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SEMINAR ON Giant cell lesions of maxillofacial region & Surgical management Presented By: Dr. Satyajit Sahu III MDS


INTRODUCTION: Cells those are larger in size than normal size of cell is called as giant cell. These contain more than one nucleoli and are called as multinucleated giant cells. These cells are found in many physiological and pathological conditions. Physiological conditions: 1) Resorption of deciduous teeth 2) Healing of extraction of teeth 3) Orthodontic tooth movement 4) Synctiotrophoblasts of placenta.

Formation: Two main mechanisms have been put forward for the formation of giant cells 1) Multiple nuclear division without division of cytoplasm. 2) Fusion of multiple cells when macrophages fails to deals with particle to be

removed. They fuse together and forms multinucleated giant cells. These have strong phagocytic and pinocytic activity. They secrete interferon, pyrogen, complement

components lysozyme and hydrolase, cytotoxic

factors. CLASSIFICATION OF GIANT CELLS: 1) Damaged striated muscle fibers: Regenerating sarcolemmal cells in damaged voluntary muscle Aschoff giant cell in heart muscle (in rheumatic fever) 2) Fused fibroblasts: giant cell fibroma 3) Osteoblasts in bone resorption 4) Tumor giant cells: These are the large tumor cells with single huge polymorphic nucleus having two or more nuclei. These nuclei are hyper chromatic and very large compare to size of cell.


Reed-Steinberg giant cells in Hodgkin’s lymphoma, Giant cell in central giant cell granuloma, Poorly differentiated astrocytoma Giant cell in the tumors like carcinoma.

5) Inflammatory giant cells: Like foreign body giant cells or Langerhan’s giant cells they have normochromic small normal nuclei, but numerous within one cell. 6) Fused cell due to viral infection: Epithelial giant cell as in HSV infection Connective tissue cells as in Meseals Warthin Finkeday cells 7) Fused macrophages: Due to reaction of foreign body ( exogenous and endogenous material Due to reaction of organisms as in TB (Langerhans giant cell) and fungal infection Touton giant cell of xanthoma. The osteoclasts have been the controversial cell with respect to its origin. Fibroblastic, macrophages, pericytic and endothelial origin of the osteoclasts have been suggested. Marks have however shown that the mononuclear precursor of osteoclasts to be the site specific extra skeletal source which are distinguishable morphologically and kinetically from precursor of osteoblasts. Current consensus about origin of osteoclasts is moving away from monocytes or macrophages which may even be derived from distinct stem cells that at least potentially arrive on the bone surface through circulation. The explanation for difficulty in finding mononuclear cells with strong enzymatic, ultra structural functional or immunocytological similarities to osteoclasts may be that the osteoclasts do not take origin from the local stromal mononuclear cells but

represent immigrant cells, brought in like many cells type of inflammatory reparative or neoplastic lesions from the circulation. The fusion of microphases may give rise to giant cell in response to presence of foreign bodies in tissue which may be living cell or non-living material which in turn may be exogenous or produced in the body. The tuton giant cell Xanthoma are fused form cells with ring like, wreath shaped arrangement nuclei. Its peripheral cytoplasm has a foamy or vacuolated appearance and the nuclei around a central area of clear eosinophilic cytoplasm. When macrophages encounter insoluble material, they fuse coalesce to form a giant cell. This is the mode of formation of the giant cell rather than nuclear division. It has been found that despite the inactive appearing nuclei in these cells, DNA synthesis does occur. Mitotic activity too has been associated with these cells mainly in the experimental situation. These cell have strong phagocytic and pinocytic activity. They secrete interferon, pyrogen, complement components, lysozyme, acid hydrolases, neutral proteases, cytotoxic factors etc. evidence also suggests that they may process antigen too. In giant cells all centrioles are found in one area of the cells, cyto filaments radiating away from the centriole towards their respective nuclei. These collection of filaments may occasionally be accentuated and become visible at light microscopic levels as so called “asteroid bodies”. The tumor giant cells are the large tumor cells with a single huge polymorphic nucleus or having two or more nuclei. These nuclei are hyper chromatic and very large compared to the size of the cell. The inflammatory giant cells or Langerhan’s giant cells have monomorphic, small, normal looking nuclei which may be numerous within one cell. Giant cell formation in tumor has been related to degree of the CLASSIFICATION OF GIANT CELL LESIONS OF ORAL CAVITY:

Lesions where giant cells in the concerned background are pathgnomic: 1) Hodgkin’s lymphoma 2) Peripheral / central giant cell granuloma 3) Giant cell fibroma

Lesions where giant cells are characteristic but not pathgnomic: 1) Tuberculosis 2) HSV infection 3) Meseals 4) Xanthoma

Lesions associated with presence of giant cell: Orofacial granulomatosis, fungal infection, foreign body reaction, neoplasm, syphilis, leprosy, fibrous dysplasia, cherubism, ossifying fibroma, ABC, Paget’s disease of bone wegners granulomatosis actinomycosis odontogenic giant cell fibromatosis. Another classification of GIANT CELL LESION: I) Physiological conditions: 1) Resorption of deciduous teeth 2) Healing of extraction of teeth 3) Orthodontic tooth movement 4) Synctiotrophoblasts of placenta. II) Non neoplastic growth: A) Soft tissue 1) Peripheral giant cell granuloma 2) Giant cells fibroma 3) Epulis fisseratum 4) Traumatic granuloma

B) Bone 1) Central giant cell granuloma 2) Brown’s tumor 3) Fibrous dysplasia 4) Paget’s disease 5) Osteomalacia 6) Cherubism.

III) Cyst and neoplasm: A) Cysts: 1) Aneurysmal bone cyst 2) Calcifying epithelial odontogenic tumor 3) Solitary bones cyst

B) Benign neoplasm: 1) Giant cells tumor 2) Osteoid osteoma 3) Osteoblastoma 4) Central hemangioma

C) Malignant : 1) Osteosarcoma 2) Hodgkin's lymphoma 3) Reticular cell sarcoma 4) Lymphosarcoma 5) Squamous cell carcinoma

IV) Infections: A) Bacterial: 1) Tuberculosis 2) Syphilis

3) Leprosy 4) Actinomycosis 5) Yaws 6) Osteomyellitis

B) Viral: 1) Herpes simplex 2) Herpes zoster 3) Mumps 4) Cytomegalo virus 5) Meseals

C) fungal: 1) Histoplasmosis 2) Candidiasis 3) Blastomycosis 4) Coccidomycisis 5) Rhinospordosis

D) Protozoal: 1) Leistmonisis.

E) Chlamydial: 1) Lymphogranuloma venerum

V) Non infective granuloma: 1) Midline lethal granuloma 2) Wegener’s granuloma 3) Plasma cell granuloma 4) Sarcodosis

VI) Periodontal condition: 1) Periodontis

2) Periapical cyst 3) Periapical granuloma 4) Chronic periapical abscess

VII) Miscellaneous: 1) Internal resorption 2) External resorption 3) Massive osteolysis 4) Spindle or epithelial cell nerve

WALDRANS 1995 --------------Aggressive & Non aggressive LUCCAS 1976 --------------------Intraossious Extraosseous CENTRAL GIANT CELL GRANULOMA: Term giant cell reparative granuloma coined by Jaffe- in 1953, for central giant cells lesions of jaws. Jaffe made study of long bones and found difference between lesions of long bones and jaw. Long bone tumor occurs between 20-55 where as jaw tumor occurs between 10-25 years. Histologically: In long bones now new bone formation In jaw bone spicules of woven bone formation. Because of this Jaffe felt that jaw condition is dysplastic rather than neoplastic. He focused on tissue of repair and hence name reparative. From their radiological appearance, central giant cell granuloma can be divided into two types. -

Central medullary type


Sub periosteal type

Clinical features: The central giant cell granulomas occurs predominantly in children or young adults, female > male, mandible > maxilla. Anterior to 1st molar and anterior segment of the jaw commonly involved and may cross the midline. Slight to moderate bulging of the jaw due to expansion of cortical plates occurs in the involved area; depend on the extent of the bone involvement. The lesion may present no syndrome and symptoms and may discovered accidentally. Central giant cell granuloma reported to be associated with pregnancy, the involved teeth may be non vital and maxillary tension may show nasal obstruction. Pain may or may not be present.

A central giant cell granuloma of the anterior mandible causing the displacement of teeth.

A central giant cell granuloma of the left angle region of the mandible, appearing as an ill-defined multilocular radiolucency, causing resorption of the distal root of the first molar (unusual). Radiological appearance: The central giant cell granuloma is centrally a destructive lesion produces radiolucent area with either relatively smooth or ragged borders. Occurs mainly in tooth bearing area, causing marked resorption of cortical plates. Thin layer of sub

periosteal bone formation. Multilocular cross hatched appearance particularly in maxilla. In sub periosteal type larger bulk on external to normal contour. Definitive loculation are often present particularly in large lesion and expanded and may become perforated by the mass. Displacement of the teeth is frequently root resorption and loss of lamina of lamina dura seen. Histological features: The central giant cell granuloma is made up of loose fibrillar connective tissue stroma with many interspersed small proliferating and small capillaries. Collagen fibers are not usually in bundles. Multinucleated giant cells (contains 3-18 nuclei) are prominent throughout the connective tissue nut not necessary abundant. Vary in size from case to case, nucleus may very from few to dozens. Numerous foci of old extravasted blood and associated hemosiderin pigment, some of its phagocytized macrophages. Differential diagnosis for radiographs: 1. Ameloblastoma 2. Odontogenic myxoma 3. Aneurysmal bone cyst

Ameloblastoma: Is uncommon in younger age and usually appears in posteriorly on the angle of mandible while giant cell granuloma occurs anterior to the I molars, ameloblastoma is multilocular giant cell granuloma uniloculated. Aneurysmal bone cyst : do not occur in the anterior of the mandible. Odontogenic myxoma :associated with missing or impacted tooth.

Treatment of central giant cell granuloma: Three primary methods of treatment of central giant cell granuloma of jaw bones have been used, curettage with peripheral osteotomy. Simple curettage and recession: Usually curettage with peripheral osteotomy is satisfactory method if recurred a second procedure of curettage and peripheral osteotomy would eradiate the lesion without further recurrence. When recurred it is classified aggressive and non aggressive clinically. After a complete soft tissue exposure, the tumor is isolated and removed, under direct observation, bone is then removed with rotary instrument to a point 2-3 mm beyond the clinically evident extent of the pathologic tissue. On the other hand if it is found that the cortex is extremely thin or cortical discontinuity exist then inter maxillary fixation and immediate autologous bone grafting may be necessary. Bleeding of the lesion to be anticipated. Radiotherapy has been used successfully in certain cases, age factor and size of the lesion and contraindication of surgical procedure may determine the use of radiotherapy usually 30Gy. This type of treatment should be used with caution and certainly not with young patient. Pre operative endodontic therapy: Is advantage to endodontic treatment preoperatively on all the teeth that give the impression in the radiograph that the roots are adjacent to radiological adjacent to or enveloped by the lesion it is the characteristic of giant cell granuloma that the disease extends to the inter radically area, often up to and involving the alveolar bone crest, if the root canal treatment is performed in advanced of curettage and peripheral osteotomy the surgeon can explore in all detections and remove suspended tissue aggressively without concern about the roots of the teeth.

Successful resolution of a lesion using intralesional injection of corticosteroids been used. First step is biopsy, to rule out the lesion, mixture of equal parts of triamcinolone acetonide (10mg/ml kenalog-10) and local anesthesia with epinephrine was injected into the lesion under pressure weekly for 6-weeks. Using 26 gauge needle & dose 2ml/2cm2. of radiolucency. PERIPHRAL GIANT CELL GRANULOMA: Synonyms: peripheral giant cell reactive granuloma, Giant cells epulis Periosteoma, osteoblastoma. Earlier it is thought that it is a true neoplasm. Some believe it is proliferative response. Lesion dose not appear truly a reactive. Etiology: Role of trauma, extraction of teeth, chronic irritation due to denture.

Clinical features: age average 25-35 years (1-65). Sex: female to male ratio == 2:1 Site: mandible > maxilla.

Location: Gingiva, and alveolar process, anterior to molars, fallowed by canine and pre molar region. It appears as an sessile or pedenculated mass arising from deeper tissue. It originate from periodontal ligament, muco periosteum. Size: 0.5 to1.5 cms not > 3 cms. Colour: dark red. Vascular/ hemorrhagic. Consistency: soft to firm. Swelling is pain less. Rarely get ulcerated if trauma from opposite teeth. If teeth present protrude inter dentally, deviation of adjacent teeth. If edentulous it occurs at the crest region. Increased size lesion of causes disturbed sleep and mastication. It also interfere with tooth brushing. Histological features: it is a non encapsulated mass of a tissue containing reticular and fibrillar connective tissue. Large number of ovoid or spindle shaped connective tissue are present. It shows multinucleated giant cells. Giant cells resembles osteoclasts but larger. Numerous capillaries particularly at periphery. Foci of hemorrhage- liberation of hemosiderin spicules of newly formed osteoid. Radiological appearance: it is not specific unless pressure resorption of underlying bone has occurred. In such cases IOPA shows saucerisation at alveolar crest, it may be well defined or irregular. Treatment: Pre operative endodontic therapy. Excision through incision around base of lesion. Excision few mm wide to avoid recurrence. Adjoining teeth preserved, if pocketing; surface curettage. Ridge is made smooth around the lesion. Site is kept under observation for few months.

HODGKINS LYMPHOMA: Hodgkin’s lymphoma is commonest type of lymphoma, can occur whenever there is lymphoid tissue. On microscopic section the involved nodes are pink gray in colour and rubbery in consistency. ETIOLOGY: Possible viral etiology for the disease in the younger age group. More cases of Hodgkin's lymphoma are seen with inflammatory monocytes. In cases of Hodgkin's lymphoma it shows elevated antibody titer to E B virus. It is found in those, whose childhood is protected from common infections. CLINICAL FEATURES: Affects young adults, commonly males (25-40) age. Second peak at age of 45 years. Present as painless progressive lymph nodes enlargement in the cervical or supra clavicular region which may or may not be associated with generalized symptoms such as malaise, fever, weight loss night sweat. Pressure effect results in superior vena cava obstruction due to enlarged mediastinal lymph node. Bone pain indicates vertebral collapse secondary to bony metastases. Recognized but unexplained symptom infection is pain in the site of disease is induced by drinking alcohol. On examination: The involved nodes tend to be discrete, non tender rubbery in consistency. Spleenomegaly, hepatomegaly with demission bony metastasis, anemia develops. Patient may also complain of edema of legs, anorexia, dysphagia, hemoptysis & malena. The course of the disease is very variable, death may fallow in weeks. With modern method of treatment the disease may be cured. Clinical stages of the Hodgkin’s lymphoma is necessary to determine accurately the extent of the disease treatment and prognosis.

Four stages of Hodgkin’s lymphoma are ANNA ARBONS CLASSIFICATION 1) Stage I


confined to one lymph nodes

2) Stage II


in more than one side either above or below


nodes involved above and below the diaphragm.

diaphragm. 2) Stage III

3) Stage IV =====

spread beyond lymphatic nodule system Eg liver, kidney.

Each stage is further sub divided into group A or group B. According to presence or absence of associated generalized symptoms such as weight loss, fever, anemia and one pain. Special investigations leading to clinical staging a)

Biopsy in diagnosis and histological grading.


Chest radiograph to demonstrate enlarged mediastinal lymph nodes.


Mediastinal scanning with Gallium 67 to demonstrate involved mediastinal lymph nodes.


Intra venous urography; may show distortion or compression of the renal calyces by retro peritoneal nodes.


Lower limb lymphangioram: will demonstrate both pelvic and retro peritoneal nodes (false positive and negative results) may present.




CT scan


Laparotomy/ spleenectomy liver and nodular biopsy to stage the Hodgkin's lymphoma.

Histological classification: 1. Lymphocyte predominate 2. Mixed cellularity 3. Nodular sclerosis

4. Lymphocyte deplicate.

Histological features: Mainly Reed stembergs cells dispensed in varying type of stroma. These cells are 15-45 micron in diametertwo halvesof nucleus appear as a mirror image of each other. (owl eye) nucleus is large well formed distinct inclusion like owl eyed nucleus surrounded by a clear halo. Another hyper segmented nucleus is also seen. Relationship between clinical and histological grade and survival: Histologically inactive disease is lymphocyte predominate clinically Stage I is potentially curable. Progressive disease: Histologically diffused fibrosis, lymphocyte depletion, domination by histiocytes clinically Stage III B and Stage INTRA VENOUS with association of systemic disease. Changing disease; mixed cellulority and nodular sclerosis in Stage III or Stage II disease. Nodular sclerosis, Stage I decrease good prognosis. Treatment: Treatment policy in Hodgkin's lymphoma is radiotherapy and combination chemptherapy Radiotherapy is treatment of choice in Stage I, II, & III A is good in divided dose over several weeks. Disease combination chemotherapy in Stage IIIB & IV disease cytotoxic drugs and steroids. Eg: commonly used combination used is _________ Nitrogen mustard (Mustine) _________ Vinblastin and Prednisone(MOPP) _________ Other combination are under trial. Results 5 years survival of 80% of cases.

BROWN TUMOR OF HYPERPARDTHYRODISUM: Brown tumor represents part of the MORPHOLOGIC SPECTR It is a disease where excessive parathyroid hormone is released. This may be due to adenoma, functional carcinoma of parathyroid. End stage renal diseases or phosphate retention. Clinical features: Age == any age common in 20-50 yrs of age. Female to male ratio == 3:1. It represents as smooth painless swelling of maxilla or mandible. If cortex is intact overlying mucosa is normal, if perforates, mucosa is thin, reddish/ purplish. It may cause pathological fracture, bone pain, stiffness of joint, sudden drifting with definite spacing between teeth.

Radiographic appearance: Bone generally shows radiolucent area which is sharply defined round/oval which may be loculated. Small cystic area can be seen. In jaw bones it gives ground glass appearance. Lamina dura is partially lost. Resorption of root is seen in some cases. Histological features:

The name Browns tumor is derived from the colour imparted to tissue by hemosidrin. Lesion composed of vascular fibrous tissue in which areas of hemorrhage and hemosiderin and occasionally islands of osteoid and bone formation. Wide spread/ nodular accumulation of giant cells are present. In hyper parathyroidisum serum calcium level is > 9-12 mg/dl. Treatment: Small Brown’s tumors are excised. In case of large tumor biopsy is taken first. In parathyroid carcinoma removal of parathyroid glands. CHERUBISM: Synonyms: (familial fibrous dysplasia of the jaws, familial fibrous swelling of the jaws, familial multilocular cystic disease of the jaws, disseminated juvenile fibrous dysplasia, hereditary fibrous dysplasia of the jaws)

A 7-year-old female with cherubism affecting the maxillofacial region.

Clinical features: First reported by Jones in 1953. It manifests itself in early child hood around 3-4 years of age. Starts as progressive painless symmetrical swelling of jaws maxilla/mandible. Jaws are firm to hard on palpation. Lymph nodes palpable in early occurrence of disease. Premature exfoliation of deciduous teeth as early as 3 years. Absence of numerous permanent teeth. Mucosa is normal and intact. Increase width of maxillary alveolar ridge and is “V� shaped.

Radiographic appearance: Extensive bilateral destruction of bones of jaw with expansion and severe thinning of cortical plates. Numerous un-erupted and displaced teeth which appear floating in cyst like spaces. Other bones of skull appear normal. Histological features: Presence of large number of large multi nucleated giant cells in a loose delicate, fibrillar and mainly small blood vessels. Small number of inflammatory cells. In older and regressing lesion appear less number of giant cells and more number of fibrous cells. Small capillaries may also be seen. Treatment:

1) Observation: Though the lesion needs Oral Surgery. Progressive in

childhood, it tends to become static and shows regression as patient shows puberty. 2) Extraction of teeth in lesional area (Jones-1965) since even if the teeth erupt

it erupt haphazardly. 3) Curettage of lesion: Some have kept wound open after curettage and


have done primary closure. 4) Surgical contouring: This is done after puberty if symptoms do not subside,

for cosmetic purpose. 5) Radiation is contraindicated.

PAGETS DISEASE: (Jaffe- 1958) Clinical features: Age 40 years and above It has familial tendency. Bone pain, severe headache, deafness, visual disturbance, facial paralysis, progressive enlargement of skull Defarmation of spine, femur, tibia, flattening of chest, waddling gait Maxilla exhibit progressive enlargement. Maxillary ridge widens palate flattens Tight dentures in case of edentulous, spacing between teeth in dentulous patient, lips appear small to cover big jaw. Radiographic appearance: Cotton-wool appearance Hyper cementosis Spacing between teeth. Histological features:

It depends on stage of disease Formation of mosaic bone Formation of reversal lines. Treatment: Administration of, Vitamins, hormones-calcitonin Fluorides therapy Radiation therapy. ANEURYSMAL BONE CYST: (Described by Jaffe & Lichten Steirs 1942)

Clinical features: Age commonly occurs in young age 20 years. History of traumatic injury. Lesions are painful upon motion Limited movement of the joint Swelling of the joint. Upon entering the lesion excessive bleeding; welling up from tissue, resembling a blood soaked sponge.

Radiological appearance: Honey comb or multiple soap bubble appearance. Cortical bone may be destroyed and periosteal reaction may be evident. Histological features: It consists of fibrous connective tissue stroma containing many cavernous and sinusoidal blood filled spaces. These spaces may or may not show thrombus. It shows young fibroblasts with multinucleated giant cells with patchy distribution similar to that of giant cell granuloma. Treatment:

Treatment modalities includes; Enucleation, curettage, cryotherapy, radiation, resection, amputation if long bones. Radiation may lead to osteosarcoma formation. In surgery all efforts should be made pre operatively to enclose the lesion is aneurysmal bone cyst. Bleeding is excepted and may be severe since wide exposure in access of afferent vessels. Rapid curettage of the lesion should be done which further stops bleeding.

OSTEOCLASTOMA: (GIANT CELLS TUMOR) Line of demarcation between very aggressive giant cells lesion and giant cells tumor cannot be drawn. Clinical features: Age it commonly occurs between 20-40 years. Mainly affects ends of long bones. History of trauma may be present on some cases. On palpation eggshell cracking may be heard and felt. Metastasis may occur to lung via blood. Radiographic appearance: Radiolucent area is seen representing osteolytic activity. Borders are regular, well defined. Some lesion shows multiple soap bubble appearance. As soon as lesion become malignant borders become irregular. Histological features: Increased nucleus cytoplasm ratio, hyper chromatic nucleus. Variation in cell and nucleus size. Abnormal mitosis is seen. Treatment:

Adequate radical surgery Growth is excised together with wider margins. Radio therapy may be necessary.

CONCLUSION: Controversy exit between the authors regarding the relation between giant cells granuloma and giant cells tumor. Waldron & Shafer: Concluded that these lesions are similar and identical. Jaffe in 1953 proposed that giant cells lesions in the jaws are different from those in the rest of skeleton. He suggested that giant cells granuloma occurs only in the oral cavity while the giant cells tumors occur in the other skeletal bones Eg. long bones. Agreed with Jaffe’s concept that the two entities are separate and distinct suggesting in addition that; some jaw lesions are giant cells tumor and same giant cells lesions outside the jaw are giant cells granuloma.

Giant cell tumor of the jaw are extremely rare, while the giant cell tumor of long bones is common. Giant cell tumor contains more nuclei. The giant cell clinically more destructive hen compared with central giant cell granuloma. In support of non neoplastic nature of the condition is the realization that in complete removal can result in cure, a small abnormal tissue which left behind may not necessary leads to recurrence. In certain cases when aggressive biopsy was taken, healing was stimulated which does not favor that the lesion is neoplastic. Majority of the modern investigator suggest that giant cell granuloma is an unusual proliferative response of the tissue of an injuries. Role of trauma plays an important role in etiology of giant cell lesion. Trauma is caused chiefly by tooth extraction, denture irritation and chronic infections. Giant cell lesion is a histological finding some represents lesions where giant cells in the concerned background are pathgnomic. Some lesions where giant cells are characteristic but not pathgnomic; some lesions associated with presence of giant cell there fore these lesions should be correlated with clinical finding for the final diagnosis and treatment plan.


By shafer Hine Levy


edition BY Malcolm A. Lynch. Vernon J. Brightman. Martin S. Greenberg. 3. FUNDAMENTALS


Second Edition By Dr. Bailoor DN & Dr. Nagesh KN 4. AN OUTLINE OF ORAL SURGERY: part II

By H. C. Kelly, G. R. Seward & L. W. Kay. 5. ORAL & MAXILLOFACIAL SURGERY. Volume two. By Deniel M. Laskin. 5. A TEXT BOOK OF ORAL & MAXILLOFACIAL SURGERY.


edition By Gustav O. Kruger. 7. Giant cells and giant cell lesions of oral cavity: Journal of Indian Dental Association. Vol. 66 November 1995.

Gaint cell lesions of bone/ dental implant courses by Indian dental academy  

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