia (Hamilton II-III) were included. Latanoprost 0.1% and placebo were applied daily for 24 weeks on two minizones on the scalp. Measurements on hair growth, density, diameter, pigmentation, and anagen/telogen ratio were performed throughout the study. At 24 weeks, an increased hair density on the latanoprost-treated site was observed compared with baseline (n = 16, P < .001) and placebo-treated site (P = .0004). Only young men with mild androgenetic alopecia were included. The results may not be applicable to other patient groups. Choice of investigational site may have affected the results. Latanoprost significantly increased hair density (terminal and vellus hairs) at 24 weeks compared with baseline and the placebo-treated area. Latanoprost could be useful in stimulating hair follicle activity and treating hair loss.
The hypothesis according to which male common baldness has developed in the human species as a compensation for the growth of a beard in order to achieve heat loss has been tested. In 100 clean-shaven men direct measurement of the area of glabrous skin on the forehead and calvaria was found to be proportional to that of the hairy skin on the lips, cheeks, chin and neck. During light hyperthermia the evaporation rate on the bald scalp was 2 to 3 times higher than on the hairy scalp. Conversely the evaporation rate was practically equal on he foreheads and chins of women and unbearded young men, while in adult clean-shaven bearded men it was 40% less on the chin than the forehead. These results support the hypothesis that male baldness is a thermoregulatory compensation for the growth of a beard in adults.
Our study was designed to measure the transcutaneous PO2 of the scalp to determine if there was a relative microvascular insufficiency and associated tissue hypoxia in areas of hair loss in male pattern baldness. A controlled prospective study was performed at Butterworth Hospital, Grand Rapids, Michigan. Eighteen nonsmoking male volunteers aged 18 years and older were studied. Nine men had male pattern baldness (Juri degree II or III), and nine were controls (no male pattern baldness). Scalp temperature and transcutaneous PO2 were obtained at frontal and temporal sites in each subject. Peripheral circulation was assessed from postocclusive transcutaneous PO2 recovery time by means of maximum initial slope measurements. Statistical significance was assessed at p < 0.05. There was no significant difference in scalp temperature between male pattern baldness subjects and controls. Temporal scalp blood flow was significantly higher than frontal scalp blood flow in male pattern baldness subjects; however, there was no significant difference in controls. Transcutaneous PO2 was significantly lower in bald frontal scalp (32.2 +/- 2.0 mmHg) than in hair-bearing temporal scalp (51.8 +/- 4.4 mmHg) in men with male pattern baldness. In controls, there was no significant difference in transcutaneous PO2 of frontal scalp (53.9 +/- 3.5 mmHg) and temporal scalp (61.4 +/- 2.7 mmHg). Transcutaneous PO2 also was significantly lower in the frontal scalp of male pattern baldness subjects (32.2 +/- 2.0 mmHg) than in either frontal or temporal scalp of controls (53.9 +/- 3.5 mmHg and 61.4 +/- 2.7 mmHg, respectively). There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. We have identified a previously unreported tissue hypoxia in bald scalp compared with hair-bearing scalp.
Lymphedema -Overview and etiology
  • L Swezey
Swezey L (2011) Lymphedema -Overview and etiology.
A Question for Scientists in Tissue Physiology
Citation: Foote S (2018) A Question for Scientists in Tissue Physiology. J Tissue Sci Eng 9: 217. doi:10.4172/2157-7552.1000217