Lymphoid lesions

1,110 views
823 views

Published on

Oral Pathology II
Forth Year

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
1,110
On SlideShare
0
From Embeds
0
Number of Embeds
4
Actions
Shares
0
Downloads
1
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Lymphoid lesions

  1. 1. For all student: main source is (Regezi) This outline not enough for exam Lymphoid lesions  Reactive lesions • • Lymphoid hyperplasia Angiolymphoid hyperplasia • Lymphoepithelial cyst  Developmental lesions  Neoplasms:  Lymphomas • Hodgkin’s lymphomas • Non-Hodgkin’s lymphoma  Myeloma/plasmacytoma Reactive lesions *Lymphoid hyperplasia Normal lymphoid tissue in/around the oral cavity: Pharyngeal tonsils Lingual tonsils Oral tonsils Regional lymph nods and lymphoid tissue 1. LH: is a proliferation of lymphocytes without cytological atypia. 2. Mitotic figures often remain restricted to the germinal center. 3. Occasionally, it may mimic the “starry-sky” appearance Follicular lymphoid hyperplasia: is a reactive condition involving the soft tissue covering the hard palate Lymphoproliferative disease of the palate: Similar to follicular lymphoid hyperplasia but always associated with malignancy *Angiolymphoid hyperplasia with eosinophilia "Epithelioid or histiocytoid hemangioma"  Nodular subcutaneous benign disease [Aggregates of lymphocytes and eosinophils]  Regional lymphadenopathy  Blood eosinophilia ALHE Clinically  Oral mucosal involvement is rare, however, it is common in the head & neck area  If occur, labial mucosa is the common site  Predominant in males  Affect persons in all ages  1-2cm. Solitary painless mobile lesion that enlarged gradually ALHE Histopathology  Well developed lymphoid follicles containing  Proliferating and dilated capillaries germinal centers
  2. 2.  Intensive infiltration of lymphocytes with eosinophils and fewer number of macrophages Treatment: Surgical excision Intralesional steroid injections might be effective *Kimura’s Disease  Similar to ALHE but without the association with regional lymphadenopathy  Different but related entity Developmental *Lymphoepithelial cyst Neoplasm Hodgkin’s Lymphomas Non-Hodgkin’s Lymphomas **Hodgkin’s Lymphomas  Affect bone or soft tissues  Painless enlargement of lymph nods or extra-nodal lymphoid tissue  Rarely affect the oral cavity  Malignant lymphoid cells  Non-neoplastic inflammatory cells  Reed-Sternberg cells Lukes-Bulter histologic classification 1. Lymphocytic predominance 2. Nodular sclerosis 3. Mixed cellularity 4. Lymphocyte depletion Ann Arbor classification  Stage I: =Involvement of single LN or single extralymphatic site  Stage II: = 2 or more LN chains  Stage III: =Positive disease in both sides of diaphragm  Stage IV: = bone marrow, liver or other extralymphatic organs Treatment and prognosis: • External radiotherapy • Chemotherapy **Non-Hodgkin’s Lymphomas  Middle-age and elderly  Gradual, asymptomatic, Focal enlargement of lymph node  Ann Arbor classification 1-Nodular lymphoma  3 subtypes: • Poorly differentiated • Mixed lymphocytic-histiocytic • Histiocytic [least favorable prognosis] 2-Diffuse lymphoma  Lymphocytic • •  Histiocytic Well-differentiated Poorly-differentiated
  3. 3.  Mixed Treatment - Stage I: radiotherapy - Other stages: chemotherapy or both *Burkett's lymphoma  Non-Hodgkin’s Lymphoma  African children lymphoma  Translocation of distal part of chromosome 8 to chr. 14. • Translocation of long arm of chromosome 22 to Chr. 9. is called Philadelphia Chr. [seen in leukemia]  Highest proliferation rate in humans Clinically African American % of all childhood malignancy Mean age Race Jaw involvement 50% 6-10% 3-10 years #100 blacks Relatively common 11 years #77% whites R. uncommon Association with EBV 90% 10% Radiographically  Poorly marginated radiolucency  Cortex: expanded, eroded or perforated Histopathologically  B-cell proliferation  Nodular or diffuse proliferation  Proliferation of lymphocytes with numerous scattered macrophages [starry-sky] Treatment and prognosis  Chemotherapy  2 years survival Plasma cell neoplasms 1-Multiple myeloma 2-Solitary plasmacytoma of bone *Multiple myeloma  What is plasma cell?  May present in soft tissue or in bone [solitary or multiple]  80% of bone plasmacytomas involve head and neck region  Mean age 63 years  May be asymptomatic. In symptomatic cases: pain, swelling, expansion, numbness or mobility of teeth. Loss of weight and anemia in some cases.  Immunoglobulin components [IgG, IgA] maybe detected in serum and urine of 91% and 97% Radiographically  85% of patients have abnormal radiographic skeletal survey  Multiple well-defined radiolucent areas Histopathology  Proliferation of plasma cells Treatment and prognosis  Chemotherapy and steroids and local radiation  Most patients die of infection or renal failure
  4. 4.  Mean survival is 2-5 years *Solitary plasmacytoma of bone  Mean age 50 years  Rarely affect jaw [angle of the mandible]  It may progress to multiple myeloma Radiographically  Well defined radiolucency  It may penetrate the cortical bone to the adjacent soft tissue  Peripheral blood picture is normal  Bone biopsy reveals proliferation of plasma cells producing immunoglobulin components Treatment Local radiotherapy Survival of patients is 10 years
  5. 5. Metabolic and Genetic jaw diseases       Paget’s disease Hyperparathyroidism Hyperthyroidism Acromegaly Cherubism Osteopetrosis Paget’s disease Chronic progressive disease of unknown etiology  3 stages: 1. Bone resorption 2. Vascular phase 3. Osteoblastic repair Clinical Features  ≈90% >55 years of age  Rare <40 years of age  Slightly more common in men (4:3)  More common in Europe mainly in England  Site: Femora, cranium, pelvis and sternum HP: according to it’s stage, activity of osteoclast and osteoblast, diagnosable…Why?]. mosaic picture [is characteristic but not Treatment: symptomatic includes analgesics, calcitonin. Hyperparathyroidism         Etiology: unknown, neoplasm or hereditary Elevated levels of [PTH] and hypercalcimia Bone demineralization Treatment: management of the primary cause and treatment of associated problems as renal failure Excessive amount of T3 and T4 hormones Common in female between 10 to 14 years Tremor, muscle weakness palpitation, diarrhea, anxiety and loss of weight Treatment:  thyroid-suppressive drugs [Thiocarbamides]  Radioactive iodine administration  Stress or epinephrine may precipitate “thyroid storm” Acromegaly  Hypersecretion of pituitary growth hormone  Common in 4th decade  Muscle weakness, paresthesia, new periosteal bone formation, enlargement of maxilla and mandible and paranasal sinuses, hypertension  Treatment: Controlling levels of growth hormone Cherubism     Children of 5 years Hereditary Bone expansion particularly the posterior region of the mandible Cervical and submandibular lymphadenopathy are common
  6. 6. Osteopetrosis  Hereditary bone condition  Generalized symmetrical increase in skeletal density and bone abnormalities  2 main types  Infantile [malignant]  Adult [benign]  Prognosis is poor, in adults is less sever  Treatment of complications Most common lesions containing large number of multinucleated giant cells are:        cherubism giant cell tumor (osteoclastoma) fibro-osseous lesions bone lesion of hyperparathyroidism hereditary hyperparathyroidism jaw tumors syndrome aneurysmal bone cyst

×