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Review

sBlackwell Science Ltd

The mast cell in wound healing

Role of the mast cell in the different stages of the wound healing process

CHIARA NOLI* and ALDA MIOLO

*Studio Dermatologico Veterinario, Via Sismondi 62, 20133 Milano, Italy;
CeDIS, Innovet, Viale dellIndustria, 8, 35030 Rubano, Italy
(Received 11 October 2000; accepted 11 July 2001)

Abstract This review describes the role of the mast cell in the pathobiology of skin healing. After illustrating
its main morphofunctional characteristics, with special reference to the dog and cat, we consider the involvement
of the mast cell in the various phases of skin repair. With the aid of a wide array of newly formed or preformed
mediators released by degranulation, the activated mast cell controls the key events of the healing phases: triggering and modulation of the inflammatory stage, proliferation of connective cellular elements and final remodelling of the newly formed connective tissue matrix. The importance of the mast cell in regulating healing
processes is also demonstrated by the fact that a surplus or deficit of degranulated biological mediators causes
impaired repair, with the formation of exuberant granulation tissue (e.g. keloids and hypertrophic scars), delayed
closure (dehiscence) and chronicity of the inflammatory stage.

Keywords: cytokines, growth factors, inflammation, mast cells, proliferative phase, skin, tissue remodelling,
wound healing.

INTRODUCTION
Although their discovery dates from over 100 years
ago,1 mast cells still represent a biological enigma.
These cells, which are ubiquitous in the connective
tissues and mucous membranes, especially in interface
tissues such as the skin, respiratory tract and gastrointestinal apparatus,2 possess a series of biochemical and
functional resources which places them at the centre
not only of protective inflammatory and immune
responses, but also of homeostatic tissue regulation
mechanisms in general.3 Even taking account of the
substantial differences in terms of morphological
heterogeneity and reactivity to secretagogues found in
various tissues and/or various species, all mast cells are
activated by stimuli of various kinds, and release, by
means of degranulation, a wide array of biologically
active mediators which are not only synthesized at the
time of the stimulus, as in all the other cells, but can
also be released with immediate kinetics because they
are stored in cytoplasmic granules (Fig. 1).46
Recognition of their ability to respond to a composite range of stimuli, and the identification of an increasing number of biochemical mediators contained in and
released by mast cells (Table 1),735 has led to an extension
of the functional role of these cells in an increasingly
wide range of diseases, from inflammatory to parasitic
disease, from fibrotic involutions to tumours.3650
In the skin, in particular, an important role was
classically reserved for the mast cell, but limited to allergic

Correspondence: Dr Chiara Noli. E-mail: pitnoli@iol.it

2001 Blackwell Science Ltd

Figure 1. Photomicrograph of skin mast cell (Safranin; 1000).

and parasitic diseases.5154 Later, as a result of continual

research into its functional characteristics, this cell
acquired increasing importance in all processes requiring
delicate biological coordination between the cells of the
skin for their correct performance. A good example is represented by the dermo-epidermal events that accompany
wound healing. Wound repair, which is conceptually
divided into the three phases of inflammation, proliferation and remodelling,55 represents a single dynamic
sequence of cell responses to damage, in which a dense network of mutually controlled molecular signals stimulates
the migration of specialized cells to the site of the injury,
induces proliferation of specific cell lines, and controls the
structural remodelling of the extracellular matrix.55 60
303

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C. Noli and A. Miolo

Table 1. Principal mediators isolated from dog mast cells

Mediator

Mast-cell origin

Function

References

-Chymase

Mastocytoma

714

Tryptase

Trachea smooth muscle

cell culture, mastocytoma
Mastocytoma
Mastocytoma

Metalloproteinase activation, matrix protein degradation,

increased extravasation, neutrophil chemotaxis, stimulation of
submucosal gland secretion, inactivation of inflammatory
neuropeptides, control of complement-mediated inflammation,
stimulation of conversion of angiotensin I to angiotensin II
Metalloproteinase activation, smooth muscle and epithelial
cell mitosis stimulation
Inhibition of histamine release, stimulation of angiogenesis
Trypsin-like effect

19
20, 21

Mastocytoma

Remodelling of connective matrix

11, 12

Mastocytoma

Intracellular activation of prochymase and protryptase

22

Lung, gastric mucosa,

skin, submandibular
gland (cat)
Heart, mastocytoma
Mast-cell culture

Vasodilatation; increased vessel permeability; increased endothelial

cell proliferation; nerve stimulation

2328

Increased expression of adhesion molecules; chemotaxis of neutrophils

Activation of TH2 lymphocytes; activation and differentiation
of B lymphocytes; eosinophil chemotaxis; up-regulation of
adhesion molecule expression; increased SCF production
Eosinophil chemotaxis; B lymphocyte activation
Fibroblast proliferation; angiogenesis

2931
32

Fibroblast proliferation and epithelial cells, leukocyte chemotaxis

Platelet proliferation and aggregation; fibroblast proliferation
Mast cell growth, differentiation and chemotaxis, mast cell adhesion
to fibronectin, upregulation of TNF release, interaction with cytokines
(IL-3, IL-4, IL-10) for maturation of mast cells, increase in natural
mast-cell mediated immunity; increase in mast-cell survival due to
suppression of apoptosis
Nerve stimulation; vasodilatation

3638
39
4047

Heparin
Protease-3
(MCP-3)
Gelatinase
(MMP-9)
Cathepsin C
(dipeptidyl
peptidase I)
Histamine

TNF
IL-4

IL-5
FGF
TGF
PDGF
SCF

PDG2

Mast-cell culture
Fibrotic lung
Rheumatoid synovial fluid
Mastocytoma
Mastocytoma
Cardiac tissue
Mastocytoma

Mast-cell culture

8, 9, 13, 1518

33
34, 35

48

MMP, matrix metalloproteinase.

Table 2. The mast cell: biological profile
The mast cell derives from undifferentiated haemopoietic precursors (CD34 +)
It matures in the peripheral tissues as a resident cell with a long mean life span (from weeks to months)
It differentiates into subpopulations with different phenotypes and proliferation potentials, depending on the stimuli it receives from the local
microenvironment
It is strategically located in close contact with the nerve endings and local microcirculation
Although it is a resident cell, it possesses considerable mobility within the tissue, and can migrate in response to stimuli of various kinds
It is characterized by cytoplasm filled with metachromatic granules containing biologically active mediators
It is activated by physical stimuli (sunlight, trauma), immunogenic stimuli (IgE, complement, cytokines and growth factors) and neurogenic
stimuli (neuropeptides)
It releases, through an exocytotic process of degranulation, an array of mediators stored in cytoplasmic granules
It adapts the degranulating potential to the homeostatic control requirements of the tissue.

This review analyses the latest literature and offers

an overview of current knowledge of the involvement
of mast cells in skin repair and its pathological dysregulation. Most data are obtained from experimental
animals or humans, and the background mechanism of
the role of mast cells in wound healing may not be
directly extrapolated to domestic animals, however, it
is likely to be similar in many aspects.

THE SKIN MAST CELL:

MORPHOFUNCTIONAL HALLMARKS
Selye61 was the first to describe human mast cells as
rounded elements with an oval nucleus and cytoplasm
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 303 313

filled with spherical metachromatic granules, typically

situated in the dermis, near the blood vessels, glandular
ducts and hair follicles.
Unlike the circulating basophil, the mast cell
reaches the tissues from the bone marrow through
the systemic circulation as an undifferentiated
progenitor cell, which acquires its morphological
and functional characteristics peripherally6264
(Table 2).
The process of differentiation is guided by specific
molecular influences [e.g. stem cell factor (SCF) and
nerve growth factor (NGF) ] which the immature mast
cell receives from the cells in the peripheral tissue, and
which determine its development, survival, proliferation and functional characteristics.65

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305

Table 3. The main mast cell subpopulations

Fixation
Metachromasia
Proteases
Proteoglycans
Location
Quantitative variations

Mucosal or atypical (MCT )

Connective or typical (MCTC )

Lead acetate (Mota solution)

Only after fixing in lead acetate or Carnoy fluid
Tryptase
Chondroitin sulfate
Mucous membranes (lamina propria,
gastrointestinal mucosa)
Increase in allergic and parasitic disease
Increase around lymphocyte TH2 activation sites
Decline in chronic immune deficiency

Formalin
Independent of fixative
Tryptase, chymase, carboxypeptidase, cathepsin G
Heparin
Connective tissue (dermis, subepithelial connective tissue
of the respiratory and digestive apparatus)
Increase in fibrotic processes
Remain unchanged in allergic and parasitic diseases
Do not change in chronic immune deficiency

This peripheral maturation determines the heterogeneity of mast cell populations, which differ in the
various tissues in terms of phenotype, granular content,
reactivity to agonistic stimuli, secretion patterns, and
tinctorial and fixative properties.6670 In rodents, the
mast cells are divided into two main types (connective
and mucosal),71,72 whereas in man they are now classified into three groups, based on their immunocytochemical characterization.73,74 Specifically, there are
mast cells containing tryptase only (MCT), which correspond to the mucosal mast cells; mast cells containing tryptase, chymase, carboxypeptidase and cathepsin
G (MCTC ), which correspond to the connective mast
cells (Table 3), and mast cells with differing tissue
locations containing chymase and carboxypeptidase
(MCC ).
This heterogeneity typical of the human mast cells
has also been identified in the dog and cat.7577
Although initially defined on the basis of the appearance of the characteristic metachromasia after fixing
in formalin,77 this heterogeneity is now more appropriately determined in those animal species on the
basis of the different content of proteolytic enzymes
(tryptase and chymase), which were recently shown to
be biochemically and immunologically similar to those
isolated in man.2,11,76,77
The greatest morphological characterization of
these cells has been achieved in the skin of the dog and
cat. Even taking account of the numerical variability
found in relation to the possible influence of the fixation methods used,2 the dog, and even more so the
cat,78 presents a large population of skin mast cells,
70% of which have a mixed protease content (MCTC ).75
These cells are preferentially located in the dermis and,
as in the other tissues, are anatomically adjacent to
nerve endings and microvascular networks.4,79,80
Although traditionally considered to be resident in
the dermis, the skin mast cells have migratory capacity
and also demonstrate extraordinary functional adaptation in response to disturbance of tissue homeostasis.4,62,81 The discovery of mast cells which superficialize
in the epidermis in response to inflammation is typical
of the cat,82 whereas the finding of subepidermal
linear alignment in dermatitis is typical of the dog.83,84
As regards the functional activation, the skin mast
cell, which is strategically located between vessels and
nerves, is stimulated directly by immunological signals
(cytokines, IgE and complement fractions)4,51,85 and

Figure 2. Schematic representation of mast cell degranulation.

Activation of mast cells may be triggered by immunogenic,
neurogenic and mechanical stimuli. Once activated, the mast cell
releases a wide array of preformed and newly synthesized biological
mediators.

by stimuli of nerve origin.79,80 The mast cells are

actually an integral part of a peripheral axon reflex
triggered by external stimuli applied to the skin.86 The
neuropeptides [NGF, substance P (SP), calcitonin
gene-related protein (CGRP) and somatostatin (SOM) ]
released by stimulated or damaged dermo-epidermal
nerve endings not only initiate the vessels response to
neurogenic inflammation,87 but also act as factors that
directly activate local mast cells, causing their degranulation.80 In addition, numerous stimuli of a physical,
chemical and/or mechanical nature (e.g. trauma, exposure to sunlight and use of radiographic contrast
media) act as agonistic stimuli.88 91 In other words, by
directly disturbing the mast cell membrane or indirectly acting by stimulating local sensory endings, they
can trigger the release, by degranulation, of mediators
with biological activity which the mast cell synthesizes
and stores in the cytoplasmic granules (Fig. 2). Once
released, cytokines, growth factors, vasoactive amines
and proteolytic enzymes influence the surrounding
cell elements, coordinating the biological response to
aggressive events of various types within a threshold
degranulation value, with defensive and reparatory
purposes. In addition, unlike rodents, in the dog and
man these mediators are released in soluble form,92
demonstrating their potential to act not only close to
the release site, but also on anatomically distant cell
targets such as circulating leukocytes or the adjacent
keratinocytes.
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THE MAST CELL IN SKIN HEALING

The morphofunctional characteristics attributed to the
mast cell have generated numerous research projects
designed to establish the role of this cell in the dynamic
physiology of skin healing.93,94 At present, it can be
said that mast cells are able to control the key events of
wound healing: the inflammatory response designed to
limit damage, revascularization of the damaged tissue,
re-epithelialization, deposition of temporary connective tissue and subsequent remodelling of the matrix
support.95,96
The mast cell and inflammation
Once activated by direct tissue injury,88 the mast cell
located at the wound edges releases, by means of
degranulation, the mediators essential to trigger the
inflammatory reaction of the injured tissue, which
mainly influence the local endothelial cells (Fig. 3).97
The mast cells, which adhere to the outer wall of the
vessels and are even distributed in the intimal layers, are
part of a vascular control system (vascular-associated
lymphoid tissue, VALT) responsible for constant
monitoring of microcirculatory homeostasis.98 In particular, through the release of vasoactive mediators,
such as histamine, protease, tumour necrosis factor
(TNF) and metabolites of arachidonic acid, they induce
vasodilatation and increase vascular permeability.99,100
The endothelial cells, in turn, influence the functional state of the mast cells. Once activated by inflammation, they release factors such as SCF, interleukin-3
(IL-3) and thrombin which enhance migration, proliferation and local differentiation of mast cells,97,101 in
practice creating a biological circuit that regulates the
functional tone of the mast cell, with the prime aim
of triggering an initial inflammation and moving on to
the subsequent repair phases. Mast cell numbers can
increase fivefold in the border of a wound, and this
increase correlates with the upregulation of the chemokine monocyte chemoattractant protein-1102 and the

Figure 3. Mast cell participation in the inflammatory phase of

wound healing. Mast cell multifunctional mediators act directly on
the local vasculature, nerve endings, macrophages and other
inflammatory cells (i.e. polymorphonuclear leukocytes).
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 303 313

production of transforming growth factor (TGF)-, an

important wound healing cytokine, which is also a
potent chemoattractant for mast cells.103
During the initial phase of healing, the skin mast cell
is also actively involved in the regulation of primary
haemostasis and the subsequent dissolution of the
temporary clot. As a result of the release of substances
such as platelet activating factor (PAF), leukotrienes
and specific cytokines (IL-1 and IL-8), the mast cell
aids platelet activation and aggregation and extravascular deposition of fibrin.104,105 By releasing mediators
such as heparin, tryptase, chymase and t-plasminogen
activator (tPA), it directly regulates the endogenous
fibrinolysis mechanisms, causing the temporary clot to
dissolve and promoting anticoagulant activities.106,107
The balance between these two opposing actions is
essential, first to seal the injured surface layer rapidly
(haemostatic action), and second to guarantee sufficient perfusion and nutrition to trigger the subsequent
repair events (fibrinolytic activity).95
As the inflammatory process develops, a crucial
event is represented by the recruitment in the injured
area of circulating leukocytes which, together with the
resident macrophage populations, perform specific
defence functions (phagocytosis) and a kind of debridement. This leukocyte recruitment is a complex phenomenon, in which the mast cells play a direct part.108
It has now been clearly demonstrated that these cells
are involved, through the release of specific mediators,
in a whole series of events ranging from initial contact
between the leukocyte and the vessel wall (rolling) to
marginalization, transendothelial migration by diapedesis and hyperafflux to the tissues by chemotactic
signals. In fact, although molecules of mast cell origin
such as TNF and histamine favour the adhesion of the
leukocytes to the vessel, increasing the expression of
endothelial adhesion molecules (selectin, integrin),109 111
other mediators, also released by the mast cell (leukotrienes, proteases and cytokines, especially IL-8), represent chemotactic signals for neutrophils, basophils and
eosinophils.112
The mast cells also contribute directly to microbiological cleansing of the wound by enhancing
macrophagic phagocytosis113,114 and by acting as
phagocyosting cells in response to stimulation by any
bacterial components, which also trigger the degranulation mechanism.115,116
The local innervation, which is profoundly altered
by the wound, is influenced by the functional state of
the skin mast cell, also involved in the electrophysiological alterations found in the injured area.117 In
particular, NGF, released by the mast cells by means
of degranulation,118 causes a reduction in the nociceptive threshold, the mechanism responsible for the
hyperalgesia which generally affects the injured
area.119121
The mast cell and proliferation
Classically, the proliferation phase of wound healing is
dominated by the formation of granulation tissue, to

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Role of the mast cell in the different stages of the wound healing process

307

Figure 4. The central role of the mast cell in the proliferative phase
of wound healing. As a source of cytokines, growth factors, vasoactive
amines, proteases and neuropeptides, the activated mast cell affects
the other cells involved in the angiogenesis and proliferation:
endothelial cells, fibroblasts, keratinocytes and nerve endings.

Figure 5. The central role of the mast cell in the remodelling phase
of wound healing. Among the numerous mediators produced and
secreted by cutaneous mast cells, there are some that also affect cell
types involved in matrix formation and remodelling, such as
fibroblasts and myofibroblasts. In addition, the mast cell promotes
the correct re-innervation of injured tissues.

which specific events, such as the formation of new

blood vessels (angiogenesis), fibroblast proliferation
(fibroplasia) and re-epithelialization, contribute.59,122
All these processes can be modulated by the mast cell
as a result of the differentiated release of biological
mediators responsible for stimulating the growth,
migration and proliferation of the elements essential
for repair: endothelial cells, fibroblasts, keratinocytes
and nerve endings (Fig. 4).122125
In particular, the mast cell coordinates neovascularization in the injured area, influencing the regrowth
potential of the endothelial cells. Vasoactive amines
(histamine), heparin, cytokines (TNF, IL-6 and IL-8)
and growth factors [platelet-derived growth factor
(PDGF), vascular endothelial-derived growth factor
(VEDGF), TGF and fibroblast growth factor (FGF)]
represent the angiogenic pool which the activated
mast cell rapidly releases by means of degranulation,
and which modulates the various stages leading
directly or indirectly to new vessel formation, aiding
the formation of a temporary substrate of connective
tissue to ensure correct migration of the endothelial
cells.97,123,126
Mast cells play an essential role in the deposition of
connective matrix through a dense two-way interplay
with the cells most involved in the process, namely the
fibroblasts. Mast cells, which are anatomically adjacent
and functionally able to release substances with specific fibroproliferative activity such as histamine,127,128
fibrogenic cytokines (IL-1, IL-4 and TNF),129 tryptase130
and growth factors (TGF and bFGF),24,25 possess the
biological weapons needed to stimulate chemotaxis,
migration, phenotype differentiation and biosynthesis
activity by the fibroblasts. Mast cell extracts can
activate fibroblasts, promoting collagen synthesis
and activation of gelatinase A, an enzyme involved in
matrix remodelling.131 This effect may be partly due to
tryptase, which has been shown to stimulate the synthesis of type 1 collagen in human lung132 and dermal

fibroblasts.133 Basically, there is a profound functional

synergy between mast cells and fibroblasts, boosted
by the recent discovery that a veritable membrane
apparatus (gap junctions) exists between these two cell
types, allowing direct physical interconnection.97,134
The mast cell mediators also influence the reepithelialization process which, by means of sophisticated processes of keratinocyte migration and
proliferation from the wound edges, leads to the formation
of new epithelium.135,136 In fact, although the activated
keratinocyte is able to influence the skin mast cell, causing
its degranulation,137 the mast cell directly influences the
functionality of the keratinocyte, modulating its proliferation and locomotion processes by releasing growth
factors [epithelial growth factor (EGF), TGF and
NGF) and specific cytokines (IL-1 and TNF).125,138,139
The regulatory influence of the mast cells is also
demonstrated by the nerve repair phenomena characteristic of the proliferation stage.140 The release of specific
mediators (vasoactive amines, tryptase, IL-4 and NGF)
of mast cell origin is essential to initiate regeneration
of damaged nerve fibres,117,119 and lead to temporary
hyperinnervation of the scar at this stage.140 142
The mast cell and remodelling
Mast cell degranulation plays an important role not
only in the deposition of temporary connective matrix,
but also in the formation of permanent matrix through
the remodelling phase (Fig. 5). Mast cells, which accumulate at the site of the wound, release mediators with
lytic activity (serine proteases and metalloproteinases),
inhibitors of this degradative enzyme and growth factors (FGF and TGF) which, when suitably balanced,
coordinate replacement of the previous temporary
substrate with connective tissue of suitable structural
composition and functional properties.143
Growth factors (FGF and TGF) and cytokines of
mast cell origin (IL-1, IL-4 and IL-6) also influence the
phenotype of the activated fibroblasts inducing, in the
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late phases of repair, the appearance of particular

cells with contractile activity (the myofibroblasts) which
ensure the changeover from fibroplasia to contraction,
and final healing of the wound.59,122,144
At this stage, the newly formed capillaries also
undergo further structural remodelling, which is
influenced by the mast cell due to its ability to release
angiogenesis-stimulating and -inhibiting factors at
different times.59,145 Thus, reduced endothelial proliferation, caused by specific factors of mast cell derivation
(TGF), and by the same products of degradation as the
preceding connective tissue matrix, is accompanied by a
perivascular increase in smooth muscle cells which, under
the influence of certain growth factors (TGF and PDGF),
lead to permanent conformation of the vessel wall.59

THE MAST CELL IN IMPAIRED

HEALING
The scientific findings reported to date clearly indicate
that mast cells are wholly involved in all phases of
wound healing.
As regards healing impairments, a probable functional link has long been postulated in the literature
between the mast cells and incorrect repair, in view of
the direct involvement of these cells in diseases with
a fibrotic component.146,147 It has also been observed
that the mast cell undergoes significant qualitative and
quantitative variations not only during correct performance of healing events,93,94,148 but also in situations
of impaired repair processes (keloids and hypertrophic
scars).149151 More specifically, the dynamic variations
(in terms of number and morphology of the mast cells
present in the injured skin) are basically associated
with the variations in degranulating activity presented
by these cells at the various phases of healing. Thus, the
rapid perilesional disappearance of the mast cells
found immediately after the injury148 can be attributed
to their degranulation, which prevents their histological
identification due to progressive loss of the granular
cytoplasm content.152 Only at the more advanced phases
of repair do the mast cells gradually recover histological
visibility and consequently their normal number,148
demonstrating reduced degranulation and therefore
gradual recovery of the set of mediators stored at granular level. Conversely, the mast cell hyperplasia found
in keloids and hypertrophic scars149151 and in the
presence of ulcers153 and chronic inflammation154 may
be correlated with greater histological visibility, resulting
from reduced release of intragranular mediators, and
therefore be predictive of altered bioavailability of the
mast cells biological apparatus.
Basically, although the mast cell acts as a homeostatic orchestrator of skin healing under piecemeal
degranulation, once the degranulation threshold has
been exceeded it turns into a damage effector, i.e. it
triggers impaired repair processes, leading to chronicity of the inflammation and altered proliferation
dynamics.95,96,155,156
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 303 313

CONCLUSIONS
Research has now clearly defined the functional profile
of the mast cell, whose balanced, piecemeal degranulation mechanism is essential to the well-being of a
tissue, unlike the uncontrolled release of mediators
with cytotoxic and tissue-damaging action, which
represents the key to pathological events of various
kinds.157,158
In the context of the biology of wound healing, the
intrinsic dynamics of this biological process require
particular attention to be paid to a cell like the mast cell
which, as a result of its calibrated degranulation, has
the potential to ensure correct performance of the
healing events.
In view of all that is said nowadays about the need to
give specific attention to wound healing, administering
suitable treatment and not merely relying on the natural healing process,159 the fact that the homeostatic
role played by the mast cell in repair has been identified
certainly opens up new possibilities for action based on
fine-tuning of the degranulation mechanism during the
repair stages.

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Rsum Cette revue dcrit le rle des mastocytes dans la pathobiologie du processus de cicatrisation. Aprs
avoir illustr les principales caractristiques morphofonctionnelles des mastocytes, en insistant sur les espces
canine et fline, nous envisageons le rle des mastocytes dans les diffrentes phases de la cicatrisation cutane.
Grce la libration dun grand nombre de mdiateurs, noforms ou prforms, les mastocytes activs
contrlent les lments cls du processus de cicatrisation: dclenchement et modulation de linflammation, de la
prolifration des cellules conjonctives et modelage final de la matrice conjonctive nouvellement synthtise.
Limportance de ce type cellulaire dans la rgulation du processus de cicatrisation est galement dmontre par
le fait quun surplus ou un dficit des mdiateurs issus de la dgranulation provoque une mauvaise cicatrisation,
avec la formation dun tissu de granulation excessif (eg: klodes et cicatrices hypertrophiques), un dlai de fermeture de la plaie (dhiscence) et un passage la chronicit de la raction inflammatoire.
Resumen Esta revisin describe el papel de los mastocitos en la patobiologa de la curacin cutnea. Despus
de ilustrar sus principales caractersticas morfofuncionales, con especial referencia al perro y al gato, consideramos la implicacin de los mastocitos en las distintas fases de la reparacin cutnea. Con la ayuda de una amplia
serie de mediadores formados de nuevo o preformados, liberados en la degranulacin, los mastocitos activados
controlan los acontecimientos clave en las fases de curacin: iniciacin y modulacin de la fase inflamatoria, proliferacin de los elementos celulares conectivos y remodelacin final de la matriz de tejido conectivo recin formado. La importancia de los mastocitos en la regulacin del proceso de curacin tambin se demuestra por el
hecho de que un exceso o un dficit mediadores biolgicos degranulados causa un impedimento de la reparacin,
con la formacin de tejido de granulacin exuberante (p.ej. queloides y cicatrices hipertrficas), retraso en el cierre
(dehiscencia) y cronicidad en la fase inflamatoria.
Zusammenfassung Diese bersicht beschreibt die Rolle der Mastzelle in der Pathobiologie der Wundheilung
der Haut. Nach Erluterung der hauptschlichen morphologischen Charakteristika mit besonderer Bercksichtigung des Hundes und der Katze diskutieren wir die Beteiligung der Mastzelle in den verschiedenen Phasen der
Hautheilung. Mit Hilfe einer grossen Menge von neu gebildeteten oder schon vorher produzierten und durch
Degranulation freigesetzten Mediatoren kontrolliert die aktivierte Mastzelle die Schlsselereignisse der Heilungsphasen: Auslsung und Modulation der Entzndungsphase, Proliferation der Bindegewebszellen und schliesslich die Umgestaltung der neu geformten Bindegewebsmatrix. Ein berschuss oder Defizit von degranulierten
biologischen Mediatoren verursacht gestrte Heilung und Entstehung von berschiessendem Granulationsgewebe (z. Bsp. Wulstnarben oder hypertrophische Narben), versptete Wundschliessung (Dehiszenz) und chronische Entzndung, was die Bedeutung der Mastzelle in der Regulation des Heilungsprozesses weiter
unterstreicht.

2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 303313

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