In most cases, a careful history and physical examination will identify a readily diagnosable cause of the lymphadenopathy, such as upper respiratory tract infection, pharyngitis, periodontal disease, conjunctivitis, lymphadenitis, tinea, insect bites, recent immunization, cat-scratch disease or dermatitis,
2. CONTENTS
Ö Introduction
Ö Anatomical Structure
Ö Physical Examination Of Lymph node
Ö Imaging based Nodal Classification for neck
metastasis
Ö Evaluation of suspected cause of
lymphadenopathy
Ö Cause Of Cervical Lymphadenopathy
Ö Management
Ö References
3. INTRODUCTION
⢠Lymphadenopathy is an abnormal increase in
size or altered consistency in lymph nodes.
⢠The condition is generally not a disease, it may
be a symptom of one of many possible
underlying problems.
4. The peripheral nodes are arranged in
two circles superficial and deep
⢠Submental
⢠Submandibuar
⢠Buccal & mandibular
⢠Pre auricular
⢠Post auricular
⢠Occipital
⢠Anterior cervical
⢠Superficial cervical
Superficial nodes
⢠Prelaryngeal and pretracheal
⢠Paretracheal
⢠Retropharyngeal
⢠Waldeyerâs ring
Deep circle of cervical lymph node
5.
6. LYMPHNODES OF
HEAD AND NECK
The entire lymph from the head and
neck drains ultimately into the deep
cervical nodes
The jugulo digastric nodes
Jugulo omohyoid nodes
11. MECHANISM OF
LYMPHADENOPATHY
There are two mechanism of
lymphadenopathy â hyperplasia and
infiltration
Hyperplasia Infiltration
It occurs in
response to
immunologic
or infectious
stimuli
It occurs by
infiltration by
various cell
types, including
cancer cells,
lipid cells or
glycoprotein
laden
macrophages.
12. PHYSICAL
EXAMINATION
& ANATOMY
OF NECK
⢠Physical Examination of a region involves
⢠Inspection
⢠Palpation
⢠To detect changes in the contour of neck
we must know the normal topography of
this region.
⢠Certain normal skeletal & soft tissue
structures of the neck are readily
identified by palpation.
⢠Normal size, contour, consistency is
necessary to identify them
NORMAL PALPABLE MASSES PATHOLOGIC ONE
13. PHYSICAL
EXAMINATION
& ANATOMY
OF NECK
â SKIN AND SUBCUTANEOUS TISSUE (Neck)
â The investing cervical fascia is attached to lower
border of mandible, mastoid process, hyoid bone
and clavicles.
â It forms the heavy membrane over the deep
structures of neck.
â The mobile skin and subcutaneous tissue are
superficial to the investing fascia.
â Thus masses arising within this area exhibit the
mobility unless fibrosis or malignancy has fixed
the deeper layer.
14. SPECIFIC REGIONS OF NECK
Submandibular
region
Parotid region
Median â
paramedian
region
Lateral region
21. Examination
of deep
cervical nodes
â Ask the patient to sit erect and turn the
head to one side to relax the
sternomastoid muscle.
â Use thumb and finger to palpate under the
anterior and posterior borders of the
relaxed muscle and repeat the procedure
on the opposite side.
â Palpate the posterior cervical nodes in the
posterior triangle close to the anterior
border of the trapezius muscle.
â Finally, check for supraclavicular nodes
just above the clavicle, lateral to the
attachment of the sternomastoid.
23. LYMPH
NODES OF
THE NECK
⪠A capillary plexus of endothelial tubes is found below
the epidermis and oral mucosa of the head and neck.
⪠It collects the fluid from the interstitial space for
return to the large venus trunks at the base of the
neck.
30. OTHER
DISORDERS
A. Castlemanâs disease (giant lymph node hyperplasia)
B. Sarcoidosis
C. Dermatopathic lymphadenitis
D. Lymphomatoid granulomatosis
E. Kikuchiâs disease (histiocytic nectrotizing
lymphadenitis)
F. Kawasakiâs disease (mucocutaneous lymph node
syndrome)
G. Histocytosis X
H. Severe hypertriglyceridemia
32. ⢠Level I:
⢠Above hyoid bone
⢠Below mylohyoid muscle
⢠Anterior to back of submandibular gland
⢠Previously classified as submental and submandibular nodes
⢠Level IA:
⢠Between medial margins of anterior bellies of digastric muscles
⢠Previously classified as submental nodes
⢠Level IB:
⢠Posterolateral to level IA nodes
⢠Previously classified as submandibular nodes
33. Level II: From skull base to level of lower body of hyoid bone
Posterior to back of submandibular gland
Anterior to back of sternocleidomastoid muscle
Level IIA: Anterior, lateral, medial, or posterior to internal jugular vein
Inseparable from internal jugular vein (if posterior to vein)
Previously classified as upper internal jugular nodes
Level IIB: Posterior to internal jugular vein with fat plane separating nodes and
vein
Previously classified as upper spinal accessory nodes
34. Level III: From level of lower body of hyoid bone to level of lower cricoid cartilage
Anterior to back of sternocleidomastoid muscle
Previously known as mid jugular nodes
Level IV: From level of lower cricoid cartilage to level of clavicle
Anterior to line connecting back of sternocleidomastoid muscle and posterolateral margin of anterior scalene
muscle
Lateral to carotid arteries
Previously known as low jugular nodes
Level V: Posterior to back of sternocleidomastoid muscle from skull base to level of lower cricoid arch
From level of lower cricoid arch to level of clavicle as seen on each axial scan
Posterior to line connecting back of sternocleidomastoid muscle and posterolateral margin of anterior scalene
muscle
Anterior to anterior edge of trapezius muscle
35. Level VA: From skull base to level of bottom of cricoid cartilage arch
Posterior to back of sternocleidomastoid muscle
Previously known as upper level V nodes
Level VB: From level of lower cricoid arch to level of clavicle as seen on each axial scan
Posterior to line connecting back of sternocleidomastoid muscle and posterolateral margin of anterior scalene
muscle
Previously known as lower level V nodes
Level VI: Between carotid arteries from level of lower body of hyoid bone to level superior to top of manubrium
Previously known as visceral nodes
Level VII: Between carotid arteries below level of top of manubrium
Caudal to level of innominate vein
Previously known as superior mediastinal nodes
36. Supraclavicular: At or caudal to level of clavicle as seen on each axial
scan
Lateral to carotid artery on each side of neck
Above and medial to ribs
Retropharyngeal: Within 2 cm of skull base and medial to internal carotid
arteries
43. INFECTIONS
UPPER RESPIRATORY INFECTION â
Acute bacterial cervical lymphadenopathy
commonly caused by bacteria and viruses that
infect the upper respiratory tract.
Viruses that frequently cause this infection include
adenovirus, influenza virus, group A beta
hemolytic streptococcus
( bacterial pharyngitis)
Other common bacteria causing infection are
Group b C and G hemolytic streptococci,
cornybacteria & several anaerobes.
44. INFECTIONS
Clinical Features â
symptoms â cough, sinus congestion,
rhinorrhea, and occasionally fever and malaise
sign â Cervical lymph nodes bilateral palpable,
and may persist for weeks after the resolution of
other symptoms.
Diagnosis â
based on symptoms.
Viral culture, serological antigen detection for
persistent infection
Management â Palliative treatment
45. LOCAL
INFECTION
⢠Local bacterial infections of the head and
neck often cause cervical adenopathy
when the infection localize within the
node.
⢠Common bacterial pathogens are
staphylococcus aureus & streptococcus
pyogens.
⢠It includes tonsillar abscess, salivary
adenitis & dental abscess
⢠Source â viral infection (herpes simplex,
coxasackie virus)
46. LOCAL
INFECTION
⢠Often affect children and adolesents
⢠Acute painful oral ulcers and oropharynx
⢠Enlarge bilateral tender lymph nodes in anterior triangle
of neck
⢠Submandibular and sub mental adenopathy
⢠Occasionally fever and malaise
⢠Do not present with other systemic complications
(hepatospleenomegaly or generalized lymphadenopathy)
Clinical features â
D/D â Acute pyogenic cervical lymphadenitis
47.
48. SYSTEMIC INFECTION ⢠Severe acute and chronic
infection cause cervical
lymphadenopathy.
⢠Cervical adenopathy is a
common features of many viral
infections
⢠Systemic viral infections may
cause acute syndrome such as
hand foot mouth diseases,
chicken pox, measles, rubella.
⢠Enlarge lymph nodes are firm
tender characteristically not
warm and erythematous.
49. Nontender
Lymphoid
Hyperplasia
⢠One or two such enlarged nodes are found
during routine papation.
⢠It represents persistent chronic lymphadenitis
or a permanently enlarged node after an acute
or chronic lymphadenitis.
⢠Features â
⢠the nodes are solitary, discrete,
asymptomatic, freely movable.
⢠Ex â submandibular and submental group
of lymphnode
50. Nontender
Lymphoid
Hyperplasia
Management â
The patient should
reexamine at two weeks
to see the mass,
changes perceptibly
If doubt still exists,
biopsy and microscopic
study are adviced
Differential
Diagnosis â
secondary carcinoma
51. CAT â SCRATCH
DISEASE
⢠Causative organism â Bartholena species
(B Henselae)
⢠Clinical Features â
â fever, headache, malaise,
â Cervical lymphadenopathy involving
parotid and submandibular gland.
â At the site of inoculation pustular skin
lesion is formed
â Nodes often warm, tender,
erythematous, may be indurated or
supporative.
52. CAT â
SCRATCH
DISEASE
⢠Serologic testing for the presence
of antibody to B Henselae
⢠Lymphnode biopsy
Investigations â
⢠Self limiting, resolving with out
treatment within 2 â 3 months.
⢠Antibiotic â trimethoprin-
sulfamethoxazole.
Management â
53. TUBERCULOSIS
Caused byâ M. Tuberculosis
(infectious communicable organism)
Clinical features â
⢠Weight loss, night sweat, fever, malaise,
anorexia
⢠Persistent cough (pulmonary TB)
⢠Hemoptysis and nonpurulent sputum
⢠Chronic granulomatous lymphadenitis
typically within nodes draining salivary
glands.
⢠Tubercular cervical lymphadenitis (scrofula)
54. TUBERCULOSIS
Investigations â
â Chest X-ray
â Tuberculin test
â Mantoux test
â Histopathologicallly gram staining
and LĂśwensteinâJensen medium
staining
55. Rheumatoid
Arthritis
⢠Autoimmune condition.
⢠Characterized by chronic inflammation of
the synovium with an affinity for small
joints often leading to destruction of bone
& cartilage.
⢠Inflammation of surrounding tendon and
joint deformity.
⢠Other clinical signs and symptoms may
include fatigue, anorexia, weakness, and
muscular pain.
56. Rheumatoid
Arthritis
⢠75% of patients with rheumatoid arthritis may
present with enlarged lymph nodes.
⢠Enlarged nodes are associated with active disease
and are often localized near an inflamed joint,
although generalized lymphadenopathy is also
quite common.
⢠Histopathology - Rheumatoid arthritis will
typically contain an extensive reactive follicular
hyperplasia and interfollicular plasmacytosis.
58. Systemic Lupus
erythematosus
⢠This disease is characterized by production of
auto antibodies and immune complex, which
lead to array of systemic complication.
⢠Specifically, the formation of immune
complex results in an immune reaction, which
activate the compliment system.
⢠The ultimate outcome is tissue injury caused
by vasculitis, fibrosis, and tissue necrosis.
⢠Lymphadenopathy is recognized as one of the
clinical manifestations of SLE.
59. Systemic Lupus
erythematosus
⢠Clinical manifestations â
⢠The classic categorization of LE into SLE
and DLE has during recent years been
supplemented with acute cutaneous lupus
erythematosus and subacute cutaneous lupus
erythematosus.
⢠SLE may also occur in concert with other
rheumatologic diseases such as secondary
SjĂśgrenâs syndrome and mixed connective
tissue disease.
⢠These lesions may form butterfly-like rashes
over the cheeks and nose known as malar
rash.
60. Histopathology
Ű A diffuse hyperplasia with small
lymphocytes, plasma cells.
Follicles may be scarce or absent,
however, there are some reports
of finding follicular hyperplasia.
61. SJĂGRENâS SYNDROME
⢠This chronic autoimmune disorder is characterized by xerostomia, xerophthalmia, and
exocrine gland involvement. When this triad is present, SjĂśgrenâs syndrome may also
be referred to as âsicca complex.â
⢠Individuals with SjĂśgrenâs syndrome display a wide spectrum of severity that may
involve multiple organ systems, including the eyes, oral cavity, salivary glands, the
lungs, kidneys, skin, and nervous system.
62. SJĂGRENâS
SYNDROME
⢠Clinical features â
â Keratoconjunctivitis,
â Hypofunction of the salivary glands,
â Vasculitis,
â Glomerulonephritis,
â Interstitial nephritis,
â Parotid gland enlargement,
â Polyneuropathies
63. SJĂGRENâS
SYNDROME
⢠Lymph node histology â
â Paracortical hyperplasia with prominent
vascular proliferation and many lymphoid
follicles with germinal centers.
â The paracortical area of the node typically
contains numerous T-lymphocytes without
cytological atypia, accompanied by a variable
number of plasma cells, B-immunoblasts, and
histiocytes.
64. SJĂGRENâS
SYNDROME
⢠Laboratory blood studies are helpful in
the evaluation of dry mouth, particularly
in suspected cases of SjĂśgrenâs syndrome.
⢠The presence of nonspecific markers of
autoimmunity, such as antinuclear
antibodies, rheumatoid factors,
elevated immunoglobulins (particularly
[IgG]), and ESR, and the presence of
antibodies directed against the extractable
nuclear antigens SS-A/Ro or SS-B/La
are important contributors to the
definitive diagnosis of SjĂśgrenâs
syndrome.
65. MALIGNANCY
⢠There are several metastatic tumors that may present
as cervical lymphadenopathy; these are tumors of the
skin and appendages, oropharynx, larynx, thyroid
gland, salivary gland, and nasophrynx.
⢠Widespread lymphadenopathy may be seen with
many solid tumors.
⢠Malignancies arising from cells in the immune system
may also cause lymphadenopathy.
66. MALIGNANCY OF LYMPHOID TISSUE
Hodgkinâs
lymphoma
Non â
hodgkinâs
lymphoma
Burkittâs
lymphoma
Primary
reticular cell
sarcoma
Leukemia
68. Hodgkinâs lymphoma
Lymphocyte predominant
abundant lymphocytes, few plasma
cells, occasional Reed-Sternberg
cell, localized involvement of one
side of diaphragm.
Mixed cellularity lymphocytes,
plasma cells, eosinophils, easily
identified Reed-Sternberg cell.
Nodular sclerosis sparse
lymphocytes, stromal cells, fibrosis
and numerous but bizarre Reed-
Sternberg cells.
Lymphocyte depletion
lymphocytes, plasma cells,
eosinophils with localized
involvement.
Types
69. ⢠Symptomsâthe involved nodes are painless. Generalized weakness, loss of weight, cough, dyspnea
and anorexia are seen. Pain in back and abdomen owing to splenic enlargement
⢠Signsâthe lymph nodes are discrete and rubbery in consistency with overlying skin being freely
mobile.
⢠Pel Ebstein fever - a cyclic spiking of high fever.
⢠It may appear in the oral cavity as an ulcer or a swelling or as an intra-bony lesion.
70. Radiographic
Features
SiteâRarely seen in jaws (posterior maxilla and
mandible).
Appearance â Irregular bone loss. There are radiolucent
areas separated from each other by normal appearing
bone which later become confluent.
Margins â The radiolucent lesions have diffuse ill defined
margins which suggest infiltration of bone.
Osteoblastic type â uncommon in jaws, but it is seen in
the vertebrae and pelvis. In it, there is frank sclerosis
with filling of the marrow spaces by bone.
71. Non-Hodgkinâs
Lymphoma
(Lymphosarcoma)
⢠Frequently widespread at the time of
diagnosis, often involving not only the
lymph nodes but also bone marrow, spleen
and other tissue. Early involvement of
bone marrow is typical.
⢠Etiology
â Viralâthe herpes virus and Epstein
barr virus.
â Immunologicalâthere may be induced
immunologic effect permitting a
malignant clone to proliferate.
72. Clinical
Features
⢠Age/Sex - all age, M>F
⢠Painless lymph node enlargement of
abdominal & mediastinal region
⢠SymptomsâPatient C/o of tiredness, loss of
weight, fever and sweating. Pain is the main
symptom of bone involvement which may
present as a pathological fracture.
⢠hepatosplenomegaly is present. The growth
is fleshy and is prone to ulceration.
⢠palatal lesions have been described as slow
growing, painless, bluish soft tissues mass
73. Radiographic
Features
⢠Small radiolucent foci scattered throughout the area.
⢠Moth eaten radiolucency with poorly defined margins.
⢠Marked expansion of bone. Erosion and perforation of
cortex may occur.
⢠Teethâcortices of unerupted tooth buds and lamina
dura of adjacent teeth are lost. Teeth may be resorbed
74. Differential
Diagnosis
⢠Multiple myeloma â Bence Jones proteins are
present in urine, borders of lesion are usually
well defined.
⢠Metastatic carcinoma â history of primary
tumor.
⢠Ewingâs sarcoma â It occurs in younger age
group.
⢠Osteosarcoma â It can be differentiated by
clinical features.
75. Burkittâs
Lymphoma
(African jaw
lymphoma)
â Etiology - Epstein-Barr virus
â Clinical Features
â Age & sex - 6 - 9 years. Males : females' ratio
of 2:1.
â maxilla > mandible, where it may spread
rapidly to the floor of the orbit.
â Symptoms - Painless swelling of jaws,
abdomen
â peripheral lymphadenopathy common.
â loosening or mobility of permanent teeth. There
is gross distortion of the face due to swelling
76. Radiographic Features
Moth eaten appearanceâsmall radiolucent foci scattered throughout the affected area. Focal areas of
radiolucency are darker and sharper than the shadow of the marrow space lined by normal bony trabeculae.
Sunray appearance seen
Marginsâill defined and non-corticated.
Shapeârapidly expand and are ballooned shaped.
Maxillary sinusâin the maxilla, there is blurring of shadow of antrum
77. Radiographic Features
TEETHâLESIONS ARE OSTEOLYTIC WITH LOSS OF LAMINA
DURA ABOUT THE ERUPTED TEETH AND CRYPTS OF
DEVELOPING TEETH ARE ENLARGED. ERUPTED TEETH IN
THE AREA ARE GROSSLY DISPLACED, AS ARE THE
DEVELOPING TOOTH CRYPTS.
EFFECT ON SURROUNDING STRUCTURESâRAPIDLY
EXPAND, CAUSING GROSS BALLOON-LIKE EXPANSION WITH
THINNING OF ADJACENT STRUCTURES AND PRODUCTION
OF SOFT TISSUE MASS ADJACENT TO THE OSSEOUS LESION.
EROSION AND PERFORATION OF THE CORTEX IS SEEN. IN
SOME CASES, ORBIT IS INVOLVED AND THERE IS
DISPLACEMENT OF ORBITAL CONTENT.
78. á´Ľ Differential diagnosis â
á´Ľ Infectious mononucleosis â
in this disease the nodes
often tender
á´Ľ Paul â Bunnel heterophilic
test is positive
80. Acute
lymphadenitis
⢠Lymphadenitis is an inflammation or infection
of a lymphnode, & it frequently occurs when
an infection is present in the tissue drained by
the particular nodes pathway.
⢠It is the 2nd most common pathologic cervical
mass and the most common painful
enlargement.
⢠Primary source of infection may be oral
cavity, nasal cavity, pharynx, tonsils.
81. ACUTE
LYMPHADENITIS
Clinical features â
⢠It is usually tender on palpation
⢠Single affected nodes are round firm , may
be movable or fixed
⢠Several nodes may be involved in such
cases accompanying inflammation cause a
firm swelling. That prevent palpation of
lymph nodes
D/D â Ludwigâs angina
infected cyst of neck
82. Management
â In most cases, when the primary mucosal
infection is eliminated, the secondary acute
lymphadenitis soon regresses.
â Adequate dose of antibiotic specific to the
organism is administered.
83. Rare varieties
of specific
lymphadenitis
⢠It results from primary infection by bacteria /
vurus
⢠The specific lesions with in lymph nodes
generated by tuberculosis, histoplasmosis,
sarcoidosis, infectious mononucleosis
⢠Investigation â
Biopsy
Culture to be one of the specific infection.
84. Kikuchi disease
⢠It is a type of cervical sub-acute necrotising
lymphadenopathy, characterised by extensive areas
of necrosis bounded by broad zones of histiocytes
and activated lymphoid cells.
⢠It is one of the important Diagnosis because it is
often misdiagnosed as lymphoma.
⢠Cervical lymphadenopathy is common clinical
condition and in most cases histopathologic
examination is enough to diagnose the etiology of
cervical lymphadenopathy.
85. EVALUATION OF
SUSPECTED CAUSE OF
CERVICAL
LYMPHADENOPATHY
Disease Clinical features Investigatory findings
Infectious
Mononucleosis
Fatigue, malase, fever,
atypical lymphocytosis
Monospot, IgM early
antibody or viral capsid
antigen
Toxoplasmosis 80 â 90 % patient are
asymptomatic
IgM toxoplasm antibody
Cytomegalo
Virus
Often mild symptoms,
Hepatitis
IgM CMV antibody, viral
culture of urine or blood
Cat scatch
disease
Fever, cervico â facial
lymph nodes are palpable
Usually clinical criteria,
biopsy if necessary
Pharyngitis due
to group A
streptococcus
Fever, Pharyngeal
exudates, cervical nodes
Throat culture on
appropriate medium
Tuberculous
lymphadenitis
Painless, chain of cervico
â facial lymphadenopathy
Purified protein
derivative, biopsy
86. EVALUATION OF
SUSPECTED CAUSE
OF CERVICAL
LYMPHADENOPATHY
Disease Clinical features Investigatory
findings
Lymphoma Fever, night sweats,
weight loss in 20 -30
% cases
biopsy
Leukemia Blood dyscreasis,
bruising
Blood smear, bone
marow
Serum sickness Fever, malase,
urthralgia, urticaria
Complement assay
Sarcoidosis Hilar nodes, skin
lesions, dyspnoea
Biopsy
kawasakidisease Fever, conjunctivitis
rash, mucous
membrane disease
Clinical criteria
87. Investigation
(FNAC)
Straw colored fluid contain cholesterol crystals, seen in some
odontogenic and fissural cyst.
Thick yellowish white &
granular fluid
epidermoid and keratocyst in which lamina is
filled with keratin
Yellowish cheesy material dermoid cyst
Sebum sebaceous cyst
Amber colored fluid thyroglossal duct cyst
Lymph fluid colorless with high lipid content, appears
cloudy and frothy. It is seen in hygroma and
lymphoma
Blue blood hematoma, hemangioma
Brighter red blood aneurysm and arteriovenous fistula
Pus abscess
Sulfur granules actinomycosis
88. Consistency
of
pathological
mass
SOFT CHEESY RUBBERY FIRM BONY
HARD
Inflammatory
hyperplasia
Cystic
hyperplasia
Cystic hygroma
Tubercular
node
Sebaceous
dermoid and
epidermoid
cyst.
Lymphoma
(hodgkinâs
lymphoma,
Nonhodgkinâ
lymphoma,
Burkitt
lymphoma)
Myxoma
Myoblastoma
Inflammation
& infection of
lynphnode
Ex â dental
abscess
Osteosarcoma
Metastatic
lymphnode
Squamous
cell
carcinoma
Malignant
lymphoma
Malignant
melanoma
Metastatic
tumor
Sarcoma
89. CONCLUSION
â An understanding of head and neck surface anatomy. Recognition of the
major structures, along with knowledge of the distribution of lymph nodes
in the head and neck, will help identify normal versus abnormal.
â It helps to describe the physical findings Thorough physical examination
includes evaluation of the skin, neck, ears, eyes, nose, and throat.
â Intraorally, the patientâs oropharynx should be visualized. The oral mucosa,
tongue, periodontium, and dentition should also be examined.
90. REFERENCES
â Wood and Goaz, Differential diagnosis of Oral and Maxillofacial
Lesions, 5th edition 521 â 539
â Dr. Nitin Upadhyayet al, cervical lymphadenopathy, Journal of
Dental Sciences & Oral Rehabilitation : Jan-March 2012
â Anil Govindrao Ghom, Textbook of ORAL MEDICINE, third
edition
â Ernesta Parisi et al, Cervical lymphadenopathy in the dental
patient: A review of clinical approach QUINTESSENCE
INTERNATIONAL,VOLUME 36, NUMBER 6, JUNE 2005
â Yogesh M. Paikrao et al, Clinicopathological study of cervical
lymphadenopathy at rural tertiary health care centre Paikrao YM
et al. Int J Adv Med. 2018 Feb;5(1):154-158 pISSN 2349-3925 |
eISSN 2349-3933
â Peter M. Som et al, Imaging-Based Nodal Classification for
Evaluation of Neck Metastatic Adenopathy, AJR:174, March 2000
â Martin S. Greenberg et al, Burketâs oral medicine Eleventh Edition,
435 - 460