• A giant cell is a cell that is larger in dimension than the cells that are
routinely encountered in histology.
• These cells are involved in many physiologic and pathological
• The giant cells may be mononucleated or multinucleated which can
be explained by the mechanism of their formation.
• A multinucleated giant cell (MGCs) is a mass formed by the union
of several distinct cells.
• They are usually of monocyte or macrophage lineage
• In chronic inflammation when macrophages fail to deal with
particles that has to be removed; fuse together and form
multinucleated giant cells.
• Thus, their role in elimination of foreign substances, damaged
tissue, and pathogens is essential for host survival.
• Furthermore, these cells are able to sequester irremovable materials
or persistent pathogens and prevent further spread of infection.
• Multinucleated giant cells were first reported in tuberculous
granulomas by Rokitansky and Langhans
• It is well recognized that cells of monocyte /macrophage lineage are
capable of fusion to form MGCs.
• However, many aspects of their recognition, adhesion, fusion, and
activation, in addition to specific intercellular and intracellular
signaling pathways, remain unknown.
• These types of cells differ markedly in their association with disease
states, location & prevalence in various tissues or organs; stimuli
that induce the formation of the respective MGCs, and subsequent
function of these cells.
• The size of giant cells varies greatly, but is usually between 40 μm
and 120 μm.
• Classification – Acc text book of pathology by Dutta
• Various types of cells:
Normally occuring gaint cell
i. Megakaryocytes/megakaryoblasts in bonemarrow
ii. Osteoclasts in bone
iii.Trophoblastic cells in placenta
Reactive giant cells – generally develop from macrophages
I. Foreign body giant cells
II.Langhan’s giant cells
III.Ascoff’s giant cells
IV.Touton giant cells
Neoplastic (tumor) giant cells-
I. Reed-Sternberg cells
• Types of Giant Cells
1. Macrophage derived
a. Langhans’ giant cells
b. Foreign body giant cells (FBGCs)
c. Touton giant cells: Xanthelasmatic giant cells.
2. Epidermal cell derived
a. Tzanck giant cells
b. Multi nucleated epidermal giant cells.‑
3. Melanocyte derived
a. Starburst giant cells
b. Giant cells in melanocytic nevus.
i. Balloon cells
ii. Giant nevus cells.
4. Other giant cells
a. Floret like multi nucleated giant cells (FMGCs).‑ ‑
Gupta G etal. Giant cells in dermatology, Indian journal of dermatology 2014;59(5):481-84
• Osteoclasts, as named by Kolliker are bone-resorbing cells that play
a pivotal role in bone homeostasis and remodeling.
• Osteoclast precursors are derived from bone marrow as early
mononuclear macrophages, which circulate in blood, and bind to the
surface of bone.
• Osteoclast formation is driven mainly by two cytokines, Receptor
Activator of Nuclear Factor Kappa β Ligand (RANKL) and
macrophage - colony stimulating factor (M-CSF).
• In addition a wide variety of factors like systemic hormones and
growth factors influence the formation and function of osteoclasts.
• They usually contain 10 to 20 nuclei per cell and are found on bone
surfaces; on the endosteal surfaces within the haversian system; and
on the periosteal surface beneath the periosteum .
Foreign body giant cells:
• Foreign body giant cells (FBGCs) are the results from the body’s
attempt to remove or wall off impregnated foreign material.
• They are seen in tissues where the size of foreign particulate is too
large to permit macrophage phagocytosis.
• These contain numerous nuclei (up to 100) which are uniform in
size and shape and resemble the nuclei of macrophages. These
nuclei are scattered throughout the cytoplasm.
•They are formed from the fusion of macrophages and is observed
as a result of the response induced by biomaterials and other
•These are seen in chronic infective granulomas, leprosy and
• Recent studies show that macrophage fusion, giant cell formation,
and the foreign body response require matrix metalloproteinase
• FBGCs most commonly are observed in foreign body granuloma
formed in response to various exogenous or endogenous materials.
• Exogenous particles are starch, talc, tattoo material, cactus bristles,
wood splinters, suture material, retained epicardial pacing wires,
bioplastique, dermalive, artecoll microimplants, injected mineral oil,
injected hyaluronic acid, pencil lead, bovine collagen, etc.,
• Endogenous are calcium deposits, urates, oxalate, keratin, and hair.
• These giant cells are also seen in Borderline tuberculoid type of
Langhans’ Giant :
• These are formed by fusion of epithelioid cells. They are not
phagocytic but secrete interleukins and help in inflammation.
• It contains more than 15 nuclei,Their nuclei are like the nuclei of
macrophages and epithelioid cells.
•These nuclei are arranged either
around the periphery in the form of
horseshoe or ring, or are clustered at
the two poles of the giant cell.
• Interactions with cluster Differentiation 40 and its ligand (CD40L)
as well as interefron gamma are essential for the formation of
Langhans’ giant cells.
• The expression of Dendritic cell specific transmembrane protein, a‑
known fusion related molecule in monocytes, is upregulated during‑
Langhans’ giant cell formation, and knock down of DC STAMP‑ ‑
expression inhibits Langhans’ giant cell formation.
• These cells are seen in following conditions:
1. Tubercular granuloma
2. Leprosy (TT Type mainly)
3. Late Syphilis
4. Deep fungal infection
7. Crohn’s disease.
Touton Giant Cell :
• It is discovered by Karl Touton.
• These are also called as xanthelasmatic giant cell, whose
characteristic appearance is determined merely by the presence of
demonstrable lipid in the cytoplasm .
• These cells are formed by fusion of lipid containing macrophages.
• It is proposed that Touton cells develop when the stimulus to cell
fusion is accompanied by a factor stimulating lipid uptake. Touton
giant cells have a central ring of nuclei while the peripheral
cytoplasm is clear due to accumulated lipid.
• These cells react positively to lysozyme, alpha 1 anti trypsin, and‑ ‑
alpha 1 anti chymotrypsin, indicating their histiocytic origin.‑ ‑
• These cells are seen in
1. Fat necrosis
Nuclei are arranged as Central ring
Aschoff giant cells:
• These multinucleate giant cells are derived from cardiac histiocytes
and are seen in rheumatic nodule.
Giant cells in tumours:
i) Anaplastic cancer giant cells.
• These are larger, have numerous nuclei which are hyperchromatic
and vary in size and shape. These giant cells are not derived from
macrophages but are formed from dividing nuclei of the neoplastic
e.g. carcinoma of the liver, various soft tissue sarcomas etc.
Anaplastic tumour giant cell with
nuclei of variable size and shape
ii) Giant cell tumour of bone.
• This tumour of the bones has uniform distribution of osteoclastic
giant cells spread in the stroma.
III) Reed-Sternberg cells.
• These are also malignant tumour giant cells which are generally
binucleate and are seen in various histologic types of Hodgkin’s
• Giant cell lesions of oral cavity have been classified based on the
etiopathogenesis as described by Chattopadhyay A (1995) (Table 1)
and Varghese et al (2011) as follows.
1. Microbial lesions
• a. Tuberculosis
• b. Leprosy
• c. Actinomycosis
• d. Sarcoidiosis
2. Tumor and tumor like lesion
• a. Central giant cell granuloma
• b. Peripheral giant cell granuloma
• c. Giant cell fibroma
• d. Osteosarcoma
• e. Rhabdomyosarcoma
• f. Hodgkins lymphoma
3. Cystic lesion
• a. Traumatic bone cyst
• b. Aneurysmal bone cyst
4. Metabolic lesion
• a. Hyperparathyroidism
5. Osteodystrophic lesion
• a. Noonan-like multiple giant cell
• lesion syndrome
6. Miscellaneous lesion
• a. Cherubism
• b. Paget’s disease
• c. Fibrous dysplasia
I. Giant cell lesions of bone
A. Reactive :
• Brown tumor
• Hemophiliac Pseudo tumor
• Intraosseous haemorrhage
B. Benign :
• GC Granuloma
• Non ossifying Fibroma
• GC Tumor
• Aneurysmal Bone Cyst
• Chondromyxoid Fibroma
• Langerhans Cell Histiocytosis
• Pigmented Villonodular Synovitis
C. Malignant :
• Clear cell chondrosarcoma
• Metastatic Carcinoma
Rosenberg AE et al; Current Diagnostic Pathology: 2001 (7)235-46
Giant cells containing lesions of bone and their Differential Diagnosis
II. Mucosal lesions with Giant Cells
A. Peripheral Giant Cell Granuloma
B. Giant cell Fibroma
C. Oral Granulomatosis
• Specific : Fungal, Bacterial, Viral infection
• Non specific : Sarcoidosis, Wegeners Granulomatosis,
A. Hodgkins Lymphoma
B. Temporal Arteritis
Central Giant Cell Granuloma
• In 1953 Jaffe first described CGCG as Giant Cell Reparative
• CGCG is described as a benign lesion affecting the mandible
and maxilla that consists of massive fibrohistocytic
proliferation with numerous heavily haemosidrin laden
multinucleated giant cells.
• It has been called as osteoclastoma, myeloid sarcoma, chronic
hemorrhagic osteomyelitis and giant cell reparative
• Etiology unknown
• The CGCG of the jaw accounts for approximately 7% of all tumors
of the jaw. It may occur at any age but is more commonly seen in
the first three decades of life.
• The incidence of CGCG in the general population is estimated to be
0.0001%. Gender predilection reports are variable, but the majority
occurs in females with a female–male ratio of approximately 2:1.
• Lesions develop twice as often in the mandible with an epicenter
anterior to the first molar in young patients and there is a tendency
for the epicenter to occur in the posterior aspect of the jaws after the
first two decades of life .
• In the maxilla, the epicentre is more commonly anterior to canine.
Ebenezer. V . Giant Cell Granuloma: A Case Report. World J. Med. Sci., 10 (2): 165-168, 2014
• Symptoms—the earliest sign of the lesion may be expansion
of bone with premature loosening and shedding of deciduous
• Usually painless, but local discomfort may be noted.
• Growth is slow or fast depending on the type.
• Teeth in the area may become mobile but maintain their
vitality, until they are exfoliated.
Based on C/F & R/F : it is classified as
• Non-aggressive—it exhibits slow growing benign behavior.
• Aggressive—it shows typical features of rapidly growing,
-Aggressive lesions may exhibit pain,rapid growth,cortical perforation and root resorptio
-Non aggressive exhibit no symptoms,slow growth,no perforation,no resorption
• Radiographically, central giant cell granulomas present as either
unilocular or multilocular radiolucencies.
• Multilocular lesions are usually larger than unilocular lesions but
either may show radiographic evidence of expansion.
• The radiolucency may be ill defined or may have corticated borders.
"Fuzzy" densities and "wispy" opacifications may be seen within the
radiolucent areas and are thought to represent mineralized
•Loss of dental lamina dura also may occur (Homer 1989).
• Root resorption and apical perforation may be evident,
particularly in those patients with age, clinically aggressive
lesions. (Chuong, Kaban 1986, Ficarra 87)]
•Margins may be either smooth or scalloped .
• Histologically, the lesion is characterized by dense proliferation of oval or
spindle-shaped mesenchymal cells as well as a varying in number of
multinucleated giant cells containing 4 to 20 nuclei (aggregated or not)
dispersed in the fibrous stroma in a perivascular or adjacent position to areas
of hemorrhage .
• Round macrophages, deposition of hemosiderin, extravasated erythrocytes,
foci of osteoid material (bone trabeculae), dystrophic calcification and
predominantly mononuclear inflammatory infiltrate, particularly
surrounding the periphery of the lesion found.
Vasconcelos .R et al, Peripheral and central
giant cell lesions: etiology, origin of giant
cells, diagnosis and treatment. J Bras Patol
Med Lab, v. 49, n. 6, p. 446-452, dezembro
• Treatment of CGCL is associated with its clinical behavior. In
milder cases, a simple surgical resection followed by a thorough
curettage is recommended. Nevertheless, in aggressive lesions,
curettage is followed by cryosurgery, peripheral osteotomy or
• Some treatments involve daily local application of calcitonin,
corticosteroids and subcutaneous injection of interferon-2α.
Intralesional injections of triamcinolone acetonide have also been
prescribed in view of its anti-inflammatory and antiangiogenic
• The combined treatment (pharmacological and surgical) is
advantageous for large aggressive lesions .
• Prognosis—recurrence rate of 12% for lesions under 2 cm and
37% recurrence for lesions over 2cm in size.
Ameloblastoma—it is uncommon in a younger age range, which
is most susceptible to giant cell granuloma.
• Seen in posterior mandible in contrast to giant cell granuloma
which occurs anterior to the first molar.
• Ameloblastoma demonstrates internal, hard curved arch like
septa whereas giant cell granuloma has lighter wispy septa.
• Ameloblastoma is usually multiloculated.
Aneurysmal bone cyst—it does not occur in anterior segment of
mandible. Aspiration produces blood.
Odontogenic myxoma—multiloculated and typical honeycomb
appearance. Missing or impacted tooth is usually a finding.
Odontogenic myxoma—multiloculated and typical honeycomb
appearance. Missing or impacted tooth is usually a finding.
Traumatic bone cyst—no bodily movement of teeth is present.
No expansion of overlying bone cortex.
Cherubism—it is bilateral in the posterior part of mandible and
there is history of familial involvement. It does not cross the
Brown tumors of hyperthyroidism—serum calcium levels are
Giant Cell Tumor
• GCT is a true neoplastic process originating from the undifferentiated
mesenchymal cells of the bone marrow
• Relatively uncommon tumor in jaw .Common in long bone like femur,
• Cooper first reported giant cell tumors in the 18th century.
• In 1940, Jaffe and Lichtenstein defined giant cell tumor more strictly
to distinguish it from other tumors.
• Giant cell tumor usually occurs de novo but also may occur as a rare
complication of Paget disease of the bone.
Lesley-Ann Goh, Wilfred CG eMedicine - Giant Cell Tumor ; June 2002
• GCTs arising in the head and neck region constitute
approximately 2% of all GCTs.
• It is generally considered as benign but severe bony destruction
may result occasionally depending on the location and clinical
presentation of the tumor, making tumor management very
challenging .GCTs are usually mono-ostotic, although they may
occasionally present in a polyostotic form, which is usually of a
high grade .
• It is more common in 3rd and 4th decades and unusual in patient
below 20 years of age common in males
• Age 20-30 years
• Usually occurs at the end of long bones
• Pain and swelling at the affected site
• Radiologic examination of GCT usually reveals a well-
circumscribed lytic lesion surrounded by little or no sclerosis.
• The tumors may infrequently break through the cortex and
invade the soft tissue or the articular space .
• A CT scan can provide a detailed assessment of GCT, showing
the soft tissue mass of the lesion, cortical perforation, amount
of bony destruction, and extension toward important adjacent
• The final diagnosis is established only on the basis of a biopsy
• Histologically, GCTs are composed of multinucleated giant
cells in a vascular stroma of epitheloid or spindle-shaped
Evenly distributed multinucleated giant cell
with surrounding stroma made up of spindle
cells are shown, which were consistent with
• Differential diagnosis :
a) Aneurismal bone cyst
c) Dermoid cyst
e) Giant cell reparative granuloma
f) Pigmented villonodular synovitis
Park. SR. Giant Cell Tumor of the Mandible. Clinical and Experimental Otorhinolaryngology Vol. 5, No.
1: 49-52, March 2012
• The treatment of choice of GCT is surgical excision.
Regardless of the site of presentation, partial resection or
curretage results in a recurrence rate of up to 70%, whereas
recurrence after wide resection is about 7%.
• Some authors have advocated the use of radiotherapy in the
management of GCT.
• Other treatment modalities including cryotherapy,
chemotherapy, and curretage with adjuvant agents have been
tried, but have yielded less effective results .
• GCTs generally recur within the first 3 years if recurrence
occurs, but continuous evaluation up to 5 years is
recommended, since late distant metastasis have been reported
• Auclair et al (1988) by histomorphometric study on GCT and
GCG found statistical significant difference between the two
• Stromal cellularity
• Even distribution of GC
• Number of nuclei
• Presence of tumor necrosis
• Presence of inflammatory cell
Aneurysmal Bone Cyst
• Jaffe and Lichtenstein in 1942, discovered a distinct
clinicopathological entity and termed it Aneurysmal bone cyst.
• First case in jaw was reported by Bhaskar & Bernier in 1958
• An aneurysmal bone cyst is an expansile osteolytic lesion with
a thin wall, containing blood-filled cystic cavities.
• It is usually considered as a reactive bone lesion rather than a
cyst or true neoplasm.
• These occasionally develop in association with other primary
lesions such as:-
-Giant cell granuloma
• Etiology remains unclear
• ABC is characterized as a false syst because it does not have
an epithelial lining.
• It has been reported most frequently in the long bones , the
vertebrae and occasionally jaws.
• An extensive study was undertaken to test the hypothesis that
the ABC is a secondary phenomenon that occurs in a primary
lesion of bone.
• It was postulated that the initiating process of the ABC is the
microcyst that forms as a result of intercellular edema in a
primary lesion with loose, unsupported stroma.
• They are solitary lesions
• Commonly seen in 2nd
decade of life
• Commonly affects females.
• Mandible>maxilla=3:2(molar areas ,ramus common site)
• ABC tend to enlarge rapidly and cause thining & perforation of
overlying cortical plate .
• Large lesions may cause displacement of teeth leading to
• Mobility, migration, resorption of teeth may occur.
• Any long bone can be affected. Mandible, femur and tibia
• Grossly lesion is soft and reddish brown; because of its rich
• Radiographically, aneurysmal bone cysts are seen as a
unilocular or multilocular radiolucency, usually multilocular
lesions frequently produce a "soap bubble" or "honeycomb
• Debska & Buracewski (1969) and Wilner (1982) described 4
stages in the radiographic appearances of ABC:
a) Intial lytic phase – well defined area of bone resorption with
no distinctive features is observed.
b)Phase of active development – there is typical subperiosteal
“blow out” expansile appearance .
c) Stabilization phase – there is distinct peripheral bony shell
with internal septa and trabaculations, resulting in the soap
d) Healing phase – progressive ossification of the cyst resulting in
a dense bony mass of irregular structure.
• Aneurysmal bone cysts may cause thinning of the cortices but
usually do not destroy them and in some instances destruction of
the cortex with soft tissue extension
• Teeth may be missing or displaced but root resorption is seldom
• The characteristic feature is blood vessels and large blood filled
• Fibrous connective tissue stroma.
• MGC are present with patchy distribution.
• Osteoid formation
• Surgical curettage or excision(appearance at time of surgery
has been likened to that of a BLOOD SOAKED SPONGE)
• Also known as ‘familial fibrous dysplasia of the jaws’,
‘disseminated juvenile fibrous dysplasia’, ‘familial multilocular
cystic disease of the jaws’ and ‘Hereditary fibrous dysplasia of the
• It was first described by W.A. Jones in 1933 as “Familial
multilocular cystic disease of the jaws”.
• He coined the term Cherubism(reflecting the characteristic of
chubby facial appearance similar)
• Disease is of developmental origin.
• Point mutations in SH3BP2 gene on chromosome 4p16
• Ueki et al (2001) described mutation in gene encoding for
SH3BP2 in cherubism.
• Demostrated MGCs in cherubism stain positive for TRAP –
• Imai Y (2003) found the MGCs positive for both TRAP and
CD68 – macrophage lineage
Yoshimichi et al :Cleft palate craniofacial journal 2003, vol 40:
A Missense mutation in SH3BP2 gene in a case of Cherubism
• Affects in early childhood - mainly 1-5 yrs.
• The characteristic feature is that it is strictly
• Painless bilateral firm swelling involving the
posterior mandible usually.
• Maxilla if involved-either tuberosity or entire
maxilla may be affected
• Eyes turned up to heaven which is mainly due to a
wide rim of exposed sclerae below the iris.
• Impaired mastication, speech difficulties, loss of
Meng XM et al; Int. J. Oral Maxillofac. Surg. 2005: 34 Clinicopathologic
study of 24 cases of cherubism
• Bilateral multilocular lesions of the mandible more often than lesions
of the maxilla. Cortices are frequently paper thin focally,
• Complete erosion and concomitant soft, tissue extension.
• Involvement of the coronoid process is common
• Condylar involvement is rare.
• Initially fibrous replacement of the bone give rise to "soap
• In the later stages of the disease ,the fine bony septa increase
both in number and density thus filling the radiolucent areas,
by adult life there is a dense bony pattern with possibly a few
small radiolucencies present.
• Seward and Hankey suggested a grading system in 1957 of
cherubism, based on radiographic location of the lesions in the
• Grade-I the lesions are confined to the mandible; first molar
upto the coronoid process.
• Grade-II there are lesions in the maxillary tuberosity in
addition to the grade I lesion.
• Grade III- both the jaws are diffusely affected
Kalantor, Motamedi, 1998,
Grade I lesions of the mandible without root resorption.
Grade II maxilla and mandible without root resorption.
Grade III aggressive lesions of mandible with root resorption.
Grade IV both jaws with root resorption.
Grade V massive , aggressive lesions, both jaws, involve maxilla,
• H/F –
• Vascular fibrous stroma is loosely arranged.
• MGC are small, few and usually aggregated
• Peculiar perivascular eosinophilic cuffing.
• Giant cell granuloma – usually unilateral , usually affects
patients between 20 & 40 yrs.
• Fibrous Dysplasia- histological examination of the classic
form of fibrous dysplasia reveals trabeculae of immature bone
resembling chinese characters within the proliferating stroma.
Treatment : generally regress by puberty . Its self-limiting
• Rarely surgery is indicated.
• Brown tumours, are unifocal or multifocal bone lesions,
represent a serious complication of advanced
hyperparathyroidism with a frequency of 1.5–1.75 percent in
secondary hyperparathyroidism and 3–4 percent in primary
• Lesion derives its name from the color of the tissue
specimen(red-brown),due to abundant hemorrhage and
hemosiderin deposition within the tumor.
Brown Tumor of hyperparathyroidism
• In 1891, Von Recklinghausen described the classic bone
disease termed osteitis fibrosa cystica.
• An osseous lesion that develops in bones affected by
• Excess PTH results in an increase in bone breakdown by
means of osteoclastic resorption with subsequent fibrous
replacement and reactive osteoblastic activity.
• The serum calcium levels are increased and serum
phosphorous levels are decreased(primary).
Freitas B et al: eMedicine - hyperparathyroidism.htm; Aug. 2002 Hyperparathyroidism,
• It usually affects especially females with varying degrees of
aggressiveness and risks of recurrence .
• Ratio 3:1. Mainly in 30 to 60 years of age.
• It can affect the base of the skull, orbits, paranasal sinuses,
spinal column ,as well femur, tibia, humerus, clavicles and
• However, it is relatively rare in the maxilla with a frequency
of 4.5–11.8 percent.
NicolaDi. Brown Tumour in a Patient with Secondary Hyperparathyroidism Resistant toMedical
Case Report on Successful Treatment after Subtotal Parathyroidectomy. International Journal of
• Classic sign is subperiosteal
erosion along the radial margin
of the middle phalenges.
• They appear as unilocular or
multilocular with variably
defined margin and may produce
• Hand bone—earliest change is
subtle erosion of bone from sub-
periosteal surface of phalanges
• Pathological calcification—punctuate and nodular
calcifications occasionally occur in kidneys and joints.
• Skull bones—entire calvarium has granular appearance
caused by loss of central trabeculae and thinning of cortical
• Pepper pot skull—evidence in the skull vault of osteopenia
producing a fine overall stippled pattern to the bone, hence it
is called as pepper-pot skull.
R/F of jaws
Lesions may be multiple within a single bone.
If solitary it may resemble CGCG or ABC.
Demineraliztion,cortical thinning,reduced bone density
changes in trabecular pattern “ground glass apearance of
numerous small trabaculae.
R/F of teeth
Loss of Lamina Dura(complete/partial)
Root may thus appear tapered due to loss of image contrast.
Similar to central giant cell granuloma.
• proliferation of vascular granulation tissue which serves as a
back ground for numerous osteoclastic MGC.
• Hemosiderin deposition .
• Vasularity and hemosiderin content imparts the color.
• Ameloblastoma—it usually shows a honeycomb appearance
accompanied with paresthesia.
• Cherubism—the lesion is bilateral, seen in children and also
there is usually familial involvement.
• Aneurysmal bone cyst and central hemangioma—it occurs in
a younger age group.
• Osteomalacia—blood calcium levels are decreased.
• Fibrous dysplasia—osseous changes are frequently localized,
loss of lamina dura is less common.
• Multiple myeloma—lesions are punched out, generalized bone
demineralization in hyperparathyroidism helps in
Immunoassay for parathormone
CT & Dual Energy X-ray Absorptiometry (DEXA) to produce
quantitative estimates of bone density.
• Surgical management
Mucosal lesions with Giant CellsMucosal lesions with Giant Cells
Peripheral Giant Cell Granuloma
• First reported as fungus flesh in 1848.
• Also called as giant cell reparative granuloma ,
osteoclastoma , giant cell epulis, myeloid epulis.
• PGCG is site specific variant of pyogenic granuloma
embedded with osteoclastic like multinucleated giant cell and
arising exclusively from the periodontal ligament enclosing
the root of a tooth
Clinical features :
• Usually seen in 4th
decade of life but no marked age
• More than 60% cases occur in females.
• Present as red /red-blue nodular mass.
• Can be sessile/pedunculated
• Size: generally larger than pyogenic granuloma , the lesion
may exceed 4cm in size and most lesions remain less than 2cm
• Common site—it occurs on gingiva and alveolar mucosa, most
frequently anterior to molars. It is common in mandible than
• Early lesion—it appears as discoloration and slight swelling
of the buccal aspect of the gingiva.
• Later lesion—the lesion increases in size and becomes
rounded and very often pedunculated.
• Hourglass appearance—sometimes, it grows in an hourglass
manner, with the waist of the lesion between two teeth and the
globular extremities presenting buccally and lingually
• Soft to firm in consistency.
• In edentulous patients, it may present as a vascular, ovoid or
fusiform swelling of the crest of the ridge, seldom over 1-2 cm
in diameter or there may be granular mass of tissue which
seems to be growing from the tissue covering the slope of the
Proliferation of MGCs within background of ovoid or spindle
shaped mesenchymal cells.
Large vesicular nuclei. Mitotic figures are common.
• The intraoral radiograph may or may not exhibit evidence of
involvement of the bone underlying the lesion.
• In edentulous areas the peripheral giant cell granuloma
characteristically exhibits superficial erosion of the bone with
pathognomonic peripheral "cuffing" of the bone
• Pyogenic granuloma
Local surgical excision down to the underlying bone
Giant Cell Fibroma
• GCF is a benign non-neoplastic lesion first described by
Weathers and Callihan (1974).
• It is a type of fibroma not associated with trauma or irritation.
• It is a localized reactive proliferation of fibrous connective
• GCF is found predominantly in Caucasians in first three
decades of life with slight female predilection.
• But few studies have reported equal sex predilection.
• Age:Any age, 60 % in first 3 decade
• Usually it manifest as an asymptomatic, sessile, or
pedunculated lesion measuring about 0.5 to 1 cm with a
bosselated or pebbly surface. Surface often appears papillary
• Sites: Gingiva, tongue, palate, buccal mucosa and lips
• Mandibular gingiva is twice affected in comparison to
• The exact etiology is largely unknown, but few authors have
suggested trauma or chronic irritation as the inciting factors
whereas few authors rule out these factors
• A possible viral origin for the tumor is also postulated.
Sonalika etal. Giant Cell Fibroma of Tongue: Understanding the Nature of an Unusual
Histopathological Entity. Case Reports in Dentistry Volume 2014, Article ID 864512, 4
giant fibroblasts with stellate
shape and some contains two nuclei
GCF is an encapsulated mass of fibrous connective tissue that
contains numerous characteristic large spindle shaped and
stellate fibroblasts some of which are multinucealted.
These cells are easily observed in peripheral areas of lesion
while in central areas contains typical fusiform fibroblsasts
• It is lymphoproliferative disorders arising from lymph nodes
and from lymphoid components of various organs.
• It is neoplastic proliferation of lymhopoietic portion of
• It was first described by British pathologist, Thomas Hodgkin
• It is characterized by painless enlargement of lymphoid tissue
throughout the body.
• The exact cause of Hodgkin’s lymphoma is not known
• It is characterized by a bimodal age incidence, peak one in
young adults and the second in the 5th decade of life with
equal distribution between genders.
• Onset—the onset is insidious, usually with enlargement of one
group of superficial nodes.
• The cervical lymph nodes are usually the first to be involved
but the disease may start in the mediastinal, axillary,
abdominal, pelvic or inguinal lymph nodes
• The involved nodes are painless. Generalized weakness, loss
of weight, cough, dyspnea and anorexia are seen.
• Pain in back and abdomen owing to splenic enlargement, due
to pressure of enlarged nodes or involvement of vertebrae.
• The lymph nodes are discrete and rubbery in consistency with
overlying skin being freely mobile.
• Some patients may manifest pruritis.
• Pel Ebstein fever is the characteristic features of this disease,
a cyclic spiking of high fever and generalised severe pruritis.
Clinical Stages (Ann Arbor Staging)
• Stage I—involvement of single lymph node region or extra-
• Stage II—involvement of two or more lymph node regions or
an extra-lymphatic site and lymph node region on the same
side of diaphragm.
• Stage III—involvement of lymph node region on the both sides
or without extra-lymphatic involvement or involvement of
spleen or both.
• Stage IV—diffuse involvement of one or more extralymphatic
tissues, e.g. liver or bone marrow.
• Subdivision—all the above stages are subdivided into A and B
categories depending on whether they have systemic
symptoms such as weight loss, fever, night sweats. A—
absence of systemic signs and B—presence of systemic signs.
• primary jaw lesions are uncommon.Secondary effect can be
seen in oral cavity in the form of infection due to reduced host
• It may appear in the oral cavity as an ulcer or a swelling or as
an intra-bony lesion which presents as a hard swelling
Rye system 4 types :
1. Lymphocyte predominant—abundant lymphocytes, few
plasma cells, occasional Reed-Sternberg cell, localized
involvement of one side of diaphragm and most favorable
2. Mixed cellularity—lymphocytes, plasma cells, eosinophils,
easily identified Reed-Sternberg cell.
3. Nodular sclerosis—sparse lymphocytes, stromal cells, fibrosis
and numerous but bizarre Reed-Sternberg cells.
4. Lymphocyte depletion—lymphocytes, plasma cells,
eosinophils with localized involvement.
Reedsternberg Cell - have paired
• Non-Hodgkin’s lymphoma—Hodgkin’s lymphoma is
differentiated from non-Hodgkin’s lymphoma by the presence
of cells known as Reed-Sternberg cells which have paired as
mirror nuclei and prominent nuclei.
• Combination of both
Giant cell arteritis
• Giant-cell arteritis and cranial arteritis, is a systemic vasculitis
of medium-sized and large-sized arteries.
• It is the most common systemic vasculitis of older adults.
• Symptoms of temporal arteritis can be either constitutional or
• Constitutional symptoms include fever, weight loss, anemia,
• Vascular-related symptoms arise secondary to arterial
inflammation with luminal stenosis and resultant end-organ
• The typical involvement of the temporal, vertebral, and
ophthalmic arteries leads to the classic clinical manifestations
of headache, facial pain, and vision problems. Pain may
radiate to maxilla , mandible.
• The incidence for temporal arteritis is 15-25 cases per 100,000
persons older than 50 years,with a mean age of 71 years at
• Temporal arteritis is the most common systemic vasculitis of
adults in Western countries.
• Women are affected at least twice as often as men.
susceptibility is associated with northern European descent
and is seldom observed in blacks and Asians
• The etiology of temporal arteritis is multifactorial and is
determined by both environmental and genetic factors.
• Data indicate that the disease is probably initiated by exposure
to an exogenous antigen.
• Numerous viruses and bacteria have been proposed as
potential precipitants, including parvovirus, parainfluenza
virus,varicella zoster virus,[5,6]
pneumoniae, and Mycoplasma pneumoniae.
• There are 3 main patterns of vascular damage in temporal
• The first is the classic pattern, characterized by marked intimal
thickening and transmural inflammation. A dense
inflammatory infiltrate composed of T cells and histiocytes is
present. Fusion of histiocytes results in the classic microscopic
appearance of granulomatous inflammation with
multinucleated giant cells (foreign body and Langhans types)
• The second pattern is the atypical pattern. A less dense
nonspecific arteritis is seen, with an inflammatory infiltrate
composed of lymphocytes, macrophages, and, rarely,
eosinophils and neutrophils.
• Moderate or marked intimal thickening and medial fibrosis are
sometimes noted (see the images below). Granulomas and
multinucleated giant cells are rare. The inflammation tends to
be most marked in the adventitia. Intimal fibromyxoid changes
and inflammation are also found
• The third histologic pattern is the healed pattern, which
demonstrates intimal and medial fibrosis.
• The intima is irregularly thickened and exhibits fibromyxoid
change and neovascularization.
• The consensus for glucocorticosteroid initiation is as follows:
Uncomplicated GCA (No jaw or tongue claudication or visual
• Prednisolone 40-60mg (not <0.75 mg/kg) daily until resolution
of symptoms and laboratory abnormalities.
• Evolving visual loss or history of amaurosis fugax: i.v.
methylprednisolone 500mg to 1 g daily for 3 days.
Established vision loss—at least 60mg prednisolone is
• The condition was originally named for Friedrich Wegener,
who described the disease in 1936.
• Wegener's granulomatosis (WG) also known as
granulomatosis with polyangiitis (GPA) is a rare disease in
which blood vessels become inflamed (a condition
called vasculitis) and localized, nodular collections of
abnormal inflammatory cells, known as granulomas, are found
in affected tissues.
• It is uncommon disease
• Exactly unknown
• Predeposing factors may be exposure to environmental
antigens such as silica and infection ( particularly
• Genetic factors .
Clinically it is classified as
• Generalized or classic Wegener’s granulomatosis—it involve
upper respiratory tract, pulmonary and renal lesions.
• Localized or limited Wegener’s granulomatosis—it affects
oral and nasal cavity and the lungs.
• Superficial Wegener’s granulomatosis—it exhibits lesion of
skin and mucosa.
• Estimated prevalence of 3 per 100,000 persons in US.
• Common in whites.
• Mean age of onset is approx 40 years.
• The most common symptom of Wegner’s granulomatosis is
nasal stuffiness with chronic discharge (rhinitis).
• Patient soon develops cough, hemoptysis, fever and joint
• There are also non-specific symptoms of malaise, arthralgia
and weight loss.
• Hemorrhagic or vesicular skin lesions may seen.
• Rapidly progressive glomerulonephritis (75%), leading
to chronic kidney failure.
Oral manifestations :
• ulceration may occur on any surface.
• Involvement of gingiva is the most common manifestation;
which is characterized by ulceration, friable granular lesions
or simple enlargement of gingiva.
• Inflamed, hyperplastic and hemorrhagic gingiva may be found
called as Strawberry gingivitis.
• Palatal lesions typically include ulceration of the palate by
extension of nose lesions and destruction of nasal septum.
Thus leading to perforation of palate.
• There may be loosening of teeth with in some cases
• After extraction of teeth patient is usually noticed poor
• Other features—cranial nerve palsies, jaw claudication,labial
mucosal nodule, oroantral fistulae, and parotid swelling.
Granulomas are illdefined with surrounded areas of necrosis.
The inflammatory infilterate can be dense, mixed and non
specific. Gaint cells are common.
Strawberry gingivitis show pseudoepitheliomatous
hyperplasia and prominent vascular component associated
with red blood cell extravasation.
• Hodgkins Lymphoma
• Cotrimoxazole—it is combination of trimethoprim and
• sulfamethoxazole. It has proved to be effective as an adjuvant
or sole therapy in both localized and generalized forms.
• Corticosteroids—regimen of cyclophosphamide 12 mg/ kg
body weight/day with prednisolone 1 mg/kg bodyweight have
been utilized to obtain complete remission.
• Others—other treatment modalities includes cyclosporine,
intravenous pooled immunoglobulin, and local irradiation.
• It is also called as Boeck’s sarcoid, Besnier-Boeck-Schaumann
• It is a multisystem granulomatous disease.
• It is characterized by depression of delayed type of
hypersensitivity, suggesting an impaired cell-mediated
immunity and raised or abnormal serum immunoglobulin,
• It is characterised by presence of non-caseating granulomas in
• Etiology is unknown
• Multiple underlying factors include:
a. Genetic predisposition
b. Infectious agents
c. Environmental exposures.
• Possible microbial triggers – mycobacterial and
propionibacterial organisms with the microbacterial catalase –
peroxidase (mkatG) protein as a potential candidate agent.
• Most commonly seen in United States and scandinavian
• Blacks are more affected than whites.
• Common in young and middle-aged adults, with approx 75%
cases in individuals younger than 40 years.
• Females are more susceptible than males.
• lesions are most common in lungs, skin, lymph nodes, salivary
glands, spleen and bones.
• Majority of the cases sarcoidosis is asymptomatic with the
disease being discovered with routine chest radiograph.
• Symptomatic patients usually present with respiratory and skin
• Dry cough , dyspnea and chest pain are frequent respiratory
• Non specific symptoms such as fever , night sweats , fatigue
and malaise are present.
• Cutaneous manifestations occur in approx 25% of patients
present with erythema nodosum and lupus pernio.
• Lupus pernio—these are the cutaneous lesions which appear
as multiple, raised red violaceous patches. It occurs in group,
grows slowly and does not ulcerate or crust.
• Erythema nodosum—it is nonspecific tender erythematous
Syndromes associated with sarcoidosis:
• Lofgren syndrome – acute form of sarcoidosis usually found in
white females, consists of erythema nodosum, bilateral
• Heerfordt syndrome(uveoparotid fever)- is characterised by
parotid enlargement , anterior uveitis, facial paralysis and
• Oral manifestation:
• Oral manifestations of sarcoidosis is uncommon as disease is
diagnosed before oral symptoms appear.
• Commonly buccal mucosa followed by gingiva , lips, floor of
mouth, tongue and Palate.
• Lesions most commonly present as submucosal masses, which
may vary in color from normal to browish-red or violaceous .
• Sarcoidosis of major or minor salivary glands leads to
Shows cluster aggregate of epitheloid histiocytes surrounded
by a rim of lymphocytes.
Multinucleated giant cells may contain laminated calciifed
structures called Schaumann bodies or stellate inclusions
known as asteroid bodies.
• Standard treatment of choice is corticosteroids.
• Refractory (does not respond to treatment) sarcoidosis—in
this case methotrexate, azathioprine, chlorambucil and
cyclophosphamide is used.
• Also known as leus
• It s a chronic sexually transmitted diseases caused by
trepenema pallidum, characterised by peroids of active disease
• It occurs world wide.
• Acc. to WHO approx 12 million new cases of veneral syphilis
occurred in 1999
• It occurs through Sexual contact
• Maternal transmission
• Predisposing factors—overcrowded living and primitive
• Acquired syphilis—contacted primarily as venereal disease
due to sexual intercourse with infected partner.
Primary—it is evident clinically 3 to 90 days after the
Secondary—it is discovered 4 to 10 weeks after primary stage.
Tertiary—this stage after several years develop the latent
Quaternary syphilis—the atypical malignant progression of
tertiary neurosyphilis in immunocompromised HIV
individuals is referred as quaternary syphilis.
Latent phase—this appear after secondary stage and in this
stage, there is no sign and symptoms are present. Serological
test is positive in this stage.
• Congenital—this is secondary to fetal infection.
Early syphilis—primary syphilis, secondary syphilis and the
early latent phase of the disease are grouped as early syphilis.
Early syphilis may last up to two years and is infectious.
Late syphilis—while late latent and tertiary are grouped as late
syphilis. Late syphilis is locally destructive and non-
• Lesion develop at the site of inoculation, approximately 3 to
90 days after the inoculation.
• It occurs most frequently on penis in males and vulva or
cervix in females.
• Recently, occurrence on extragenital sites have increased as a
result of increase in orogenital.
• Extragenital sites of involvement include fingers, perianal
region, nipples, lips, tonsils and intraoral structures such as
tongue and palate.
• The chancre begins as a painless papule that becomes
ulcerated and frequently accompanied by regional
• Chancre vary in size from 5mm to few centimetres.
• The primary lesion resolves spontaneously within 4-6 weeks
with or without treatment.
• Because the ulcers are usually painless many individuals are
not diagnosed at this stage.
• It results fromm orogenital contact .
• Active lesion as solitary ulcer ( Chancre) with indurated
margins are present on the lips, tongue or palate.
• Ulcer is usually deep and accompanied by crevical
• Ulcer heals spontaneously within 7-10 days.
• Haematogeneous dissemination of the pathogen results in
manifestation of secondary syphilis.
• Approx occurs after 6-8 weeks of primary stage.
• Most common manifestation of this stage is mucopapular rash
affecting the flank , shoulder ,arm , chest, back , hands and
• Generalized lymphadenopathy is present.
• Other features are condyloma lata, alopecia , myalgia,
meningities, pulmonary and neurologic involvement are
• The secondary lesions resolve with or without treatment and
infection enters to latent stage where there are no clinical
• Transmission of syphilis is by contact and occurs through
individuals with the primary or secondary stages of disease.
• Mucopapular and nodular mucosal lesions are common.
• Superficial mucosal erosions called ,mucous patches are seen
on lips , tongue , palate and pharynx.
• Mucous patches are usually painless , oval to crescentic
erosions , surrounded by a red periphery.
• Snail track ulcers are serpiginous lesions that may arise
denovo, or form by coalescence of number of mucous patches
• Condyloma lata are broad based verrucous plaques .
• In 1/3rd
of individuals after many years tertiary syphilis may
• Tertiary syphilis develop as gummatous form, cardiovascular
form and neurosyphilis, i.e. general paresis and tabes dorsali.
• Cardiovascular syphilis is the result of endarteritis obliterans
of the vasa vasorum which provides the blood supply to large
vessels, leading to aortitis , aortic regurgitation , aortic
aneurysm or coronary arterial stenosis.
• It occurs due to obliteration of small vessel artery involving
vasa vasorum of aorta and other large vessels of the central
nervous system (neurosyphilis).
• Neurosyphilis is manifested as tabes dorsalis and general
• Tabes dorsalis is the syphilitic involvement of dorsal column
of spinal cord and dorsal root ganglion.
• Due to syphilitic involvement of cerebral tissue, General
• Gummas are foci of granulomatous inflamation which may
occur in any tissue and present as nodular ulcerative lesions .
• Punched out ulcer with vertical walls and dull red
granulomatous base is the typical clinical feature of ulcerative
• The most commonly involved sites are skin , skeletal system,
mouth , upper respiratory tract , larynx.
• Single cerebral gumma may produce symptoms suggestive of
• Gummas are the common finding.
• They are caused by endarteritis obliterans and tend to involve
the hard palate , tongue or lower alveolus.
• It usually starts as small, pale, raised, nodular mass which
ulcerates and rapidly progresses to the zone of necrosis.
• Punched out ulcer with vertical walls and dull red
granulomatous base is the typical clinical feature of ulcerative
• Leutic glossitis—complete atrophy of papillary coating and
firm fibrous texture seen. Initially, it is thought to be
precancerous but nowadays, this concept is disputed. Loss of
papillae is probably due to endarteritis leading to circulatory
deficiency of lingual vasculature
• It is infection of fetus established by the passage of spirochetes
from mother, through the placenta.
• It has got three diagnostic features called as Hutchinson’s triad
which includes hypoplasia of permanent incisors and 1st
permanent molars, eight nerve palsy( deafness) and interstitial
• Hutchinson teeth includes screwdriver shaped incisors that
may show notching of the incisal edge. Mulberry molars .
• Other features like frontal bossing , saddle shape nose are
• Rhagades are linear scars at the angles of mouth caused by
secondary bacterial infection.
• They appear as red or copper colored linear areas covered with
a soft crust .
• Frequent on the lower lip
Syphilitic gumma consists of central coagulative necrosis
surrounded by zone of palisaded macrophages with
lymphocytes, plasma cells, giant cells and fibroblast.
• Fungal infections
• Parenteral long acting penicillin G is the drug of choice.
• Patient should give benzathine penicillin (2.4 million units
IM) aqueous crystalline penicillin tetracycline hydrochloride
(500 mg orally 4 times a day for 15 days). Patients who are
allergic to penicillin erythromycin (500 mg orally 4 times a
day for 15 days).
• T pallidum disappears from infectious lesion within 24 hours
of instituting therapy.
Leprosy (hansen’s disease)
• First observed by Hansen in 1868.
• Chronic infectious disease produced by Mycobacterium
• It is a chronic infectious disease affecting skin and peripheral
• Acc to WHO about 720,000 new cases of leprosy are reported
• Precise mechanism is still unknown.
• After entry in the body the bacilli reach the lymphatic and
bloodstream and are taken up by Schwann cells in peripheral
nervous system, where they start multiplying.
• When the host cell immunity is deficient a generalized form of
the disease lepromatous leprosy develops.
• Incubation period vary from 3-5years , with a range of few
months to 30 years.
• Leprosy represents maily two patterns
• Third is borderline leprosy-it can be tuberculoid borderline or
Tuberculoid type or paucibacillary type:
• Incubation period is of 2 to 5 years
• Males are affected more commonly than females with ratio of
• Skin lesions are hypopigmented, erythematous and flat or
raised cutaneous lesions.
• Nerve involvement occurs early in the course of the disease
and sensory, motor, autonomic nerves are affected, with
resulting hypoesthesia, muscle weakness and anhidrosis.
• Early tuberculoid leprosy manifests as hypopigmented macules
which are sharply demarcated and hyperesthetic.
• Intermediate tuberculoid lesions are larger with elevated and
circinate margin. There is peripheral spread and central
healing. At the end of this stage, the symptoms are those of
irritation of nerve ending in the skin, persistent or recurrent
paresthesia and numbness localized to certain area with no
accompanying visible alteration in the corresponding skin
Lesion of tuberculoid leprosy showing peripheral spread
• Fully develop lesions are densely anesthetic and loose normal
skin organs (sweat glands and hair follicles).
• There may be severe neuritic pain.
• Loss of eyebrows and eyelashes are prominent features.
• The sequelae of peripheral nerve involvement may develop in
some cases and this may give rise to muscle atrophy, like
contracture of hands and feet, loss of phalanges, exposure
keratitis and corneal ulceration leading to blindness.
Lepromatous type or multibacillary leprosy:
• This form is more commonly seen in children and females as
compared to males.
• The disease includes widespread involvement of body skin,
peripheral nerves, mucous membrane, lymph nodes, eyes,
skeleton, testes and other internal organs it develops early as
erythematous macules or papules without subsequently lead to
progressive thickening of skin and the characteristic nodules..
Macular lesion seen on the leg of
patient in lepromatous leprosy
• The borders of the lesion are ill defined and centers of the
lesion are indurated and convex.
• Ear lobe becomes pendulous and loss of lateral portion of
eyebrows is common.
• Painless inguinal and axillary lymphadenopathy is common
along with sterility and gynecomastia.
• Nerve involvement is a late phenomenon
• More frequent in lepromatous leprosy .
• Includes papules , plaques , nodules, non-specific erosions and
ulcerations involving the tongue , buccal mucosa and palate.
• Small tumor like masses called as lepromas develop on the
tongue, lips or hard palate. These nodules have a tendency to
break down and ulcerate. Continuous infection may lead to
scarring and loss of tissue.
• In long standing lepromatous leprosy, invasion of the pulp by
granulomatous tissue causes pulpal necrosis leading to a
pinkish discoloration of crown. Anterior teeth are most
In lepromatous leprosy there is
proliferation of macrophages with foamy
change particular around blood vessels,
nerves and dermal appendages.
The foamy macrophages are called lepra
cells / virchow cells.
In tuberculoid leprosy the dermal
lesions show tubercles composed of
epitheloid cells, langhans giant cells
and peripheral mantle of lymphocytes
• Gummatous lesion of syphilis —VDRL test should be
• Paucibacillary leprosy—it is treated with 6 month regimen of
rifampin and dapsone. Patient allergic to rifampin are treated
with clofazimine, ofloxacin and minocycline.
• Multibacillary leprosy—this is treated with 24 months therapy
of rifampin, dapsone and clofazimine.
• Tuberculosis is a common worldwide infection caused by
bacteria belonging to Mycobacterium tuberculosis.
• Most frequent and important agent of human disease is M.
• M.bovis is transmitted by unpasteurized milk and cause of
small percentage of cases in developing countries.
Other risk factors for TB includes-
• Excessive alcohol consumption
• End stage renal failure
• WHO estimates approx. 2 billion people of worlds population
are infected with M.tuberculosis in 2010 with 1.4 million
deaths caused by it yearly.
• Transmitted by air borne spread of droplet nuclei produced by
patients with infectious pulmonary TB.
• Droplets aerosolized by coughing, sneezing or speaking are
• Thus transmission of infection is enhanced by crowded
conditions and poorly ventilated areas.
• Primary tuberculosis—it occurs in previously unexposed
person and it involve lung.
• Secondary tuberculosis—in this reactivation of bacteria and it
occur in, compromised host defense.
• Miliary tuberculosis—it spreads through bloodstream and
there is wide involvement of many organs like kidney, liver
and is called as miliary tuberculosis.
• Pott’s disease—if tubercular involvement of spine occurs in
children, it is called as Pott’s disease.
• Scrofula—if it spreads by lymphatics to lymph nodes, it is
called as scrofula ( mainly cervical and supraclavicular sites)
• Patient may suffer episodes of fever and chills, easy
fatigability and malaise.
• There may be gradual loss of weight accompanied by
persistent cough with or without hemoptysis.
• Local symptoms depend upon the tissue or organs involved.
• Tuberculosis lyphadenitis is most common extrapulmonary
form. Usually present as painless swelling of lymphnodes ,
usually discrete in early stage later develop into caseous
necrosis & form fistulas through overlying skin.
• Involved nodes may radiographically appear calcified.
• Most common manifestation is pain less ulcer.
• Tongue is most commonly affected followed by palate, lips,
buccal mucosa and gingiva.
• The lesion may be preceded by an opalescent vesicle or
nodule, a result of caseation necrosis. It breaks down into an
ulcer which is usually superficial or deep and painful.
• Margins of the ulcer are undermined with minimum
induration. It tends to be increased slowly in size. Mucosa
surrounding the ulcer is inflamed and edematous. Base of
ulcer is yellowish and granular.
• TB osteomyelitis has been reported in jaws and appears as ill-
defined areas of radiolucency.
•Tubercle composed of
epitheloid cell, lymphocytes,
Multinucleated Giant Cell.
•Central foci of caseous
•Giant cells of the Langhans
type are clearly visible.
Staining methods include:Z-N
staining and other Acid fast
• Chemotherapy—short term chemotherapy, isoniazid (5 mg/kg
with maximum of 300 mg daily or 15 mg/kg two to three times
weekly) and rifampicin (10 gm/kg), ethambutol (25 gm/kg
daily for not more than 2 months).
• Other drugs—other drugs which can be used are streptomycin,
para-aminosalicylic acid, pyrazinamide, thiacetazone,
ethionamide and cycloserine.
• Text book of pathology . Harsh mohan 6th
• White and Pharoah. Oral Radiology Principles and
• Wood and Goaz. Differential Diagnosis of Oral and
• Shafers text book of oral pathology 7th
• Text book of oral medicine . Burkitts 11th
• Oral medicine oral diagnosis & oral radiology – Ongole .2nd
• Text book of oral medicine – ghom 2nd