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Fig. 4.8 Vascularization strategies: (a) vasculogenesis,
(b) angiogenesis, and (c) inosculation
perfusion of the prefabricated microvascular network in a couple of days. The process is unfortunately not as easy as it sounds. The seeding of a
scaffold with endothelial cells does not always
guarantee the development of new blood vessels
invitro. Vasculogenesis depends not only on the
seeded endothelial cells but also on the coordinated release of a variety of signaling factors
such as vascular endothelial growth factor
(VEGF) and platelet-derived growth factor
(PDGF) and involves other cell types, including
smooth muscle cells (SMCs) and pericytes,
which are normally found under invivo but not
necessarily invitro conditions [39]. The attempt
to mimic this cellular “environment” resulted in
the emergence of what is called co-culture techniques in which endothelial cells (ECs) are cocultured with target tissue cells and broblasts
and then seeded as a mixture into scaffolds [40].
The role of co-culturing could be related to
higher levels of vascular growth factor release
and/or to the direct cell-to-cell contact effect in
inducing stable vascularization [41]. Yet, coculture for promoting angiogenesis is technically
difcult. Reaching a homogeneous distribution
of the seeded cells throughout a large threedimensional (3D) construct could pose a technical challenge. Another challenge would be the
selection of the cells to be co-cultivated. For
example, co-cultivation of ECs together with
broblasts, pericytes, or vascular smooth muscle
A. Eweida and R. Horch
cells (SMCs) in a brin gel did not lead to capillary networks, whereas younger or embryonic
broblasts were able to support such endothelial
organization in other gel systems [42].
Another major concern in the vasculogenesis
process is the 3D conguration of the cultured
cells. Establishing construct vasculogenesis
should not only act on the biological and cellular
aspects of vasculogenesis but should also mimic
the 3D hierarchal structure of a capillary network. Fabrication of scaffolds with channels
mimicking the vascular networks led to the
development of constructs with a preformed capillary “pattern.” Creating such microcirculatory
networks within the scaffolds has led to the evolution of highly sophisticated techniques of
microvascular engineering, such as soft photolithographic techniques [43], and to the development of computational simulation models of
vascular assembly and remodeling [44].
Because so much effort is required to mimic a
natural scaffold, recent approaches have shown
that naturally occurring scaffolds can be decellularized and processed so that they retain the
growth factors and structural elements that are
important regulators of angiogenesis. For example, elastic bers of an extracellular matrix scaffold were shown to act as “micro-guides” for
endothelial cell and pericyte migration during
capillary sprouting [45]. Ott etal. [46] have succeeded in creating a whole-heart scaffold with an
intact 3D geometry and vasculature by
de- cellularizing cadaveric hearts using detergents
for coronary perfusion. Porcine jejunal segments
were de-cellularized using a similar technique
and seeded with porcine microvascular endothelial cells [47]. Naturally occurring scaffolds,
however, have their own disadvantages, such as
rapid degradation, potential to harbor infection,
and the possible immunological response of the
host to such implants.
4.6.6.2 Angiogenesis (Fig.4.9)
The predominant physiological mechanism of
microvascular formation in the human body is
that of sprouting angiogenesis. Angiogenesis
starts from a preexisting vascular bed through
migration, proliferation, and co-option of the
t.me/Dr_Mouayyad_AlbtousH
4 Swellings oftheJaw
Fig. 4.9 Types of angiogenesis: (a) intrinsic (prefabrica-
tion), (b) extrinsic, (c) prelamination
existing endothelium [48]. Sprouting angiogenesis commences mainly with proteolytic degradation of the basement membrane around
endothelial cells (ECs) of a preexisting capillary
or venule [49].
The majority of currently applied approaches
rely on the so-called extrinsic mode of angiogen-
esis for the vascularization of tissue constructs.
In extrinsic angiogenesis, neovascularization
starts invading the construct from its periphery.
Vascularization, in this case, does not depend on
a denite vascular axis [50]. This method is suitable for vascularization of small constructs with a
tissue thickness ranging from 2 to 3 mm [51].
The delay in blood vessel growth into larger scaffolds leads to central necrosis due to the limited
perfusion and oxygen supply to the deeply
implanted tissues. This extrinsic type of vascularization also requires an optimal, wellvascularized, implantation site so that the
construct can get its adequate blood supply. This
is seldom available after cancer extirpation due to
extensive tissue loss and eventual irradiation of
the surgical eld.
An intrinsic mode of angiogenesis, however,
depends on a denite vascular axis, which can
serve as a source of new blood vessels for prefabrication of tissues before transplantation.
Prefabrication is a technique of revascularization
of a tissue graft by implanting an arteriovenous
loop (AVL) or a vascular pedicle underneath or
within a tissue graft, resulting in spontaneous
angiogenic development from the loop or pedicle
and subsequent revascularization of the tissue
graft [52]. This mode of vascularization is also
99
known as “intrinsic axial vascularization” and
would be more suitable to regenerate tissues in
harsh environments such as after cancer ablation
(Fig.4.9) [33, 53, 54].
4.6.6.3 Inosculation
“Inosculation” refers to the development of direct
connections between the already existing capillaries of a tissue graft or construct and angiogenic
recipient site vasculature [55]. This occurs via an
interaction between the implanted microvascular
network and the microvasculature of the host site.
It was previously suggested that the host vasculature plays an active role and that the vessels
within the tissue graft only provide a conduit for
ingrowing wound bed (recipient) vessels, known
as “internal inosculation.” Other recent studies,
however, have provided evidence that the preformed microvascular network of the graft
actively contributes to the process of revascularization, leading to “external inosculation” [56].
This process may be observed when the angiogenic activity of the preformed microvascular
network of the construct is high enough to induce
angiogenesis well before it is initialized at the
host site [57]. Whether the external or internal
inosculation will predominate depends on many
factors, such as the extent of host tissue hypoxia
and the maturation stage of preformed blood vessels within the tissue construct, as well as the tissue type and degree of the inammatory reaction
to the construct at the host site.
Successful engraftment of the construct to the
host tissues not only includes the development of
vascular connections between the host and the
graft but also includes the remodeling of the construct vasculature after implantation. The microvascular network that is implanted may be
completely different or absent after remodeling
invivo [49]. Vascular remodeling and even vascular regression are crucial for maturation and
integration after construct implantation, yet premature vessel remodeling and regression would
destroy the whole engraftment process [58].
The postulated vascularization strategies show
that vasculogenesis requires a highly sophisticated
technology that is still far from clinical practice.
Recent trials to augment angiogenesis using
t.me/Dr_Mouayyad_AlbtousH
100
A. Eweida and R. Horch
microvascular techniques seem to be more feasible, and some studies have already shown good
results at the preclinical and the clinical levels [50,
54, 59, 60]. Selecting a strategy for construct vas-
cularization would depend on the size and cellular
load of the construct, the vascular status of the
recipient site, and the availability of nearby vascular axes. A small tissue construct (2–3mm thick)
would benet from extrinsic angiogenesis.
Intrinsic angiogenesis could be applied for larger
constructs wherever a local vascular axis is available. Vasculogenesis could be applied in case of
large cell-loaded constructs where immediate perfusion of the core tissue is required [61].
A major concern in the application of regenerative therapies after cancer, especially cellbased therapies, is whether these new techniques
would increase the risk of tumor recurrence.
Unfortunately, the factors that govern tissue
regeneration and revascularization are also critical to cancer growth and metastasis [62].
4.7 Summary
The concept of reconstruction has dramatically
changed during the last few decades from just
“defect lling” to a more global concept concerned not only with structure but also with function. Reconstruction is no more tailored to defects;
nowadays, it is tailored to the patient as a whole
where the patient themselves actively contribute
to the decisions concerning various reconstructive
modalities. A major advance in this context is the
emergence of regenerative medicine as an interdisciplinary eld of medicine aimed at harnessing
the human body to regenerate its own tissues.
With the rapid progress in this emerging eld,
reducing or even abolishing the donor site morbidity will probably be the standard practice in
mandibular reconstruction in the near future.
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t.me/Dr_Mouayyad_AlbtousH
Surgery oftheOral Cavity
AhmadEweida
5
5.1 Surgical Anatomy
The oral cavity extends from the lips anteriorly to
the palatoglossal folds posteriorly. This includes
the tongue, oor of the mouth, lips (posterior to
the junction of the skin and vermilion border),
hard palate, inner cheek mucosa, including the
vestibule of the mouth, and the gums. The oor
of the mouth represents the area situated below
the movable part of the tongue bounded by the
dental arch and situated above the muscular diaphragm (mylohyoid muscle) that separates the
oral cavity from the neck. Due to their anatomical
and physiological proximity, the lesions of the
oral cavity are usually discussed as one entity.
The tongue occupies most of the oral cavity
and is richly innervated with ve cranial nerves
(V, VII, IX, X, and XII) contributing to the complex innervation of this multifunctional organ.
The embryologic origins of the tongue rst
appear at 4 weeks’ gestation. The body of the
tongue is formed from the derivatives of the rst
branchial arch. This gives rise to two lateral lingual swellings and one median swelling (known
as the tuberculum impar). The lateral lingual
swellings slowly grow over the tuberculum impar
and merge, forming the anterior two-thirds of the
tongue. Parts of the second, third, and fourth
branchial arches give rise to the base of the
tongue. Occipital somites give rise to myoblasts,
which form the intrinsic tongue musculature [1].
The lymphatic drainage of the tongue is complex. Lymphatics from the tip of the tongue travel
to the submental lymph nodes (LNs). This can be
either ipsilateral or bilateral depending on the
location of the lesion and its proximity to the
midline. Lymph from the medial anterior twothirds of the tongue drains into the deep cervical
lymph nodes (DCLNs), and lymph from the lateral anterior tongue drains into the submandibular LNs. The tongue-base lymphatics drain
bilaterally into the deep cervical LNs.
Examination of the tongue is the mainstay of
the examination of the head and neck. Various
signs would indicate various localized or systemic pathologies.
In this chapter, we will briey discuss the
lesions with surgical interest related to the tongue
and oral cavity.
5.2 Swellings oftheOral Cavity
According to the National Health and Nutrition
A. Eweida (*)
Department of Head and Neck and Endocrine
Surgery, Faculty of Medicine, Alexandria University,
Alexandria, Egypt
e-mail: ahmadeweida@alexmed.edu.eg
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
M. Sakr (ed.), Head and Neck and Endocrine Surgery,
https://doi.org/10.1007/978-3-031-64102-2_5
t.me/Dr_Mouayyad_AlbtousH
Examination Survey, the point prevalence of
tongue lesions is 15.5% in US adults. Lesion
prevalence is increased in those who wear dentures or use tobacco [2]. A recently appearing
103
104
A. Eweida
tongue mass or swelling is usually a clinically
suspicious sign. A wide spectrum of causes could
be responsible for either diffuse or localized
tongue swellings (Table5.1). These may include
developmental, traumatic, inammatory, or neoplastic causes. A tongue swelling could also be a
reection of a systemic disorder. Oral cavity
swellings due to benign or malignant neoplasms
will be discussed later in this chapter.
5.2.1 Ranulae
A ranula is a large mucous retention cyst on the
oor of the mouth (in Latin, “ranula” means a
small frog) probably due to an unnoticed trauma
of the duct system.
It usually occurs in children and young adults,
affecting both genders equally. The main complaint is a swelling on the oor of the mouth that
usually ruptures and rells. Physical examination
reveals a small spherical cyst (only the top onehalf is seen), about 1–5cm in size, on the oor of
the mouth, between the symphysis menti and the
Table 5.1 Most common varieties of oral cavity
swellings
Localized swellings (masses) Diffuse swellings
A.Cystic swellings
– Retention mucous
cyst (ranula)
– Sublingual dermoid
cyst
– Thyroglossal cyst (at
the foramen cecum)
– Hemangioma
– Chronic abscess
– Degenerated solid
tumor (sarcoma)
– Softened gumma or
tuberculous (TB)
nodule
– Hydatid cyst
B.Solid swellings
– Stone in Wharton’s
duct
– Neurobroma
– Papilloma
– Lingual thyroid
– Carcinoma (usually
an ulcer)
– Sarcoma
– Vascular
malformations
– Multiple
neurobromatosis
– Congenital causes:
1. Cretinism
(muscle
hypertrophy)
2. Mongolism
– Glycogen storage
disease
– Amyloidosis
(amyloid
inltration)
– Diffuse carcinoma
– Glossitis
1. Acute glossitis
2. Chronic diffuse
syphilitic
glossitis
– Allergy
tongue, just to one side of the midline. Ranulae
occasionally extend into the submandibular triangle of the neck (plunging ranula or deep cervical
ranula). The cyst is characteristically translucent
and has a bluish tinge. It is smooth and covered by
tortuous veins, and the submandibular duct is displaced and stretched over it. The edge is difcult to
feel, and the cyst cannot be compressed or reduced.
Treatment options include marsupialization
(de-roong of the cyst and suturing the edges to
the oor of the mouth) and total or partial exci-
sion of the sublingual gland through an intraoral
approach [3].
5.2.2 Sublingual Dermoid Cysts
When the face and neck are formed by the fusion
of the facial processes, a piece of skin may get
trapped deep in the midline just behind the jaw,
which later forms a “sublingual dermoid cyst.”
Such cysts usually lie in the midline or may be
slightly lateral. They may lie above or below the
mylohyoid muscle (supra- or infrahyoid,
respectively).
It usually occurs between 10 and 25 years,
affecting both genders equally. The patient usually
complains of a swelling under the tongue, which
becomes painful and tender if it gets infected.
Physical examination reveals a smooth, spherical,
clearly dened, spherical swelling, about 2–5cm
in size, occupying the midline between the tongue
and the inner surface of the chin. It may bulge into
the submental triangle of the neck below the chin.
The mucous membrane appears normal. It can be
felt bimanually (with one nger in the mouth and
the other beneath the chin). It is characteristically
opaque and uctuant.
Treatment is by surgical excision through the
oral route rather than the cervical route because
of the hidden scar.
5.2.3 Stone inWharton’s Duct
Stones and infection of the submandibular gland
and duct are common. When such a stone
migrates to the mouth of the submandibular duct
t.me/Dr_Mouayyad_AlbtousH
5 Surgery oftheOral Cavity
105
(Wharton’s duct), it forms a tender lump on the
oor of the mouth. The lump bulges slightly into
the mouth and, through the surrounding edema,
feels hard. Occasionally, the surface of the stone
can be seen through the open end of the duct. The
submandibular gland is usually swollen and tender. The majority of stones (60%) reside in the
proximal duct or hilum of the submandibular
gland.
Small mobile stones (<4 mm) of the parotid
gland could be retrieved using baskets (via endoscopes or radiologically guided techniques). An
extracorporeal lithotripter is relatively inefcient
in eliminating submandibular stones (only 30%
clearance). These stones are dealt with by an
intraoral surgical technique either under local
anesthesia or, for patients undergoing a day case
procedure, general anesthesia. Based on a review
of the treatment of 4600 salivary stones, a submandibulectomy should be recognized as an
uncommon event representing a minority of cases
in the modern surgical practice (<3%) [4].
5.2.4 Vascular Malformations
About 50% of all vascular anomalies occur in the
head and neck regions [5]. Although such lesions
are usually of aesthetic concern, a lesion located
on the tongue or closely related to the oropharyngeal airway may lead to more serious problems
such as spontaneous bleeding or even hematemesis [6]. Though uncommon, progressive asymmetric growth of the tongue (macroglossia) can
also be observed. In contrast to hemangiomas,
malformations are not neoplasms and thus do not
exhibit mitosis or increased endothelial cell turnover. Instead, vascular malformations are dened
as structural abnormalities of the capillary,
venous, lymphatic, and arterial system that grow
in proportion to the child [7].
5.2.4.1 Classication
According to the classication of the International
Society for the Study of Vascular Anomalies
(ISSVA) approved in April 2014 [8], vascular
malformations are classied according to their
origin mainly into four main categories:
1. Simple (capillary, venous, lymphatic, arteriovenous (AV) stula, arteriovenous
malformation)
2. Combined (lymphatic venous, capillary lymphatic venous, etc.)
3. Malformations of the major named vessels
4. Associated with other anomalies
Vascular malformations could be further classied according to their ow pattern into highand low-ow malformations. The capillary,
venous, and lymphatic variants belong to the
low-ow pattern group, and those with an arterial
component belong to the high-ow one. Common
vascular malformations on the tongue and oral
cavity include venous malformations, arteriovenous stulae, and lymphatic malformations.
Venous Malformations
Pathology
Congenital venous malformations consist of
either localized or diffuse ectatic veins with
abnormal collections of irregular venous channels. Although mostly on the skin, venous malformations are also commonly found on the
cheek, tongue, lip, and mandible. They may be
present in deep tissue, bone, muscle, or brain.
Recently, a loss-of-function mutation has been
discovered on the angiopoetin receptor gene
TIE2/TEK in many solitary and multiple sporadic venous malformations [9]. In addition,
upregulation of several factors, including tissue
growth factor-beta (TGF-beta) and basic broblast growth factor (bFGF), has also been discovered in patients with venous malformations [10].
Clinical Presentation
A venous malformation is always present at birth
but is not always evident. It may rst become
noticeable in childhood or even adulthood, and it
does not spontaneously involute. Small lesions
are usually asymptomatic or patients may complain only of disgurement. Intravascular coagulation due to trauma or venous stasis may
sometimes cause pain. For large lesions with signicant thrombosis, distal embolization may subsequently occur. When malformations are
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106
A. Eweida
extensive, a blood coagulation prole should be
performed. These patients are particularly at risk
for a pulmonary embolus following surgery, and
they require anti-thromboembolic prophylactic
treatment [11]. Trauma, infection, and hormonal
changes during puberty and pregnancy can be
associated with growth of the lesions, probably
because progesterone receptors have been discovered in these malformations [12, 13].
Supercial venous malformations have a bluish compressible mass with no palpable thrill or
audible bruit. These lesions often enlarge in a
dependent position or with Valsalva maneuver.
Phleboliths are commonly seen on radiographs.
Doppler echocardiography, MRI or magnetic
resonance angiography (MRA), and direct puncture phlebography may be required to conrm the
diagnosis and assess the extent of the lesion.
Treatment
Treatment depends on the location and extent of
the venous malformation. When a lesion is symptomatic, localized, and accessible, surgical exci-
sion remains one of the most superior treatment
options and may offer a cure for localized lesions.
Excision of complex lesions remains difcult due
to intraoperative bleeding. Preoperative sclero-
therapy (sometimes multiple sessions) can be
used prior to excision (24–48h) to decrease surgical risk. Complete cure is not to be expected in
patients with extensive disease, but combined
modality therapy may offer long-term control of
the disease. Supercial lesions or the supercial
component of deep lesions can be treated with
Nd:YAG laser [14].
Arteriovenous Fistulae
Pathology
Arteriovenous stulae or malformations (AVMs)
are congenital vascular lesions associated with a
variable degree of arteriovenous shunting. They
are clinically evident in childhood or during
puberty. Rapid expansion has also been reported
following pregnancy and trauma, including inadequate surgical intervention. A defect in vascular
stabilization is believed to cause AVM, but it
remains unclear whether these lesions are primar-
ily congenital in origin. An acquired AV stula
can also occur due to direct trauma to the vessels;
however, this is uncommon in the oral cavity.
Clinical Presentation
The presentation of AVMs is commonly a warm
swelling with a palpable thrill and an audible
bruit. Oral lesions can present early due to gingival involvement, disruption of deciduous teeth,
and profuse periodontal bleeding. Traditional
angiography or MRA to demonstrate their vascular anatomy is essential for conrming the diagnosis and developing a treatment plan. Moreover,
CTA allows evaluation of the local effects on the
surrounding tissues and bones and can dene
individual arterial feeders as well [15].
Treatment
Treatment of AVMs could be problematic, especially with large and diffuse lesions due to complete replacement of normal tissues by the diseased
vessels. Such lesions require reconstruction after
excision. Recurrence is also common after embolization or even after surgical excision due to
recruitment of new vessels [16]. When a lesion is
small and asymptomatic, a period of observation
is often the most convenient initial strategy. Large
and diffuse lesions are usually symptomatic, and a
delayed treatment may lead to cardiac decompensation. Intra-arterial embolization, combined with
surgical excision, currently offers the best chance
for cure. Excision is performed 24–48 h after
embolization. This helps control blood loss and
dene the surgical margins of the lesion. Complete
excision is sometimes impossible because of the
location and extent of the malformation.
Lymphatic Malformations
Pathology
Lymphatic malformations, previously known as
“cystic hygromas” or “lymphangiomas,” are
composed of dilated lymphatic vessels with inappropriate communication, lined by endothelial
cells and lled with lymphatic uid. Their incidence is approximated to be 1in 2000–4000 live
births [17]. Lymphatic malformations are classically classied into macrocystic, microcystic, or
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5 Surgery oftheOral Cavity
107
mixed according the cyst size (2cm3) [7]. What
usually affects the oral cavity is the microcystic
or mixed variant. These small noncompressible
vesicles can weep and at times cause pain or
minor bleeding. Microcystic disease usually carries a worse prognosis and could be more aggressive, invasive, and difcult to control [18].
Clinical Presentation
Symptoms are usually related to the extent of the
disease, which can be dened by an MRI. The
patient usually suffers from pain, dysphagia, and
odynophagia.
Treatment
As spontaneous resolution is usually not anticipated, management of symptomatic disease is
usually mandatory. Treatment is usually easier
and carries a more favorable prognosis with the
macrocystic type. Treatment modalities include
sclerotherapy [19], carbon dioxide laser [20], and
surgical excision (with/without reconstruction).
Multiple combined treatment modalities are
sometimes necessary for disease control.
5.3 Ulcers oftheOral Cavity
5.3.1 Etiological Classication
The most common varieties of oral cavity ulcers
are summarized in Table5.2.
5.3.1.1 Traumatic Ulcers
Dental Ulcers
Dental ulcers are caused by trauma from a broken tooth or ill-tting dentures. The ulcer
mostly occurs at the side of the tongue. It is
painful, with sloping serrated edges, an elongated shallow oor covered with granulation
tissue, and a soft or mildly indurated base. It
heals in a few days when the cause is removed;
otherwise, it should be biopsied, particularly if
a malignancy is suspected. Treatment is by
extraction of the ragged tooth plus good oral
hygiene. Antibiotics are used if superadded
infection occurs.
Frenular (Pertussis) Ulcers
A frenular ulcer results from trauma of the frenulum of the tongue by the teeth during coughing in
children with whooping cough, between 6 and
8 months of age due to eruption of the lower
teeth. Treatment of the cause results in healing of
the ulcer.
5.3.1.2 Inammatory Ulcers
Herpetic Ulcers
Herpetic ulcers are caused by herpes simplex
(HS) virus in patients with low resistance (for
example, following pneumonia). They appear
on the tongue and angles of the mouth, as multiple, small, painful ulcers, preceded by
vesicles.
Tuberculous (TB) Ulcers
Tuberculous ulcers result from active pulmonary
TB or infected milk (causing ulcers or diffuse
brosis—woody tongue). They usually appear at
the tip and sides of the tongue as multiple, painful, shallow ulcers with undermined edges, a
yellowish oor, and a soft base. Treatment is by
anti-tuberculous drugs and hygienic measures.
Table 5.2 A list of the most common varieties of oral cavity ulcers
Traumatic ulcers Inammatory ulcers Dyspeptic ulcers Malignant ulcers
– Dental
ulcers
– Frenular
ulcers
– Herpetic ulcers
– Tuberculous ulcers
– Syphilitic ulcers
– Chronic supercial
(nonspecic) glossitis
Aphthous (metabolic or
dyspeptic) ulcers
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– Epithelioma
– Lymphoepithelioma
– Adenocarcinoma
– Basal cell
carcinoma
– Malignant
melanoma
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