Soft Tissue and Bone Face Tumors

With each child accepted as a patient in the dental office comes the
responsibility to oversee not only the patient‘s dental health, but also overall oral
health and well-being of that individual. It is all too easy to focus attention
strictly on the dental needs of the patient and remain oblivious to subtle or even
not to subtle lumps, bumps, swelling, or change in texture or color that may
signify the presence of a reactive or a hamartomatous overgrowth of tissue or a
benign or malignant disease state. Oral tumors occur too often for the
practitioner to take the attitude that this lesions happen only in someone else’s
patients. The practitioner who believes that oral desease states are not foundwith
enough frequency in his or her patients to justify a thorough examination of the
oral facial hard and soft tissues in every child has simply not been looking.
The purpose of this is not to present a comprehensive treatise on oral tumors in
children but to provide the undergraduate dental students, pediatric dental
graduate student, or the denal practitioner to beush up on the nuances of
pediatric dentistry with an overview of some of more frequently encountered
tumors of the oral soft tissues and bone in children.

A tumor is a lump or mass of tissue that forms when cells divide

uncontrollably. A growing tumor may replace healthy tissue with abnormal
tissue. It may weaken the bone, causing it to break (fracture). Aggressive tumors
can lead to disability or death, particularly if signs and symptoms are ignored.
Tumors in children are different from adult in their etiology,
pathomorpholocical structure and clinical appearance. 12,4% of maxillofacial
tumors are occur in children, however, 95% are benign, and 5% malignant.
Most of the tumors are disembryogenesis origin, that mean they are
proceed from genetic program disorders during intracellular multiplication,
growth and differentiation of the embryo. That is demonstrated by the
examinations showing that most of the tumors in children are occur before 5
years, mesenchimal origin of the tumors (no epithelial), very othen tumors are
combine with others malformations. Most of the soft tissue tumors in
maxillofacial region in children arise from conjunctive tissue (vessels tumors).
Oral tumors a connecting with odontogenesis and arise from odontogenic
epithelium.

Tumors are likely to develop from immature or ectopic tissue and may
appear in conjunction with obvious developmental anomalies such as an
unerupted displaced tooth. They may arise in areas of rapid growth. Other
theories indicate heredity.
Frequency. In general, benign soft tissue tumors occur at least 10 times
more frequently than malignant ones, although the true incidence of soft tissue
tumors is not well documented. However, some insight regarding the incidence
of soft tissue sarcomas can be derived from the National Cancer Institute's
Surveillance, Epidemiology, and End Results (SEER) Program, which, between
1973 and 1983, accumulated data on 6883 such tumors. 1. Overall, age-adjusted
annual incidence of soft tissue sarcomas ranges from 15-35 per 1 million
population. The rate increases steadily with age and is slightly higher in men
than in women. 2. Malignant soft tissue tumors occur twice as often as primary
bone sarcomas. 3. Approximately 45% of sarcomas occur in the lower
extremities, 15% in the upper extremities, 10% in the head-and-neck region,
15% in the retroperitoneum, and the remaining 15% in the abdominal and chest
wall. Visceral sarcomas, arising from the connective tissue stroma in
parenchymal organs, are not common.
According to the United States date childhood cancer is relatively rare --
only about 2 percent of all cancer cases occur in children. Each year, about one
out of every 15,000 children gets cancer. In 1998, the most recent year for which
there are data, about 12,400 U.S. children under 20 were found to have cancer.
That same year, 2,500 children died from the disease. Rates of childhood cancer
have risen over the past few decades, so the disease is more common now than it
once was. Cancer kills more children than any other disease, and is the second
most common cause of death in children, behind injuries. But while the number
of new cases of childhood cancer has risen, the death rate has decreased for most
forms since 1970, largely because of improved treatments. Childhood cancer
increased significantly from the early 1970s to the early 1990s, rising about 1
percent each year during those two decades. Since the 1990s, rates of childhood
cancer seem to have leveled off, but there is no evidence of a decline back to
pre-1980 rates.
Etiology. 1. Genetic conditions: Good evidence exists sugesting that
certain genetic disorders and gene mutations are predisposing factors for some
benign and malignant soft tissue tumors. 2. Radiation: Similar to postirradiation
bone tumors, postirradiation fibrosarcomas have been described. The
pathogenetic mechanism is the emergence of radiation-induced genetic
mutations that encourage neoplastic transformation. 3. Chronic lymphedema: as
observed in patients with late-stage breast carcinoma, chronic lymphedema may
predispose individuals to the development of lymphangiosarcoma. 4.
Environmental carcinogens: an association between exposure to various
carcinogens and an increased incidence of soft tissue tumors has been reported.
The occurrence of hepatic angiosarcoma, for example, has been linked to
arsenic, thorium dioxide, and vinyl chloride exposure. 5. Infection: a classic
example of an infection-induced soft tissue tumor is Kaposi sarcoma resulting
from human herpesvirus type 8 in patients with human immunodeficiency virus
(HIV). 6. Trauma: the relationship between trauma and soft tissue tumors
appears to be coincidental. Trauma probably draws medical attention to a pre-
existing lesion.
 Pacularities. Children's cancer is not only less frequent than adult cancer,
it is also different. None of the most common adult cancers -- prostate, breast,
lung, colon -- are found in children. Instead, children tend to get leukemias,
brain tumors and other cancers of the blood and connective tissues. Adult
cancers are thought to occur because of years of cumulative damage to the cells.
In children, this kind of long-term damage has not had a chance to take place.
Their cancers are thought to occur, instead, during periods of vulnerability
during early development, when the organs are still forming.
Tumors at the pediatric skull baze can be broadly categorized into
congenital (nazal glioma, encephalocee, and dermoid cyst as well as teratoma,
hamartoma and choristoma) and true neoplasma (olfactory neuroblastoma,
angiofibroma, nazopharyngeal carcinoma and rhabdomyosarcoma). Clinical
evaluation often gives significant clues as to the nature of skull base pathology.
The time of onset (at birth or postnatal), localization ( near the lines of fusion or
not), and tumer progression (static or enlarging) all contribute to the accurancy
of diagnosis.
In children and adolescents, neoplastic lesions are often benign and are of
mesenchymal origin. Choung and Kaban were of the opinion that tumor
histology in this age group did not correspond to their clinical behaviour.
There are significant differences that must be considered in the surgical
management of skull base lesions in the pediatric patient. Neoplastic lesions as
well as surgically manipulated tissue dynamically interact with growth potential
of the regional anatomy before and after treatment. This impact on growth is an
iportant distinction between pediatric and adult skull base surgery that has to be
considered during oncologic surgery as well as reconstruction.
There are differences between age group in terms of etiology,
pathophysiology, and treatment of the pediatric neck mass. In adult neck mass is
to be considered maligmant until proven otherwise. The etiology of the pediatric
neck mass is more often infectious or congenital.
Proper diagnosis of any desease proces begins with history and physical
examination. In the case of pediatric neck masses, this is a crutial step. In
younger patients, the parents will need to provide the history. Whereas
congenital lesions frequently present at birth, some not be noticed until later
infancy (e.g. vascular malformations), early childhood (e.g. vascular
malformations) early childhood (e.g. thyroglossal duct cysts), or young
adulthood (e.g. branchial cleft cysts). Granulematous diseases such as scrofula
usualy follow a chronic course, acompanied by fever or low-grade temperature.
Acute bacterial infection such as supperative sialoadenits usually presents
suddenly with pain and discomfort, inflammatory signs, an fever. Neoplasms
typically have either an asymptomatic presentation or nonspecific constitutional
symptom complex (e.g. Hodgkin”s lymphoma). Few malignat lesions are
present at birth, with the exeption of rhabdomyosarcoma, or an occasional
neuroblastoma presenting in the cervical region. Malignant lesions tend to
present in the teenage years. The spectrum of malignancies in children is age
related and different from that of adult. Pain associated with these lesions
usually is seen in late stages. The masses may result in airway compromise
because of direct compression. Increased tenderness and swelling during meals
may be associated with obstruction of a salivary gland duct by stricture or stone.
Enlagment of the neck mass during crying mai be assotiated with filling of
vascular channels as a result of decreased venous return.
Environmental factors must be considered in the ethiology of the pediatric
neck mass. Radiation exposure is associated with an increased risc of thyroid
cancer and salivary tumors. Dilantin and other drugs may lead to cervical
adenopathy. Tropical diseases may appear in those immigrants from endemic
areas, or in those with recent travel histoties to those areas. Breakage of skin by
a cat’s claws may lead to cat screach fever. Cockroaches and cat have been
known to carry toxoplasmosis. Fungal diseases have been associated with
swimming in contaminated waters.
The physical examination of a pediatric patient may pose unique
challenges. Compliance may be difficult or impossibile to obtain. In any case,
one must make the best attempt, so as to acquire the most information about the
patient’s condition. Although the area of concern is typically smaller than in the
adult, one should keep in mind that the neck of a child not a smaller version of
the adult. The cartilaginous infant trachea is less prominent and found more
cranially than in the adult. Pediatric pathology is more apt to show metabolic or
embriologic abnomalities than the adult population. There are also marked
differences between subgroups of the pediatric population. Minimal changes in
the shape or volume of underlying structures can produce masses that serve as
the primary motivator for parents to seek medical advic. The pediatric neck has
an abundane of adipose tissue until the age of 9 months when the amount of
baby fat startsto decrease, continuing throughout the second year of live. This
may lead to a delay in seeking medical advice and more a challenge in diagnosis
and treatment.
Inspection in the pediatric neck exam, includes the identification of
normal landmarks. Assymmetry, deformities, masses, scars, pulsations,
discolorations, sinuses, or fistular are noted. The oral cavity and oropharynx
must be visually inspected. Havimg the patient swallow wil also help identify
abnomalities. Masses attached to thyroid gland, as well AS hyroglossal duct
cysts, move with deglutination or tongue protrusion. Dermoid cysts are usually
attached to and therefore move with the skin. Cavernous hemangiomas tend to
increase i size when the head is lowered as a result of venous congestion.
Palpation may prove to be a challenge in young children, paticularly those
with tender lesions. One should attempt to to control head motion with the
opposite hand while palpating. Location of a mass, may point to the diagnosis.
The sternocleidomastoid muscle serves as a landmark that divide the neck into
the anterior and posterior triangular spaces. Cervical masses are more commonly
found in the anterior triangule. Approximately two yhird of all neck masses in
children are inflammatory. Of the remaning lesions, the most common mass of
the anterior triangle is the branchial cleft cyst. Midline lesions are commonly
thyroglossal duct cysts.
Physical examination characteristics of the lesion are also important
factors. Sebaceous cysts are usually firmly attached to the epidermis, and
therefore one is not able to roll the skin over the surface. Benign masses usually
are not attached to skin or deep structurie and thus are usually mobile.
Malignizations, both primary and metastatic, can be attached to a skin and
adjacent organs. Cancer are usually localized lesions in the pediatric population.
Degenerative lesions of salivary glands (Sjogren syndrom)present as diffuse
disease. Lipomas typically feel soft and localized. Benign lymph nodes feel soft,
well defined, and mobile. Advanced malignancies typicaly feel woody and hard.
Limphomas tend to feel rubbery. Cysts feel as through there is an interface
between solid and liquid. Cavernous hemangiomas may feel like a ‚bag of
worms’ with occational fiemness from particles of calcium (phleboliths).
Abscess are tender and feel fluctuant. Air in the neck is perceived as crepitance.
Pulsation may be derived from an aneurysm or carotid body tumor.

Classification. Soft tissue tumors are a large and heterogeneous group of

neoplasms. Traditionally, tumors have been classified according to histogenetic
features. (Fibrosarcoma, for example, is categorized as a tumor arising from
fibroblasts.) However, histomorphologic, immunohistochemical, and
experimental data suggest that most, if not all, sarcomas arise from primitive,
multipotential mesenchymal cells, which in the course of neoplastic
transformation differentiate along one or more lines. A liposarcoma appears to
arise from a lipoblast but may actually develop through lipoblastic
differentiation of a precursor multipotent mesenchymal cell. At the clinical
level, soft tissue tumors are classified according to various parameters, including
location, growth pattern, likelihood of recurrence, presence and distribution of
metastases, patient age, and prognosis. WHO (2002) Classification of Soft
Tissue Tumors

 Adipocytic tumors
o Benign
 Lipoma
 Lipomatosis
 Lipomatosis of nerve
 Lipoblastoma/lipoblastomatosis
 Angiolipoma
 Myolipoma
 Chondroid lipoma
 Extrarenal angiomyolipoma
  Extra-adrenal myelolipoma
 Spindle cell/pleomorphic lipoma
 Hibernoma
o Intermediate (locally aggressive)
 Atypical lipomatous tumor/well-differentiated liposarcoma
o Malignant
 Dedifferentiated liposarcoma
 Myxoid liposarcoma
 Round cell liposarcoma
 Pleomorphic liposarcoma
 Mixed-type liposarcoma
 Liposarcoma, not otherwise specified
 Fibroblastic/myofibroblastic tumors
o Benign
 Nodular fasciitis
 Proliferative fasciitis
 Proliferative myositis
 Myositis ossificans
 Fibro-osseous pseudotumor of digits
 Ischemic fasciitis
 Elastofibroma
 Fibrous hamartoma of infancy
 Myofibroma/myofibromatosis
 Fibromatosis colli
 Juvenile hyaline fibromatosis
 Inclusion body fibromatosis
 Fibroma of tendon sheath
 Desmoplastic fibroblastoma
 Mammary-type myofibroblastoma
 Calcifying aponeurotic fibroma
 Angiomyofibroblastoma
 Cellular angiofibroma
 Nuchal-type fibroma
 Gardner fibroma
 Calcifying fibrous tumor
 Giant cell angiofibroma
o Intermediate (locally aggressive)
 Superficial fibromatoses - Palmar/plantar
 Desmoid-type fibromatoses
 Lipofibromatosis
o Intermediate (rarely metastasizing)
 Solitary fibrous tumor and hemangiopericytoma - Including
lipomatous hemangiopericytoma
  Inflammatory myofibroblastic tumor
 Low-grade myofibroblastic sarcoma
 Myxoinflammatory fibroblastic sarcoma
 Infantile fibrosarcoma
o Malignant
 Adult fibrosarcoma
 Myxofibrosarcoma
 Low-grade fibromyxoid sarcoma
 Hyalinizing spindle cell tumor
 Sclerosing epithelioid fibrosarcoma
 So-called fibrohistiocytic tumors
o Benign
 Giant cell tumor of tendon sheath
 Diffuse-type giant cell tumor
 Deep benign fibrous histiocytoma
o Intermediate (rarely metastasizing)
 Plexiform fibrohistiocytic tumor
 Giant cell tumor of soft tissues
o Malignant
 Pleomorphic 'MFH'/undifferentiated pleomorphic sarcoma
 Giant cell 'MFH'/undifferentiated pleomorphic sarcoma with
giant cells
 Inflammatory 'MFH'/undifferentiated pleomorphic sarcoma
with prominent inflammation
 Smooth muscle tumors
o Angioleiomyoma
o Deep leiomyoma
o Genital leiomyoma
o Leiomyosarcoma - Excluding skin
 Pericytic (perivascular) tumors
o Glomus tumor (and variants)
 Malignant glomus tumor
o Myopericytoma
 Skeletal muscle tumors
o Benign
 Rhabdomyoma
 Adult
 Fetal
 Genital type
o Malignant
 Embryonal rhabdomyosarcoma - Including spindle cell,
botryoid, anaplastic
 Alveolar rhabdomyosarcoma - Including solid and anaplastic
  Pleomorphic rhabdomyosarcoma
 Vascular tumors
o Benign
 Hemangiomas of subcutaneous and deep soft tissue
 Capillary
 Cavernous
 Arteriovenous
 Venous
 Intramuscular
 Synovial
 Epithelioid hemangioma
 Angiomatosis
 Lymphangioma
o Intermediate (locally aggressive)
 Kaposiform hemangioendothelioma
o Intermediate (rarely metastasizing)
 Retiform hemangioendothelioma
 Papillary intralymphatic angioendothelioma
 Composite hemangioendothelioma
 Kaposi sarcoma
o Malignant
 Epithelioid hemangioendothelioma
 Angiosarcoma of soft tissue
 Chondro-osseous tumors
o Benign
 Soft tissue chondroma
o Malignant
 Mesenchymal chondrosarcoma
 Extraskeletal osteosarcoma
 Tumors of uncertain differentiation
o Benign
 Intramuscular myxoma - Including cellular variant
 Juxta-articular myxoma
 Deep ("aggressive") angiomyxoma
 Pleomorphic hyalinizing angiectatic tumor
 Ectopic hamartomatous thymoma
o Intermediate (rarely metastasizing)
 Angiomatoid fibrous histiocytoma
 Ossifying fibromyxoid tumor - Including atypical/malignant
 Mixed tumor
 Myoepithelioma/parachordoma
o Malignant
 Synovial sarcoma
  Epithelioid sarcoma
 Alveolar soft-part sarcoma
 Clear cell sarcoma of soft tissue
 Extraskeletal myxoid chondrosarcoma - "Chordoid" type
 Primitive neuroectodermal tumor (PNET)/extraskeletal
Ewing tumor
 Peripheral PNET
 Extraskeletal Ewing tumor
 Desmoplastic small round cell tumor
 Extra-renal rhabdoid tumor
 Malignant mesenchymoma
 Neoplasms with perivascular epithelioid cell differentiation
(PEComa)
 Clear cell myomelanocytic tumor
 Intimal sarcoma

As part of this 2002 WHO classification, soft tissue tumors are divided into the
following 4 categories.

 Benign - These usually do not recur locally, and if they do, the recurrence
is nondestructive and almost always readily curable by complete local
excision. Morphologically benign lesions, which are extremely rare, may
give rise to distant metastases, which cannot be predicted on the basis of
routine, contemporary histologic evaluation. This is best documented in
rare, cutaneous benign fibrous histiocytoma.
 Intermediate (locally aggressive) - These tumors show an infiltrative and
locally destructive growth pattern. However, although they may recur
locally, they do not metastasize. They usually require excision with a
wide margin of normal tissue for better local control. The example in this
category is desmoid (fibromatosis).
 Intermediate (rarely metastasizing) - These tumors are often locally
aggressive, but in some cases, they also have a tendency to produce
distant metastases (usually in a lymph node or lung). This risk is low
(<2%), but histomorphologically, it is not reproducibly predictable. The
classic examples in this group are plexiform fibrohistiocytic tumor and
angiomatoid fibrous histiocytoma.

 Malignant - Soft tissue sarcomas are locally destructive with the potential to
recur. The risk of distant metastasis is significant. (Depending on histologic
type and grade, the potential ranges from 20% to almost 100%).
Histologically low-grade sarcomas have a lower chance of metastasis (only
2-10%).18 However, the recurrences of such tumors may advance in grade and
attain a higher risk of metastatic potential similar to that associated with
 myxofibrosarcoma and leiomyosarcoma. Diagnostic Procedures
Laboratory Studies. Other than histologic and cytogenetic analysis, no
specific laboratory tests exist for diagnosing soft tissue tumors.
Biopsy usually is indicated for a soft tissue mass arising in a patient
without a history of trauma or for a mass that persists for more than 6 weeks
following local trauma. All soft tissue masses larger than 5 cm, as well as any
enlarging or symptomatic lesions, also should be biopsied. Small,
subcutaneous lesions that persist unchanged for years may be considered for
observation rather than biopsy. A high level of suspicion is necessary to
ensure early treatment.
Early tissue diagnosis is the most important component of
multimodality treatment for soft tissue tumor. Proper and timely biopsy is
critical. An inadequately performed biopsy may complicate patient care and
result in loss of limb or life. Several biopsy techniques are available,
including FNAB, core needle biopsy, incisional biopsy, and excisional
biopsy. The choice of biopsy is based on the size and location of the mass
and the experience of the surgeon. Excisional biopsy is indicated only for
small, superficial masses (<3-5 cm in greatest dimension), in which the
probability of malignancy is low. Effective reexcision is more likely for
smaller malignant lesions that initially are unintentionally treated as benign.
o Fine-needle aspiration biopsy
 This is a cytologic technique involving the use of a fine-
gauge (usually 21- to 25-gauge) needle to aspirate individual
tumor cells and microfragments from the mass. The aspirated
material can be examined as a cytology smear, with
immediate evaluation of specimen adequacy.

Imaging Studies. In the past 2 decades, imaging studies have contributed

greatly to the management of soft tissue tumors. Imaging studies should be
obtained before biopsy to ensure that a biopsy of a potentially malignant lesion
is taken in a manner that will not preclude limb-salvage surgery. Imaging should
also be performed before biopsy, to prevent the biopsy tract from adversely
affecting the capture of anatomic detail by magnetic resonance imaging (MRI).
The relationship of the tumor and surrounding normal structures to the planned
biopsy site should be evaluated, as should the functional status of the involved
limb, signs of lymph node involvement, and any other factors that could
compromise optimal surgical or radiation therapy.

 Because prognosis is primarily dependent on the disease stage rather than

the histologic tumor type, evaluation of local and distant extent is pivotal
in the ultimate management of soft tissue sarcoma. Imaging methods
commonly used for such evaluation include plain radiographs, computed
tomography (CT) scanning, MRI, and bone scintigraphy (bone scan).
 Positron emission tomography (PET) scanning is being used more
frequently to assess the metabolic activity and, presumably, the biologic
aggressiveness of a lesion. Angiography to evaluate any vascular
involvement by soft tissue tumors has essentially been replaced by MRI.
o CT scanning
 Check for presence and number of pulmonary metastases.
 Consider performing a CT scan of the liver in cases of intra-
abdominal or retroperitoneal tumors.
o MRI
 In contrast to CT scanning, MRI is not limited to the
transverse (axial) plane. Coronal, sagittal, and oblique planes
may be imaged.
 MRI best defines the relationship between a tumor and
adjacent anatomic structures, such as compartment
boundaries, nerves, vessels, and muscle.7,8
 Although for most patients MRI alone suffices, the
information obtained from CT scanning and MRI of the
primary tumor occasionally may be complementary. Bony
involvement may be better assessed with a CT scan, as may
the boundary between normal muscle and fibrous lesions

Medical Therapy
High-grade soft tissue sarcomas often are treated with ifosfamide- and
doxorubicin-based chemotherapy. This is controversial, as no definitive studies
exist proving that adjuvant chemotherapy contributes to prolonged overall
survival.20,21
Surgical Therapy
Localized tumors. Complete local excision is adequate treatment for
benign soft tissue tumors. However, a variety of treatment options, including
surgery alone or combined with radiation therapy or chemotherapy, may be
considered for treatment of localized primary and recurrent sarcomas.
Extremity sarcoma. Extremity sarcomas may be treated surgically, with
or without radiation therapy and adjuvant chemotherapy.
Surgery is the most important component of any treatment plan for a clinically
localized primary or recurrent soft tissue sarcoma. On the basis of the achievable
margin, 4 types of excisions may be performed.

 Intracapsular excisions and amputation - The excision or amputation

passes within the tumor itself. The tumor inside the pseudocapsule is
removed (often piecemeal). Incidence of local recurrence with these types
 of excisions is virtually 100%; these procedures are performed only in
unusual circumstances.
 Marginal excisions and amputation - The excision is performed through
the pseudocapsule surrounding the tumor. Shelling-out procedures and
most excisional biopsies belong to this category. The chance of local
recurrence is 20-75%, depending on the nature of the tumor and whether
or not radiotherapy is used.
 Wide excisions and amputation - The tumor is excised with a wide margin
of surrounding normal tissue but within the muscular compartment.
Without adjuvant therapy, the incidence of local recurrence following
wide excision varies but may reach 30%; the rate of recurrence depends
on the selection criteria used and the adequacy of the histologically
assessed surgical margin. A wide amputation is performed through the
normal tissue proximal to the reactive zone around the tumor but remains
within the involved compartment. Limb-sparing procedures belong to this
category.
 Radical excisions and amputation - These are en bloc excisions of the
tumor along with the entire muscle compartment. Amputation with
disarticulation of the joint proximal to the involved compartment is called
radical amputation. The risk of local recurrence is lowest with this
procedure.

For better local control, many patients undergoing surgical excision receive
radiation therapy. In patients who refuse or cannot tolerate surgery, radiation
alone can be an effective treatment for certain extremity sarcomas.

 Postoperative radiation therapy - Following wide surgical excision,

radiation therapy enhances local control for primary extremity sarcomas.
The concept of limb-sparing surgery with postoperative radiation has been
validated by randomized trials of amputation versus wide local excision. 22
Usually, a total dose of about 60 grays (Gy) is adequate.
 Brachytherapy - Postoperative radiation can also be delivered to the tumor
bed by means of brachytherapy (in which radioactive sources are
implanted in the patient). The advantage of this approach is that it requires
a much shorter time for initiation and completion of therapy than does
external radiation. External beam radiation is used for 6 weeks beginning
a month or more following surgery; brachytherapy usually is started
within a week of surgery and completed in 4 or 5 days. Because of its
technical complexity, brachytherapy requires an experienced radiation
oncologist during the operating procedure. Brachytherapy and external
beam radiation appear to be equally effective when properly administered.
 Preoperative radiation therapy - The employment of preoperative
radiation therapy may allow less radical forms of surgery to be used,
 specifically on large tumors that otherwise may compromise limb-sparing
procedures. Radiation-induced tumor shrinkage decreases the magnitude
of resection needed and reduces the risk of seeding by viable tumor cells.
Local fibrosis may make the resection more challenging.

Follow-up. General follow-up care includes surveillance studies to evaluate

local recurrence and distant metastasis of malignant and intermediate tumors.
The precise interval between and the duration of various follow-up studies are
not well defined. In general, vigorous surveillance continues for 3-5 years after
treatment. Benign tumors generally do not require such surveillance.

Papilloma. The papilloma is a relatively common, benign neoplasm of

unknown origin that arises from the surface epithelium. It is typically an
exophytic lesion with a cauliflower-like surface or with finger-like projections
generaly arisingfrom apedunculated base. Althoughthe average age of
occurrence is the fourth decateof life. The most common sites of occurrence
appere to be on the palatal complex and tongue, following by the lips, gingia,
and buccal mucosa, floor of the mounth, retromolar pad, alveolar ridge, and
buccal vestibular regions.

Oral verruca vulgaris, or oral warts, are e-phytic papillomatous lesion

indistinguishable clinically from oral squamous cell papillomas. In their skin
counterpart, the common wart, (veruca vulgaris), they are a viral disorder caused
by a human papillomavirus and may be spread to oral cavity through
autoinoculation by a finger thumb-sucking habit. Because oral papillomas
cannot be distinguished clinically from verruca vulgaris and have a similar
histomorphology, it is entirely possible that many oral papillomas have a viral
cause.

Histologically, the papilloma is seen as a preparation of the spinous cell layer in

a papillary patern often with hyperkeratosis, acanthosis and siliar hyperplasia.
Mitotic figures may be promire. The supporting fibrous connective-tissue
stromaten contains prominent numbers of small blood selsas well as an
inflammatory cell infiltrate thouth the presenceof a coarse keratohyaline
granular cell layer and the presenceof vacuolated cells with piknotic nuclei
(koilocytes) have been used by some to differentiate verruca vulgaris from a
papilloma, they are accurately distinguished on the bases of ultrastructures,
immunohistological findings, or the use of molecular hydridization techniques to
probe for DNA.

Fibroma. The fibroma is the most common benign soft-tissue tumor

found in the oral cavity. It is characteristically a dome-shape lesion with a
sessile base and a smooth surface that is usually the color of the surrounding
mucosa. It may vary from firm to flaccid in texture, most commonly occurring
in sites predisposed to irritation or trauma, such as the buccal mucosa, lip,
tongue gingiva and hard palate. It may occur at any age. Although generally
classified as benign connective-tissue neoplasm most if not all of those lesions
occurring in the oral cavity are reactive in nature, being basically either a
reactive type of fibrous hyperplasia or in some cases a healed pyogenic
granuloma that has undergone scleroses.

Histologically, the fibroma is a dome shape lesion composed of a fibrous

connective tisure stroma that may vary from loose and delicate to quite dense in
its appearance, with an overlying layer of stratified squamous epithelium.

Pyogenc granuloma is a relatively common soft-tissue tumor that arise

from fibrous connecrive tissue of the skin or mucous membranes. Originally
believed to be a botryomycotic infection it is known to be a reactive
inflammatory process in which there is seen an exuberant fibrovascular
proliferation of the connective tissue secondary to some low grade, cronic
iritant.

Cllinicaly, the pyogenic granuloma is a raised lesionon eithera sessile or a

pedunculated base. Its surface may be smooth or lobulated or occasionally warty
apperance that is erythematous or often ulcerated. Depending on the age of the
lesion it will vary in texture from soft to firm and is suggestive an fibroma.
Becuase of their pronounced vascularity, these lesion often bleed easily when
probed. In 70% incidence of occurrence on the gingia, most commonaly the
maxillary anterior followed by mandibullar anterior labial gingia, lips, tounger,
buccal mucosa, palate, mucolabial or mucobuccul fold.

Histologically the pyogenic granuloma presentsas a remarkabale proliferation of

plumb fibroblasts and endothelial cells with the formation of prominent numbers
thi-walled endotheliun-lined vascullar channels. A polymorphous inflammatory
cell infiltrate is present and the overlinying surface epithelium is often ulcerated.

Peripheral ossifying fibroma which is also has been called the peripheral
odontogenic fibroma is a reactive lesion believed to be of periodontal ligament
origin that occuers exclusively on the gingia. 50% of the lesions were noted to
occur between 5 and 25 years of the age, with the pick incidence of 13 years.
The lesion is equally divided between the maxilla and the mandible, with over
80% of the lesions in both jaws occurring anerior to the molar area.
Histologically the peripheral ossifying fibromais a proliferation of plump
fibroblasts in a characteristic stroma of delicate, underlacing collon fibrils.
Osteoid and calcified material varying from distrophic calcification to spicules
of lamellar may be found on the lesion. The surface epithelium is often
ulcerated.
 The peripheral ciant cell granuloma like pyogenic granuloma and
peripheral ossifying fibroma may represent an unusual response of tissues to
injury. Occurred between the 7- 15 years of age. The lesion were noted on
gingia of the alveolar ridge and involving mandibular more often than maxilla.
The histomorphology of the peripheral giant granulomais essentially identical to
that of central giant granuloma.

Neurofibroma and neurofibromatos. Neurofibroma is a benign

neoplasm of neural sheaph origin. It may occuer as a solitary lesion or as part of
clinical spectrum of neurofibromatosis. Isolated neurofibromas do not differ
from those found in association with neurofibromatosis. Neurofibromatosis is an
autosomal dominant inherited disease characterized by the presence of cafe au
lait spots and neurofibromas on the skin. On clinical significance is the
tendency, in patient with neurofibromatosis toward the malignant degeneration
of neurofibromas in from 3% to 15% of cases. In persons were multiple
neurofibromas have not been yet noted, the presence of six and more cafe aulait
spots, each larger than 1.5 cm diameter, is considered diagnostic of the desease.

Clinically, neurofibromas are usually seen as nudular lesions on either a sessile

or pedunculate base, often with a normal pink mucosal color. They are most
frequently found on the tonger ad buccal mucosa but occasionally present as
intraoesseous lesions ocurring most commonly in the posterior part of the
mandibular.

Although a great deal of histomorphologic vary ability may be noted, the

neurofibroma, the neurofibroma is primarially composed of fascicles of
neoplastic Schwann cells and collagen within a myxoid matrix. Solitay soft
tissue lesionsare best treated by simple surgical excision.

Congenital epulis of new born. Is a rare lesion of unknown originthat appears to

occur exclusively in new born infants chiefly on the maxillary anterior alveolar
ridge and less commonly on the mandibular alveolar ridge. Clinically it is a
pedunculated mass. Over 90% of cases occur in females.

Althoughits histognesis is uncertain, the congenital epulis is hidtologically

similar to the granular cell myoblastoma except that the latter is characterized by
pseudoepithelomatous hyperplasia of the overlying epithelium, whereas the
epithelium over the congenital epulis is generaly thin without rete ridge
formation.