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giant cell lesions

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giant cell , classifications , description of the lesions

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giant cell lesions

  1. 1. GIANT CELL LESIONSGIANT CELL LESIONS
  2. 2. Contents • Introduction • Types of GC • Physiologic GC • Pathologic GC • Giant cell lesions • Conclusion • References
  3. 3. Introduction : • 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 processes. • 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
  4. 4. • 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
  5. 5. • 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.
  6. 6. • 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
  7. 7. • 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
  8. 8. Osteoclasts : • 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.
  9. 9. • 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 .
  10. 10. 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.
  11. 11. •They are formed from the fusion of macrophages and is observed as a result of the response induced by biomaterials and other foreign bodies. •These are seen in chronic infective granulomas, leprosy and tuberculosis.
  12. 12. • Recent studies show that macrophage fusion, giant cell formation, and the foreign body response require matrix metalloproteinase 9(MMP 9).‑ • 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 leprosy.
  13. 13. 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.
  14. 14. • 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.
  15. 15. • These cells are seen in following conditions: 1. Tubercular granuloma 2. Leprosy (TT Type mainly) 3. Late Syphilis 4. Deep fungal infection 5. Sarcoidosis 6. Leishmaniasis 7. Crohn’s disease.
  16. 16. 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.
  17. 17. • 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 2. Xanthoma 3. Xanthogranulomas 4. Dermatofibroma. Nuclei are arranged as Central ring
  18. 18. Aschoff giant cells: • These multinucleate giant cells are derived from cardiac histiocytes and are seen in rheumatic nodule.
  19. 19. 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 cells. e.g. carcinoma of the liver, various soft tissue sarcomas etc. Anaplastic tumour giant cell with nuclei of variable size and shape
  20. 20. 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 lymphomas.
  21. 21. Giant cell lesions
  22. 22. • 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. Classification 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
  23. 23. 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
  24. 24. Chattopadhyay A (1995) (Table 1)
  25. 25. Classification  INFLAMMATORY - Chronic osteomyelitis, Orofacial graulomatosis, Periapical cyst, Sarcoidosis  INFECTIOUS - Fungal, Bacterial, Viral infection  IDIOPATHIC - External root resorption involving bone.  REACTIONARY - PGCG, CGCG, GC Fibroma  METABOLIC - Hyperparathyroidism  DEVELOPMENTAL - Cherubism  VASCULAR - Aneurysmal bone cyst  BONY LESION - Paget’s disease  NEOPLASTIC - True giant cell tumor, Hodgkins Lymohoma, Fibrous histiocytoma
  26. 26. Classification 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 • Chondroblastoma • Chondromyxoid Fibroma • Langerhans Cell Histiocytosis • Pigmented Villonodular Synovitis
  27. 27. C. Malignant : • Osteosarcoma • 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
  28. 28. 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, Xanthogranuloma A. Hodgkins Lymphoma B. Temporal Arteritis
  29. 29. Giant Cell lesions of Bone
  30. 30. Central Giant Cell Granuloma • In 1953 Jaffe first described CGCG as Giant Cell Reparative Granuloma. • 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 granuloma. • Etiology unknown
  31. 31. • 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
  32. 32. • Symptoms—the earliest sign of the lesion may be expansion of bone with premature loosening and shedding of deciduous teeth. • 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, destructive lesion.
  33. 33. -Aggressive lesions may exhibit pain,rapid growth,cortical perforation and root resorptio -Non aggressive exhibit no symptoms,slow growth,no perforation,no resorption
  34. 34. Radiographic features • 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 trabeculae.
  35. 35. •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 .
  36. 36. HF: • 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 2013
  37. 37. • 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 enbloc resection. • 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 properties. • The combined treatment (pharmacological and surgical) is advantageous for large aggressive lesions .
  38. 38. • Prognosis—recurrence rate of 12% for lesions under 2 cm and 37% recurrence for lesions over 2cm in size. Differential Diagnosis 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.
  39. 39. 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.
  40. 40. 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 midline. Brown tumors of hyperthyroidism—serum calcium levels are elevated.
  41. 41. 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, tibia. • 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
  42. 42. • GCTs arising in the head and neck region constitute approximately 2% of all GCTs. CF: • 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
  43. 43. • 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 anatomic structures.
  44. 44. • 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 mononuclear cells. Evenly distributed multinucleated giant cell with surrounding stroma made up of spindle cells are shown, which were consistent with GCT.
  45. 45. • Differential diagnosis : a) Aneurismal bone cyst b)Chondroblastoma c) Dermoid cyst d)Chondrosarcoma 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
  46. 46. • 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
  47. 47. • Auclair et al (1988) by histomorphometric study on GCT and GCG found statistical significant difference between the two lesions: • Stromal cellularity • Even distribution of GC • Number of nuclei • Presence of tumor necrosis • Presence of inflammatory cell
  48. 48. 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.
  49. 49. • These occasionally develop in association with other primary lesions such as:- -fibrous dysplasia -Giant cell granuloma -osteosarcoma • Etiology remains unclear
  50. 50. • 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.
  51. 51. Clinical Features: • They are solitary lesions • Commonly seen in 2nd and 3rd 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 .
  52. 52. • Large lesions may cause displacement of teeth leading to malocclusion • Mobility, migration, resorption of teeth may occur. • Any long bone can be affected. Mandible, femur and tibia are common • Grossly lesion is soft and reddish brown; because of its rich blooad supply.
  53. 53. Radiographic features • Radiographically, aneurysmal bone cysts are seen as a unilocular or multilocular radiolucency, usually multilocular lesions frequently produce a "soap bubble" or "honeycomb pattern“ • 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 bubble appearance.
  54. 54. 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 seen.
  55. 55. • HF: • The characteristic feature is blood vessels and large blood filled spaces. • Fibrous connective tissue stroma. • MGC are present with patchy distribution. • Osteoid formation • Rx: • Surgical curettage or excision(appearance at time of surgery has been likened to that of a BLOOD SOAKED SPONGE)
  56. 56. Differential diagnosis Giant cell granuloma Ameloblastoma Cherubism(because of giant cell-like features)
  57. 57. Cherubism • 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 jaws’. • 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
  58. 58. • Ueki et al (2001) described mutation in gene encoding for SH3BP2 in cherubism. • Demostrated MGCs in cherubism stain positive for TRAP – osteoclastic nature. • 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
  59. 59. Clinical Features: • Affects in early childhood - mainly 1-5 yrs. • The characteristic feature is that it is strictly bilateral • 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 normal vision(rare) Meng XM et al; Int. J. Oral Maxillofac. Surg. 2005: 34 Clinicopathologic study of 24 cases of cherubism
  60. 60. Radiographic features • 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.
  61. 61. • Initially fibrous replacement of the bone give rise to "soap bubble” • 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.
  62. 62. • Seward and Hankey suggested a grading system in 1957 of cherubism, based on radiographic location of the lesions in the jaw. • 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
  63. 63. 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, mandible .
  64. 64. • H/F – • Vascular fibrous stroma is loosely arranged. • MGC are small, few and usually aggregated focally. • Peculiar perivascular eosinophilic cuffing.
  65. 65. Differential diagnosis • 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 condition. • Rarely surgery is indicated.
  66. 66. • 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 hyperparathyroidism. • 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
  67. 67. • In 1891, Von Recklinghausen described the classic bone disease termed osteitis fibrosa cystica. • An osseous lesion that develops in bones affected by hyperparathyroidism. • 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, Primary
  68. 68. • 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 scapula. • 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 Therapy: Case Report on Successful Treatment after Subtotal Parathyroidectomy. International Journal of
  69. 69. Radiologic features • 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 cortical expansion. • Hand bone—earliest change is subtle erosion of bone from sub- periosteal surface of phalanges of hand.
  70. 70. • 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 tables. • 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.
  71. 71. 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.
  72. 72. R/F of teeth  Loss of Lamina Dura(complete/partial)  Root may thus appear tapered due to loss of image contrast.
  73. 73. • HF: 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.
  74. 74. D/D • 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 distinguishing.
  75. 75. Investigations :  Immunoassay for parathormone  CT & Dual Energy X-ray Absorptiometry (DEXA) to produce quantitative estimates of bone density. Treatment – • Surgical management
  76. 76. Mucosal lesions with Giant CellsMucosal lesions with Giant Cells
  77. 77. 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
  78. 78. Clinical features : • Usually seen in 4th to 6th decade of life but no marked age prelidiction . • 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 in diameter.
  79. 79. • Common site—it occurs on gingiva and alveolar mucosa, most frequently anterior to molars. It is common in mandible than maxilla. • 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
  80. 80. • 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 ridge.
  81. 81. Proliferation of MGCs within background of ovoid or spindle shaped mesenchymal cells. Large vesicular nuclei. Mitotic figures are common.
  82. 82. R/F • 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
  83. 83. D/D • Pyogenic granuloma Treatment: Local surgical excision down to the underlying bone
  84. 84. 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 tissue.
  85. 85. C/F • 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
  86. 86. • 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 maxillary.
  87. 87. • 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 pages
  88. 88. H/P 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
  89. 89. D/D • Irritational fibroma Treatment • Surgical excision
  90. 90. Hodgkins lymphoma • It is lymphoproliferative disorders arising from lymph nodes and from lymphoid components of various organs. • It is neoplastic proliferation of lymhopoietic portion of reticuloendothelial system. • It was first described by British pathologist, Thomas Hodgkin in 1832. • It is characterized by painless enlargement of lymphoid tissue throughout the body. • The exact cause of Hodgkin’s lymphoma is not known
  91. 91. C/F : • 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
  92. 92. • 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.
  93. 93. Clinical Stages (Ann Arbor Staging) • Stage I—involvement of single lymph node region or extra- lymphatic sites. • 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.
  94. 94. • 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 immune response. • 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
  95. 95. H/F: 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 prognosis. 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.
  96. 96. Reedsternberg Cell - have paired mirror nuclei
  97. 97. D/D: • 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. Treatment : • Radiotherapy • Chemotherapy • Combination of both
  98. 98. 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 vascular-related. • Constitutional symptoms include fever, weight loss, anemia, and fatigue. • Vascular-related symptoms arise secondary to arterial inflammation with luminal stenosis and resultant end-organ
  99. 99. • 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 presentation. • Temporal arteritis is the most common systemic vasculitis of adults in Western countries. • Women are affected at least twice as often as men.[2] Disease susceptibility is associated with northern European descent and is seldom observed in blacks and Asians
  100. 100. • 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] Chlamydia pneumoniae, and Mycoplasma pneumoniae.
  101. 101. H/F • There are 3 main patterns of vascular damage in temporal arteritis. • 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)
  102. 102. • 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
  103. 103. • 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.
  104. 104. D/D: Migrane Cluster headache Treatment : • The consensus for glucocorticosteroid initiation is as follows: Uncomplicated GCA (No jaw or tongue claudication or visual symptoms): • Prednisolone 40-60mg (not <0.75 mg/kg) daily until resolution of symptoms and laboratory abnormalities. Complicated GCA: • 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 administered.
  105. 105. Wegener's Granulomatosis • 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.
  106. 106. Etiology : • It is uncommon disease • Exactly unknown • Predeposing factors may be exposure to environmental antigens such as silica and infection ( particularly stapylococcus aureus). • Genetic factors .
  107. 107. 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.
  108. 108. • The most common symptom of Wegner’s granulomatosis is nasal stuffiness with chronic discharge (rhinitis). • Patient soon develops cough, hemoptysis, fever and joint pains. • 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.
  109. 109. 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.
  110. 110. • 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 spontaneous exfoliation. • After extraction of teeth patient is usually noticed poor healing. • Other features—cranial nerve palsies, jaw claudication,labial mucosal nodule, oroantral fistulae, and parotid swelling.
  111. 111. H/F 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.
  112. 112. D/D: • Hodgkins Lymphoma • Sarcoidosis Treatment: • 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.
  113. 113. Sarcoidosis • It is also called as Boeck’s sarcoid, Besnier-Boeck-Schaumann disease. • 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, suggesting lymphoproliferation. • It is characterised by presence of non-caseating granulomas in affected organs.
  114. 114. • 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.
  115. 115. • Most commonly seen in United States and scandinavian population. • 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.
  116. 116. • 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 manifestations . • Dry cough , dyspnea and chest pain are frequent respiratory complaints. • Non specific symptoms such as fever , night sweats , fatigue and malaise are present.
  117. 117. • 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 nodule.
  118. 118. Syndromes associated with sarcoidosis: • Lofgren syndrome – acute form of sarcoidosis usually found in white females, consists of erythema nodosum, bilateral hilarand arthralgia. • Heerfordt syndrome(uveoparotid fever)- is characterised by parotid enlargement , anterior uveitis, facial paralysis and fever.
  119. 119. • 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 xerostomia.
  120. 120. H/P 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.
  121. 121. D/D: Tuberculosis Treatment : • Standard treatment of choice is corticosteroids. • Refractory (does not respond to treatment) sarcoidosis—in this case methotrexate, azathioprine, chlorambucil and cyclophosphamide is used.
  122. 122. Syphilis • Also known as leus • It s a chronic sexually transmitted diseases caused by trepenema pallidum, characterised by peroids of active disease and latency. • It occurs world wide. • Acc. to WHO approx 12 million new cases of veneral syphilis occurred in 1999
  123. 123. • It occurs through Sexual contact • Maternal transmission • Predisposing factors—overcrowded living and primitive housing.
  124. 124. Classification: • 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 exposure. Secondary—it is discovered 4 to 10 weeks after primary stage. Tertiary—this stage after several years develop the latent phase. Quaternary syphilis—the atypical malignant progression of tertiary neurosyphilis in immunocompromised HIV individuals is referred as quaternary syphilis.
  125. 125. 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- infectious.
  126. 126. Primary syphilis: • 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.
  127. 127. • 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 lymphadenopathy. • Chancre vary in size from 5mm to few centimetres.
  128. 128. • 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. Oral manifestations: • 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 lymphadenopathy. • Ulcer heals spontaneously within 7-10 days.
  129. 129. Secondary syphilis: • 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 feet. • Generalized lymphadenopathy is present.
  130. 130. • Other features are condyloma lata, alopecia , myalgia, meningities, pulmonary and neurologic involvement are present. • The secondary lesions resolve with or without treatment and infection enters to latent stage where there are no clinical manifestations. • Transmission of syphilis is by contact and occurs through individuals with the primary or secondary stages of disease.
  131. 131. Oral manifestation: • 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 .
  132. 132. Tertiary Syphilis: • In 1/3rd of individuals after many years tertiary syphilis may occur. • 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.
  133. 133. Neurosyphilis: • 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 paresis. • Tabes dorsalis is the syphilitic involvement of dorsal column of spinal cord and dorsal root ganglion. • Due to syphilitic involvement of cerebral tissue, General paresis occurs.
  134. 134. • 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 gummatous lesion • The most commonly involved sites are skin , skeletal system, mouth , upper respiratory tract , larynx. • Single cerebral gumma may produce symptoms suggestive of brain tumor.
  135. 135. Oral manifestation: • 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 gummatous lesion
  136. 136. • 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
  137. 137. Congenital Syphilis • 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 keratitis. • 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 present.
  138. 138. • 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
  139. 139. H/P: Syphilitic gumma consists of central coagulative necrosis surrounded by zone of palisaded macrophages with lymphocytes, plasma cells, giant cells and fibroblast.
  140. 140. D/D • Fungal infections Treatment : • 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.
  141. 141. Leprosy (hansen’s disease) • First observed by Hansen in 1868. • Chronic infectious disease produced by Mycobacterium leprae. • It is a chronic infectious disease affecting skin and peripheral nerves. • Acc to WHO about 720,000 new cases of leprosy are reported each year.
  142. 142. Pathogenesis: • 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.
  143. 143. • Leprosy represents maily two patterns Tuberculoid leprosy Lepromatous leprosy • Third is borderline leprosy-it can be tuberculoid borderline or lepromatous borderline.
  144. 144. Tuberculoid type or paucibacillary type: • Incubation period is of 2 to 5 years • Males are affected more commonly than females with ratio of 3:1. • 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.
  145. 145. • 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 Lesion of tuberculoid leprosy showing peripheral spread
  146. 146. • 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.
  147. 147. 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
  148. 148. • 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
  149. 149. Oral manifestations: • 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 commonly affected.
  150. 150. 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 H/P
  151. 151. Differential Diagnosis • Gummatous lesion of syphilis —VDRL test should be performed. Treatment: • 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.
  152. 152. Tuberculosis • Tuberculosis is a common worldwide infection caused by bacteria belonging to Mycobacterium tuberculosis. • Most frequent and important agent of human disease is M. tuberculosis. • M.bovis is transmitted by unpasteurized milk and cause of small percentage of cases in developing countries.
  153. 153. Other risk factors for TB includes- • Diabetes • Smoking • Excessive alcohol consumption • End stage renal failure • HIV • 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.
  154. 154. Pathogenesis: • Transmitted by air borne spread of droplet nuclei produced by patients with infectious pulmonary TB. • Droplets aerosolized by coughing, sneezing or speaking are inhaled. • Thus transmission of infection is enhanced by crowded conditions and poorly ventilated areas.
  155. 155. Types • 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)
  156. 156. C/F • 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.
  157. 157. • Involved nodes may radiographically appear calcified. Oral manifestation: • 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.
  158. 158. • TB osteomyelitis has been reported in jaws and appears as ill- defined areas of radiolucency.
  159. 159. •Tubercle composed of epitheloid cell, lymphocytes, Multinucleated Giant Cell. •Central foci of caseous necrosis present. •Giant cells of the Langhans type are clearly visible. Staining methods include:Z-N staining and other Acid fast stains H/P
  160. 160. Treatment : • 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.
  161. 161. References : • Text book of pathology . Harsh mohan 6th ed. • White and Pharoah. Oral Radiology Principles and Interpretation.6th ed. • Wood and Goaz. Differential Diagnosis of Oral and Maxillofacial lesions.5th ed. • Shafers text book of oral pathology 7th ed. • Text book of oral medicine . Burkitts 11th ed. • Oral medicine oral diagnosis & oral radiology – Ongole .2nd ed. • Text book of oral medicine – ghom 2nd ed.

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