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Contents
1. Introduction
2. Classification
5. References
Introduction
• Presence of giant cell can be pathognomic or characteristic feature of a lesion.
• Most of time they have active participation in lesion , sometime only present in cellular
background.
• They have various source of origin which may determine their functioning.
1. Based on etiopathogenesis
Classification
A. Where giant cells are present in the concerned background
and are pathognomic:
1. Hodgkin’s syndrome
2. Peripheral giant cell granuloma
3. Giant cell fibroma
1. Tuberculosis
2. Herpes simplex virus infection
3. Measles
4. Xanthoma Continued…
C. Diseases associated with the presence of giant cells:
1. Orofacial granulomatosis
2. Fungal infection foreign body reactions
3. Neoplasms
4. Syphilis
5. Leprosy
6. Fibrous dysplasia
7. Cherubism
8. Paget’s disease of the bone
9. Aneurysmal bone cyst
10. Ossifying fibroma
11. Wegener’s granulamatosis
12. Actinomycosis
13. Chronic diffuse sclerosing osteomyelitis
14. Odontogenic giant cell fibromatosis
15. Heerfordt’s syndrome.
2. Based on type of lesion
Giant Cell Lesions
Osteosarcoma
Rhabdomyosarcoma
Continued…
Hodgkin’s lymphoma
Giant Cell Lesions
Fibrous
Dysplasia
3. Based on type of giant cell present
Continued…
III. Lesions with reactive osteoclastic giant cells formed secondarily by the activation of
primary lesional stromal cells
• Chondroblastoma
• Chondromyxoid fibroma
C. Oral granulomatosis
• Specifc: Fungal, bacterial, viral infection
• Non-specific: Sarcoidosis, Wegener ’s granulomatosis
Giant cell
• Giant cells are those cells which are having larger dimension (usually 40
µm to 120 µm diameter) then cells present in a region.
1. Macrophage derived:
3. Melanocyte derived:
a. Starburst giant cells
b. Giant cells in melanocytic nevus
i. Balloon cells
ii. Giant nevus cells
3. Simultaneous fusion
• Two or more macrophage try to ingest the same particle
• Simultaneous fusion occurs
• Leading to formation of multinucleated giant cells.
4. Viral induced
A) Attachment of viral envelope
• When viral envelope attach to a cells
• Cell surface coat thickness is reduced
• Approximation of lipid bilayer of adjacent cell
• Leading to fusion
B) Incorporated virus
• Proteins coded by virus are coated on surface of cell
• Thus infected cell has modified surface
• Promote fusion with uninfected cells.
5. Tumor giant cells
• Tumor cell release extracellular enzymes.
• Reduce surface coat thickness of adjacent cell.
• Causing close approximation of lipid bilayers of cell.
• Leading to fusion.
Microbial giant cell lesions
Oral Tuberculosis
Epitheloid cells
Histopathological
• Treatment
Antitubercular drugs
World Health Organization recommendation, 4th Edn
Tuberculoid Lepromatous
High immune response Reduced immune response
Localized Diffuse
Inoculation period 2 – 5 years 8-12 years
Lepromin test positive Lepromin test negative
Granuloma formation with less Significant number of
number of microorganisms microorganism in cells
Erode basal layer of epidermis. Does not erode basal layer of
Predilection for dermal nerves epidermis
• Leprosy can be also classified according to bacterial load as:
1. Paucibacillary leprosy
(Pauci: few)
Facies Leprosa
Destruction of
•Anterior maxilla and alveolar ridge.
• Anterior nasal spine
•Nasal complex destruction
Infection of lip can lead to macrocheilia
Oral Lesions
Histopathology:
• Tuberculoid leprosy
Granuloma consisting of caseating necrosis surrounded by epitheloid
cell, lymphocytes Langhans’ giant cells . Erosion of basal layer of
epidermis. Invasion of epitheloid cells, Giant cells and lymphocytes
into peripheral dermal nerves.
• Lepromatous
Facial paralysis
Swelling of face and lips Cheilitis granulomatosa
Fissured tongue
• Treatment
Multidrug therapy
Paucibacillary:
Rifampin (600mg once a month)
Dapsone(100mg daily) for 6 months.
Mutibacillary:
Rifampin(600mg once a month)
Dapsone(100mg daily)
Clofamizimine (300mg once a month + 50 mg daily) for 12-24 months.
Syphilis
• It is a Sexually transmitted disease (STD)
•Caused by Spirochaetes Treponema pallidium.
• Mode of transmission
1. Sexual intercourse
2. Intimate person to person contact
3. Materno foetal transmission
• Stages of syphilis
According to period after which lesion is appeared:
1. Primary syphilis
2. Secondary syphilis
3. Tertiary syphilis
Primary Syphilis
•Primary syphilis is characterized formation of chancre at site of inoculation.
•The external genitalia and anus are the most common sites.
•Initially a papule is formed followed by central ulceration.
1. Painless lymphadenopathy
2. Sore throat
3. Malaise
4. Headache
5. Weight loss
6. Fever
7. Musculoskeletal pain.
• The rash may also involve the oral cavity and appear as red, maculopapular areas.
Mucous Patches formation
• Some patients may show focal areas of intense exocytosis of
inflammatory cell and spongiosis (intracellular edema)
leading to zones of sensitive whitish mucosa known as mucous
patches
•Malignant syphilis.
•In this there is absence of any lesions and symptoms, known as latent syphilis.
•Following this some patient enter into third stage known as tertiary syphilis.
Tertiary Syphilis
Systemic complications of tertiary syphilis
1. Arteritis
2. Aneurysm of the ascending aorta
3. Left ventricular hypertrophy
4. Aortic regurgitation
5. Congestive heart failure
Gumma
Luetic glossitis
Hutchinson tried
1. Hutchinson’s teeth
2. Ocular interstitial keratitis
3. Eight nerve deafness
Fiumara NJ, Lessel S: Manifestations of congenital syphilis: an analysis of 271 patients. Arch
Dermatol.1970;102-78.
Investigations
1. Smear or biopsy
Demonstration of microorganism by specific immunofluorescent antibody
or
Serological test VDRL (Venereal Disease Research Laboratory )
and RPR (Rapid Plasma reagin)
• Clinical evidence of this reaction occurs about 8 hours after the first injection
of penicillin
1. Cervicofacial 50%
“Lumpy jaw”
Y. Sasaki,et al .Actinomycosis in the Mandible: CT and MRI findings. Am J Neuroradiol. Feb 2014;35:390–94 .
Investigation
2. Lesional Biopsy
• Antigen is unknown.
• Mostly lymphoid, pulmonary cutaneous and ocular lesions are most common
but any organ in body can be affected.
Lungs
Skin
Ocular
Salivary glands
• Enlargement
• Xerostomia
Intraosseous
•Less frequently, the skull, nasal bones, ribs, and vertebrae are affected.
Oral lesions
Löfgren’s syndrome
1. Erythema nodosum
2. Bilateral hilar lymphadenopathy,
3. Arthralgia
1. Parotid enlargement
2. Anterior uveitis of the eye
3. Facial paralysis
4. Fever
Differential Diagnosis
1. Sjögren Syndrome
Rheumatoid arthrirtis
Systemic Lupus Erythematosus
Collagen disorder
2. Kveim test
•Clinical features
4. Older lesions may show considerable fibrosis of the stroma and foci of
osteoid formation.
Radiographic findings
Location :
In older individuals
this lesion can occur in greater frequency in the
posterior aspect of the jaws.
Periphery
If present which characteristically , emanate at right angles from the periphery of the
lesion. A small indentation of the expanded cortical margin is seen at the point where
this right-angled septum originate.
Effect on surrounding structure
B) Multilocular radiolucency
1. Ameloblastoma
2. Aneurysmal bone cyst
3. Odontogenic myxoma
Treatment and Prognosis
• Surgical : Curettage
•They are not true neoplasm but reactive lesion caused by local irritation or
trauma.
1. Osteoclast
Some researchers suggest it is soft tissue counterpart of CGCG.
That eroded through cortical plate into gingival soft tissues.
2. Common in females
4. Dense fibrous connective tissue separate giant cell proliferation from mucosa.
Radiographic findings
1. Pyogenic granuloma
2. Fibroma
3. Hemangioma
4. Lymphangioma
Treatment
•Commonly Bilateral.
•They appear in Children and young adults and disappear in old age.
1. Fibroma
Treatment
Surgical excision
Recurrence is rare
Clinical features:
Extragnathic
• Bimodal age distribution.
•Most arise in patients between10 and 20 years, with a lesser
number diagnosed in adults older than age 50.
•Common site :
Distal femoral and proximal tibial metaphysis.
•In older patients, the axial skeleton and flat bones are
involved most frequently.
•Mandibular tumors arise more frequently in the posterior body and horizontal ramus
Maxillary lesions are discovered more commonly in the inferior portion
(alveolar ridge, sinus floor and palate) than the superior aspects (zygoma, orbital
rim).
•As jaws are situated closely to tissue that commonly receive therapeutic radiation.
thus they are common site for postirradiation bone sarcomas.
There can be dense sclerosis, mixed sclerotic and radiolucent lesion or completely
radiolucent lesion
When periosteum
is raised,
breached in
centre. But it
maintains its
osteogenic
potential at
periphery.
Internal Structure
• Completely radiolucent, mixed radiolucent- radiopaque or radiopaque.
The tumor cells may have uniform round or spindle-shaped cells or highly
pleomorphic cells with bizarre nuclear and cytoplasmic shapes.
These malignant cells of tumour may also form chondroid or fibrous connective
tissue
Mixed
•Chondrosarcoma
•Peripheral fibroma with calcifications
•Chronic osteomyelitis
Treatment and prognosis
Clinical features:
•Age : Young age
Various reviews reported mean age of 6 to 16 years.
1. Embryonal
2. Botryoid
3. Alveolar
4. Pleomorphic.
1. Embryonal
•Better prognosis
• Histolopathologically:
•Histopathological:
•Less cellular(mesenchymal ) with prominent myxoid stroma.
•Presence of peripheral zone of rich cellularity known as “cambium layer”.
Expansile osteolytic lesion of right maxilla
Embryonal rhabdomyosarcoma
3. Alveolar
•Common in extremities
•Can be seen in head and neck region.
•Poor prognosis
•Histopathological:
•Aggregates of poorly differentiated round to oval cells separated by fibrous septa.
•The peripheral cells of these aggregates adhere to the septal walls in single layer.
•Histopathological:
•Hodgkin’s disease primarily arise within lymph node followed by extranodal sites
secondarily .
Etiology
the cause of this disease is unknown, but could be related with Epstein Barr Virus.
They are precursors of mononuclear cells that continue division and fusion with
each other that leads to formation of multinucleated giant cells .
Clinical Features
• The most common sites of initial presentation are the cervical and supraclavicular
nodes .
Followed by axillary and mediastinal node, abdominal and inguinal lymph nodes.
• Constitutional symptoms:
1. Weight loss
2. Low grade fever
3. Night sweats
4. Generalized pruritus (itching).
5. Malaise
Stage Features
Types :
• Lymphocyte rich
• Nodular sclerosis
• Mixed Cellularity
• Lymphocyte deplition
• Unclassifiable
Type Reed – Sternberg cell Additional Features
Most common
Mixed Cellularity Abundant Classic cells Mixture of plasma cells,
small lymphocytes,
eosinophils and
histiocytes also present
Lymphocyte Bizzare giant Reed Few lymphoctes
deplition Sternberg cells present Most aggressive type
Unclassifiable They do not fit into above subtype thus designated
as unclassifiable.
Differential diagnosis
Patients with stage III or IV disease require chemotherapy and radiation therapy
Prognosis
Histological types
Lymphocyte predominant and Nodular sclerosis : Best prognosis
Because benign, empty, or fluid containing cavity within bone that does not
have epithelial lining .
3. Large lesion may cause expansion of the cortical plates without erosion.
Producing hard bulge on jaw.
Location :
Most common in the mandible.
In rare cases they develop in the maxilla.
2. Walls of the defect may be lined by a thin band of vascular fibrous connective
tissue .
3. Thickened myxofibromatous proliferation intermixed with trabeculae of
cellular and reactive bone can be present as lining.
1. Radicular cyst:
Non vital tooth, absence of lamina dura, a radiolucency with epicenter at periapex of
tooth.
PCOD is not more than 0.7 cm in diameter ; Traumatic bone cyst are larger than 1 cm.
PCOD is seen in patients over 30 years of age
Common site mandibular central incisors
Show maturational changes (calcification)
5. Malignancy
On surgical exposure bone defect will be seen which is usually empty cavity with
smooth, shiny bony walls.
Some times the cavity will contain small amounts of serosanguineous fluid.
The mandibular neurovascular bundle may be seen lying free in the cavity.
But continually effusion with circulating blood from the injured vessels is seen
in developing ABC ,
Not in granuloma .
5. Aneurysmal bone cyst as secondary lesion
•On occasion, the wall contains an unusual lacelike pattern of calcification that is
uncommon in other intraosseous lesions.
Location :
•The septa bear a striking resemblance to the wispy, illdefined septa seen in giant cell
granulomas.
•Another similar finding is septa positioned at right angles to the outer expanded border.
Differential Diagnosis
2. Ameloblastoma
Common in older age (30-70 years)
3. Cherubism
Multifocal bilateral disease
Treatment
Primary hyperparathyroidism
Secondary hyperparathyroidism
1. Common in females
Other soft tissues that may show ectopic calcification are the
subcutaneous tissues, walls of blood vessels, articular
cartilages, and joint capsules.
Lithiasis frequently develops in the pancreas and salivary glands.
Classically known as
“Salt and paper” skull
4. Bone remodelling leads to replacement of normal trabeculae by numerous small
randomly oriented trabeculae, resulting in “ground glass apperarence”.
Normal
2. Secondary
High dietary calcium and vitamin D supplementation.
Calcitriol, an inhibitor of PTH syntheses and secretion.
Miscellaneous lesion
Langerhans cell Histiocytosis
Histiocytosis X Langerhans cell granuloma
Langerhans cell disease Langerhans cell granulomatosis
Idiopathic histocytosis Self healing histocytosis
Eosinophilic granuloma
Definition
Clinicopathological presentation
Clinical features
5. Other bones affected are Femur, Ribs, Vertebra, Pelvis, Humerus and Scapula.
Oral manifestation
1. Sore mouths
2. Most commonly ulcerative lesions
3. Halitosis
4. Gingivitis and suppuration
5. Unpleasant taste
6. Loose and sore teeth with early exfoliation of teeth
7. Failure of healing of tooth sockets following extraction
Histopathology
• Langerhans cell stain positive to S-100 protein and peanut agglutinin and
demonstrate rod shaped cytoplasmic structures called as Birbeck or
Langerhans cell granules.
Birbeck or Langerhans cell granules has dilated terminal ends giving tannis racket
appearance.
Treatment
• If treatment is required
Inapproachable : irradiation
Chemotherapy : Prednisone, Vinblastine, cyclophosphamide
Cherubism
Clinical features
•It is autosomal dominant genetic defect that affects bone
remodeling in specific anatomically confined limits of
embryologic mandible and some time mandible and maxilla.
Both.