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2013-03-17 01:54:59

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  1. MMP
    • mucous membrane pemphigoid
    • IgG: BP180 laminin targets lamina lucida & hemidesmosomes

    • IF: linear band IgG and C3
    • Oral: gingival desquamative gingivitis, + Nikolsky
    • Other: conjunctiva
  2. Bullous pemphigoid
    • rare in oral, usually skin
    • healing w/no scarring
  3. epidermolysis bullosa acqueista
    • AI collagen VII(7)->subepithelial split
    • bullous lesions 1/2 in oral cavity
    • IgG deposits on bullae floor
    • looks like MMP
  4. Pemphigus
    • cell-cell desmosomes
    • suprabasilar spinus separation
    • Demoglein3
    • inhibilitating
    • Indirect IF
    • fishnet IF
  5. Lichen Planus
    • chronic AI: epithelial basal cells
    • T-cells
    • Hep C
    • histo: lymphocyte band along BM, basal degeneration/inflammation
    • SCC can result
    • CD8+
  6. LP tx
    dexamethasone, glucocortacoid, retinoid
  7. Discoid Lupus Erythematous
    • cutaneous H&N lesions
    • lichenoid similar to erosive LP w/ atrophic erythematous center
  8. Lupus has high morbidity from predominantly which organ?
    • kidneys
    • also warty veg in heart
    • IgM, IgG C3 + band test
  9. Pemphigus vulgaris
    • Dsg3, Tzank Cells
    • most common
    • mediterranean
    • suprabasilar acontholysis, Dsg3 oral cavity
  10. PV vs PF
    vulgaris vs foliaceus
    • vulgaris: suprabasilar (Dsg3)
    • foliaceus: subcorneal (more superficial) (Dsg1)
  11. PV tx
    • prednisone 1mg/kg
    • myclophenolate mofetil (cellcept) T,B cell inhibitor
    • gold & methotrexate
    • tetracyclines/nicotinamide
    • IVIg: expensive, refractory pemphigus
    • Rituximab: b cell antibody
    • Oral tx: dexamethasone rinse, nystatin (antifungal)
    • avoid: thiol, isothicynates, phenols or tannins
  12. Reticular LP
    • Wickman's stiae: interlacing keratotic lines
    • buccal mucosa, tongue
  13. plaque LP
    • multifocal
    • tongue buccal mucosa
  14. erosive LP
    • fibrinous ulcers surrounded by erythematous mucosa
    • keratotic stria
  15. lichenoid
    allergic like rxn amalgam
  16. lupus criteria
    • need 4
    • malar rash
    • discoid rash
    • photosensitivity
    • oral nasal ulcers
    • arthritis
    • CV-pulmonary
    • neuro
    • renal
    • hematologic
    • immunologic
    • ANA
    • pterygium
    • vascularization extends iris
    • arcus senilis
    • doesnt affect vision
    • cholesterol deposits
    • xanthelasma
    • yellow papules
  17. Atopy
    hx of hay fever, asthma, eczema
  18. spa pool foliculitis
    Pseudomonas aeruginosa
  19. RAS
    • recurrent aphthous stomatitis
    • T-cell
    • decrease CD4/CD8
    • increased TNF-alpha, IL-2,6
    • HLA A2, B12, B51, Cn7 Dr5
    • stress
    • drugs: beta blockers, nicorandil, antiarrhythmic
    • dilatory: Fe, folic, zn B1,6,12
    • food sensitivities
    • non-keratinized mucosa
    • minor, major, herpatiform
  20. RAS tx:
    • topical anti-inflammatories, anesthetics
    • cauterizing agents: thymol, phenol, silver nitrate
    • covering: milk of mgsia kaolin, pectin
    • B12 sublingual
    • tetracyclin, peridex (CHX)
  21. aphthous minor
    • most common
    • spontaneous heal (2 weeks)
    • painful
    • less keratinized tissues
  22. major aphtae
  23. Behcet's disease
    • blood vessel inflamation vasculitis
    • recurring apthous ulcers
    • pathergy test sterile needle prick-> pustule
    • sedimentation, CRP elevation
    • HLA B51
    • Anticardiolipin antibodies
  24. Reactive Arthritis (Riter’s Syndrome)
    • inflammation joints, urethra, eyes
    • STD: chlamydia
  25. erythema multiforme (EM)
    • Blistering, ulcerative mucocutaneous
    • drug hypersensitivity: barbituates, sulfonamides
    • infection: HSV, TB histoplasmosis
    • oral: diffuse ulcers epithelial necrosis, crusty vermillion
    • Minor: bullseye
    • Major: stevens johnson
    • chronic types
  26. EM tx
    • heres induces: antivirals zovirax, valtrex
    • symtoms: antihistamines, acetomenophen, topical anesthetics
    • antibiotics, corticosteroids IVIg
  27. EM Major
    • Stens-jonhsons
    • muliple bullae
  28. Toxic epidermal necrolysis (TEN
    • most severe EM
    • Drug rxn
  29. Geographic Tongue
    • (erythema margins, benign migratory glossitis)
    • unknown cause
    • psoriasis, seborrheic dermatitis, atopy
    • dekeratinization, desquamation of filiform papillae
  30. Allergic Contact Stomatitis
    • Oral mucosa resistance:
    • High vascularization,  Low density Langerhans cells and Tcells, saliva dilution 
    • Oral flavorings (balsam of peru, cinnamon,
    • cinnamric aldehyde, menthol, peppermint, eugenol)  preservatives, and dental materials, such as metals, acrylates, resins, and impression compounds, are the most common cause of allergic delayed-type hypersensitivity reactions of the oral mucosa.
    • -Ageusia (loss of taste)
    • -Dysgeusia (Change of taste)
    • -Tongue numbness, burning sensation.
    • -Lichenoid reaction, epithelium sloughing
  31. Orofacial
    • -UNCOMMON 
    • lymphatic blockage, leading to the diffuse swellings of the lips and other sites from
    • lymphoedema
    •  -Persistent and or recurrent labial
    • enlargement, oral ulcers
    • -Mucosal swelling
    • -Gingival enlargement
    • -Fissuring of the tongue
    • -Facial swelling and erythema
    • -Facial nerve palsy
    • -Cervical lymphadenopathy
    • -History of allergic Rxn and occasional
    • associations with food intolerance (monosodium glutamate and food
    • preservatives and chocolate)
    • -Delayed hypersensitivity to dental materials

    • - Normal epithelium covering connective
    • tissue showing perivascular inflammatory infiltrate
    • consisting primarily of lymphocytes and
    • plasma cells with Multiple discrete epithelioid granulomas

    • -Removal of amalgam has caused reduction of
    • swelling of buccal mucosa and lips of OFG in isolated cases
    • -Remove the allergen by discovering the
    • initiating cause
    • -Intralesional injections of high
    • concentration of triamcinolone once a week for 4 weeks
    • -First line of treatment is prednisone
  32. Wegener’s Granulomatosis
    • -Uncommon-
    • Necrotizing granulomatous lesions of the respiratory tract, glomuroneprhitis
    • -Hypersensitivity response to an inhaled
    • antigen
    • -Nasal ulcers, purulent discharge
    • -Systemic vacuities of small arteries and
    • veins
    • -Oral lesions can be the only clinical
    • evidence.
    • -Strawberry gingivitis is the key.
    • -Granular hyperplasia, bulbous projections
    • -Oral ulcers can also occur
  33. Hyperparathyroidism
    • -Primary, functioning parathyroid adenoma
    • -Secondary,  compensatory for hypocalcaemia kidney or liver failure or poor absorption of vitamin D
    • - Female, 30-60 y
    • -Renal calculi, peptic ulcers, psychiatric
    • problems, bone and joint pain
    • - Loosening, drifting and loss of teeth
    • -Elevated serum PTH levels
    • -Elevated serum calcium levels in primary and low serum calcium levels in secondary hyperparathyroidism
    • -Serum ALP might be elevated
  34. Only 10% develop a radiographic picture
    • -Demineralization of skeleton
    • -Osteitis fibrosa generalisata
    • -Brown tumors
    • -Pathologic calcifications
    • -In the jaws and calvariae: demineralization
    • of skull that acquires a granular appearance, thinning or loss of cortical
    • outlines (inferior md border, md canal, sinus walls, lamina dura, etc)
    • -Brown tumors radiographically and histology
    • resemble central giant cell granuloma OR ABC[MT1]
  35. Vitamin D Deficiency
    • rickets, osteomalacia
    • -Vitamin D and or calcium deficiency in diet
    • -Malabsorption syndromes of small bowel
    • -Renal tubular dysfunction leading to excess
    • calcium loss in urine
    • -Lack of sunlight exposure

    • Rickets:
    • - Tetany and convulsions from hypocalcaemia
    • -Craniotabes, swelling of wrists and ankles
    • -Short stature, deformities of extremities
    • -Delayed development of dentition and teeth
    • eruption
    • Osteomalacia:
    • - Bone pain and muscle weakness, waddling,
    • tetany, greenstick fractures

    • Rickets
    • - Widening and fraying of epiphyses of long
    • bones, bowing of weight bearing bones, greenstick fractures
    • - Thinning of cortical outlines (border of md
    • and md canal, lamina dura etc), thinning of trabeculae that are reduced in
    • number
    • Osteomalacia
    • - Pseudofractures in ribs
    • - Jaws show an overall radiolucency, with
    • sparse and thin trabeculae and thin cortical outlines, might show no
    • radiographic signs in the jaws
  36. osteoporosis
    • -A deficiency of bone tissue per unit volume
    • of bone
    • -Primary osteoporosis:  bone loss due to aging, F >> M,
    • postmenopausal or senile, compressed fracture of vertebrae, hip fractures,
    • hormone replacement therapy
    • -Secondary osteoporosis: due to abnormal or
    • iatrogenic causes (corticosteroid therapy, Cushing’s syndrome, malnutrition,
    • etc)
    • *Treat with bisphosphonates (increase in
    • osteoradionecrosis!)
    • -Thinning of bone cortices, sparse and thin
    • trabeculae
  37. hyperpituitarism, GH excess
    • Excess RELEASE of Growth Hormone, from a
    • functioning adenoma of the anterior lobe of the pituitary gland (pituitary adenoma)
    •  -“Gigantism” infant and children, before
    • growth ceases, prominent growth ceases, prominent growth with growth
    • potential (md and hands)
    • -Acromegaly: adults, affects soft tissues
    • (lips, tongue, nose) and bones with growth potential (md and hands)
    • -Enlargement of the hypophyseal fossa,
    • diffuse thickening of the outer table of skull, enlarged paranasal sinus,
    • spaces between teeth md prognathism in acromegaly
    • -Frontal bossing and mandibular pronathism,
    • mandible is elongated
  38. Sicklecell anemia/ Thalassemia Hemolyticanemia)
    • -Autosomal recessive
    • -Abnormal hemoglobin protein due to gene mutations
    • -Destruction of red blood cells by the spleen
    • -Hyperplasia of the bone marrow to compensate à LARGE MARROW SPACES
    • -Radiographic appearance follows bone marrow changes
    • -Large marrow spaces, thin and delicate trabeculae, thinning of cortical plates,
    • enlarged maxilla, small sinuses, radial striations in the deploic space of
    • the skull (“hair-on-end”)     
    • Expansion of the maxilla, obliteration of the
    • sinuses. Display the hair on end in the calveria.  (x-rays on the left)
  39. Paget’s Disease
    • Chronic inflammation of bones
    • osteitis deformans
    • Slow virus infection?
    • -Initial osteoclastic activity followed by vigorous osteoblastic activity-Skull, femur, sacrum, pelvis (most common is skull)-Affects MEN more than women
    • -Malignant transformation (osteosarcoma)-PRONE to osteomyelitis
    • -Maxilla is more frequently affected than the mandible-Usually bilateral involvement of the oral-facial area (can be but not every patient has bilateral involvement)-Hypercementosis, tooth displacement and mobility
    • -Enlargement of the alveolar process, frontal bossing (need to have their dentures adj. all the time!!)
    • -Bone pain 80%, deformity 20%, fractures 10%
    • -Neurological symptoms: headache, deafness, blindness, facial palsy, neuralgias (constriction of nerve by bones) Early stage: Radiolucent, well defined “osteoporosis circumscriptia” Second stage: Mixed density with various amounts of opacities: granular, ground-glass, cotton wool (osteoblasts start picking up!) Late stage: More radiopaque-Gross bone enlargement and deformity. -Cemento lines
    • – indicate area of resoprtion and bone apposition. More of a mosaic along one edge where the osteoblasts are.
  40. Scleroderma
    • -Autoimmune disease causing excessive fibrosis throughout the body.
    • -Affects 30-50 y/o-Affects Females more commonly than males
    • - Affects Skin, GI tract, musculoskeletal, kidney, heart, lungs
    • -Depends on affected tissues: Thickened, immobile, hidebound skin, sclerodactyly, heart and renal failure, respiratory insufficiencies
    • -Limited mouth opening (leads to dental disease!!) , xerostomia, dysphagia, altered tongue function
    • -Dental and periodontal disease
    • -Uniform widening of PDL space, smooth systemic erosions of the angle, coronoid and condylar process
  41. Langerhans’ Cell Histiocytosis (Histocytosis X)
    • -Langerhans proliferation= dendritic mononuclear cells normally found in the epidermis, mucosa, lymph nodes, and bone marrow (process and present antigens to T lymphocytes)
    • -Monoclonal proliferation (neoplastic process)
    • Acute disseminated LCH (Letterer-Siwe
    • disease):
    • <3 years, multiple soft-tissue and bony granulomatous foci,
    • hepatosplenomegaly, lymphadenopathy, anemia, thrombocytopenia, pulmonary lesions
    • (cutaneous, visceral and bone marrow)
    • -Unifocal LCH (eosinophilic granuloma): older children or young adults, bone lesions: ribs,
    • pelvis, skull, face, long bones. (Solitary or multiple bone lesions without
    • visceral involvement)
    • -Multifocal LCH: childhood, fever, soft-tissue and bone lesions, mild
    • hepatosplenomegaly, lymphadenopathy
    •  Hand-Schuller-Christian triad: bone
    • lesions, diabetes insipidus and exophthalmos (also known as chronic
    • disseminated histocytosis)
    • -Men younger than 15
    • -Bone lesions are solitary or multiple in the skull, ribs, vertebrae, and mandible

    • Well defined and non-corticated in the parietal bone and in the occipital bone.
    • Lateral oblique projections, with a well
    • defined radiolucency around the second molars
    • -Bone involvement in the mandible usually occurs in the posterior areas—characteristic of “scooped out” appearance when
    • superficial alveolar bone is destroyed
    • -Bone destruction and loosening of teeth may resemble severe periodontitis
    • -floating teeth (extensive alveolar involvement)

    -Diffuse infiltrate of pale-staining Langerhans cells intermixed with numerous red granular eosinophils
  42. Neutropenia
    • (neutrophils below 1500 / mm3) in an adult 
    • -Drugs (bone marrow toxicity or other mechanisms), infections or B12 deficiency - increase in susceptibility of patient to bacterial infections
    • -Infection of the oral mucosa may be the initial sign of the disease
    • -NORMALLY lower neutrophils in Africans and middle Eastern  benign ethic neutropenia
    • -Oral lesions consist of ulcerations usually shows a reduced number OR absence of neutrophils
    • -Bacterial invasion of host tissue may be apparent in some instances
    • Bone loss in a patient with neutropenia! -Biopsy specimen of neutropenic ulceration usually shows a reduced number or absence of neutrophils
    • -Bacterial invasion of host tissue maybe apparent in some instances
  43. Agranulocytosis
    • -granulocytic series, particularly neutrophils are absent
    • -decreased production or increased destruction 
    • -diopathic but MOST are caused by exposure to one or several drugs (anti hemotherapeutic agents inhibit normal mitotic division and maturation of HPSC, other drugs trigger an immunologic reaction that results in destruction of granulocytes) -Typically develops within a few days after a person ingests the offending drug
    • -Oral lesions are common and include necrotizing, deep, punched-out ulcerations of the buccal mucosa, tongue and palate. Gingivae are especially susceptible to infection, often resembling the pattern of necrotizing ulcerative gingivitis (NUG)
    • - NO or FEW granulocytes in the tissue **STOP THE OFFENDING MEDICATION as reasonably as possible!!
  44. cyclic neutropenia
    • -RARE idiopathic
    • periodic reduction in the neutrophil(4 weeks)
    • infections ulcerating necrotizing lesion of the gingiva.
    • Severe periodontitis is NOT explained by local factors.
    • Bone loss stimulating perio disease
    • -Does not occur in rather uniformly spaced episodes USUALLY a 21 day cycle
    • -Recurrent episodes of fever, anorexia, cervical lymphadenopathy, malaise, pharyngitis, and oral mucosal ulcerations
    • -Other GI mucosal areas include colon, rectum, and anus may be affected by recurrent ulcerations
    • -Similar to those of neutropenic and granulocytopic ulcerations IF biopsy is preformed during nadir of neutrophil count
    • DIAGNOSIS is- Established by sequential complete blood counts (typically 2-3x/wk for 8 wks) to determine whether cycling of neutrophil levels occurs
    • -Supportive care in form of optimal oral hygiene
    • -Symptoms seem to diminish after 2nd decade of life even though cycling continues
  45. thrombocytopenia
    • Decreased number of circulating blood platelets (formed elements derived from megakaryocyte precursors in the bone marrow)
    • -Normal platelet count: 200,000-400,000/ mm3 
    • Cause: Reduced production, increased destruction, sequestration in the spleen
    • Special types: 
    • -Severity of involvement is directly related to EXTENT of platelet reduction
    • -Detected because of presence of oral lesions
    • -Minor traumatic events are continuously inflected on oral mucosa during CHEWING and Swallowing – capillaries are damaged during this process and sealed off w/ microscopic thrombi (thrombi are not formed properly—pinpoint hemorrhagic lesions—petechial or bruises or hematomas)
    • -Spontaneous gingival hemorrhages or bleeding from minor trauma
    • -Similar hemorrhagic events occur throughout the body
    • -Severe thrombocytopenia  massive bleeding from GI or urinary tract is fatal, epistaxis, hemoptosis (significant pulmonary hemorrhage), intracranial hemorrhage is also fatal OTHER INFO (since there are not x-rays)
    • --Idiopathic (immune) thrombocytopenia (ITP) – childhood, classically after nonspecific viral infection, symptoms appear quickly and severely, most cases resolve spontaneously within 4-6 weeks, and 90% of patients recover by 3-6 months
    • --TTP—thrombotic thrombocytopenic purpura
  46. Polycythemia Vera
    • -RARE idiopathic hematologic disorder that is best thought of as an increase in the MASS of the RED blood cells
    • - Increased blood viscosity (and increased platelets) leads to thrombus formation (TIA, CVA, and MI)
    • Immediate attempt to reduce red blood cell mass
  47. Leukemia
    • malignancies of HPSC derivation
    • -malignant transformation of one of the stem cells 00> which initially proliferates in the bone marrow and eventually overflows into the peripheral blood of the affected person
    • -Problems arise when the leukemic cells crowd out the normal defense cells and erythrocytes
    • ORGIN: Myeloid  several different pathways produce malignant cells show features of granulocytosis or monocytes, and less frequently, erythrocytes or megakaryocytes
    •  Lymphoblastic/ lymphics
    • -Chronic myeloid leukemia: Chromosome abnormalities (Philadelphia chromosome) Acute: if untreated run an aggressive course and often result in DEATH w/ in moths, acute lymphoblastic leukemia of childhood can be controlled
    • Chronic: follow more indolent course, end result is the same
    • -MANY of the clinical signs are related to marked REDUCTION in the numbers of normal WBC and RBC due to crowding out of normal HPSC by malignant proliferation (myelophthistic anemia)  fatigue, easy trying, dyspnea on mild exertion (reduced red blood cell count), malignant cells may also infiltrate other organs and often cause splenomegaly, hepatomegaly and lymphadenopathy
    • -Easy bruising and bleeding (lack of blood platelets due to megakaryocytes being crowded out of the marrow)
    • -Petechial hemorrhages in the posterior hard palate and soft palate, spontaneous gingival hemorrhage (esp w/ platelet counts less than 10,000-20,000/mm3
    • -Ulceration of the oral mucosa (impaired to fight bact) – bact around teeth, herpetic infections most common are viral lesions and involve oral mucosa rather than being confided to keratinized mucosa as in immunecompentent pts
    • -soft tissue tumor (leukemia)  usually from myelomonocytic type of leukemia -Diffuse infiltration and destruction of normal host tissue by sheets of poorly differentiated cells with either myelomono-cytic characteristics or lymphoid features -Confirm the presence of poorly differentiated leukemia cells in the peripheral blood and bone marrow
    • -Classifying the type of leukemia requires establishing the immune-phenotype by using immunehisto-chemistry
    • markers to identify cell surface antigens expressed by the tumor cells - Chemo  destroy as many atypical cells in a short time to induce remission (HIGH DOSES)
    • -Remission has induced, stage must be maintained (maintenance chemo –LOWER dose long time period)
    • -New treatment- monoclonal antibodies against surface antigens CD20
    • -Prognosis depends o the pt age and the cytogenic alteration
    • -Chronic myeloid leukemia—neoplastic goes to blast transformation less differentiated and pt dies 3-6 mo.
    • -Chronic lymphocytic leukemia – incurable, but course is highly variable and depends on the stage of the disease, patients with limited disease have average survival time of >10 years
  48. Hodgkin’s Lymphoma
    • -Neoplastic cells (Reed-Sternberg cells  B- cell origin) make up only about 1-3% of the cells in the enlarged lymph nodes that characterize this condition 
    • -Linked to EBV
    • - Almost always begins in lymph nodes, Most common sites of initial presentation are cervical and supraclavicular nodes or axillary and mediastinal nodes
    • -Usual presenting sign is identification by patient of persistently enlarging, nontender, discrete mass or masses in one lymph node region
    • -Early stages: involved lymph nodes often rather movable
    • -As condition progresses: nodes become more matted and fixed to the surrounding tissues
    • -If untreated: condition spreads to other lymph node groups and eventually involves the spleen and other extra lymphatic tissues, such as bone, liver, and lung
    • -Oral involvement is rare
    • -About 30% of patients have weight loss, fever, night sweats, and generalized pruritis (itching) - absence of these symptoms = better prognosis (staging)
    • -Category A = no systemic signs
    • -Category B = systemic signs
    • -Reed-Sternberg cells with “owl-eye” nucleus -Successful treatment!!
    • Prognosis fairly good (best treatment results in early stages)
    • -Stage I or II: 80-90% relapse free 10year survival rate
    • -Stage III or IV: 55-75% 10 year survival rate
  49. Non-Hodgkin’s Lymphoma
    • -Include a diverse and complex group of malignancies of lymphoreticular histogenesis and differentiation
    • -Initially arise within lymph nodes and tend to grow as solid masses
    • - Contrasts with lymphocytic leukemias, which begin in the bone marrow and are characterized by a large proportion of malignant cells that circulate in the peripheral blood
    • -Most commonly originate from cells of the B-lymphocyte series
    • -T-lymphocyte derivation less common, true histiocyte-derived lymphomas even rarer
    • -Bacteria can induce formation of MALT lymphoma of the stomach
    • -Antibiotic treatment of Helicobacter pylori infection usually cures it
    • -Most commonly develop in lymph nodes but there are extra nodal varieties
    • -Nodal: Nontender mass that has been slowly enlarging for months, Lesion typically involves a local lymph node collection (i.e. cervical, axillary, or inguinal nodes); one or two freely movable nodules are noticed initially, As malignancy progresses: nodes become more numerous and are fixed to adjacent structures or matted together. Gradually, process involves other lymph node groups, and invasion of adjoining normal tissues occurs
    • -Extra nodal: In oral cavity, lymphoma usually is extra nodal. Oral lesions are often component of more widely disseminated disease, although sometimes lymphoma begins in oral tissues. Malignancy may develop in the oral soft tissues or centrally within the jaws. Soft tissue lesions appear as nontender, diffuse swellings
    • -Staging is adopted from Hodgkin's lymphoma Lesional cells of lymphoma consisting of population of poorly differentiated cells of the lymphocytic series with minimal cytoplasm -Low grade lymphomas - controversial in treatment
    • -Some recommend no particular treatment because tumor is slow growing and tend to recur despite chemo-therapy
    • -Watch and wait strategy (usually arise in older adults and median survival rate is 8-10 years)
    • Approximately 40% transform into high-grade lymphoma  patient's demise
  50. Burkitt’s Lymphoma
    • endemic EBV-related;
    • chromosomal translocation.
    • -Malignancy of B-lymphocyte origin that represent an undifferentiated lymphoma
    • -It is mostly kids, mostly presents in jaws, usually in the posterior.
    • -Multiple quadrants may be involved -Radiograph: malignant process with destruction of bone with ragged, ill-defined margins
    • - 4-year old child had evidence of bone destruction with tooth mobility in all four quadrants of his jaws. Note patchy, ill-defined loss of bone
    • -Almost 100% of the cells are in the process of replicating.
    • -Classic "starry-sky" appearance (interspersed histiocytic cells with abundant cytoplasm ("stars") set against a background of malignant, darkly staining lymphoma cells ("night sky"))
    • -Undifferentiated, small, dark lesional cells with numerous histiocytes
    • -High 5 year event free survival!!
  51. Multiple Myeloma
    • -Relatively uncommon malignancy of plasma cell origin that often appears to have multicentric origin within bone
    • -Cause of condition is unknown, although sometimes a plasmacytoma may evolve into multiple myeloma
    • -Abnormal plasma cells that compose this tumor are typically monoclonal
    • -Probably arise from single malignant precursor that has undergone uncontrolled mitotic division and has spread through the body -Because neoplasm develops from a single cell, all the daughter cells that comprise the lesional tissue have the same genetic makeup and produce the same proteins
    • -Proteins are the immunoglobulin components that the plasma cells would normally produce, although in the case of this malignant tumor the immunoglobulin are normal or functional
    • -Signs and symptoms of this disease result from the uncontrolled proliferation of the tumor cells and uncontrolled manufacture of their protein products
    • - Renal failure (kidneys become overburdened with the excess circulating light chain proteins of the tumor cells):
    • - 15% of patients show deposition of amyloid in various soft tissues of the body may be the initial manifestation of the disease
    • -Amyloid deposits are due to accumulation of abnormal light chain proteins
    • -Sites classically affected include: oral mucosa, tongue (diffuse enlargement and firmness and nodular appearance) -Multiple, well-defined, punched-out radiolucencies or ragged radiolucent lesions
    • -Especially evident on skull film
    • -Jaws involved in up to 30% of cases
    • -Radiolucent areas contain abnormal plasma cell proliferations that characterize multiple myeloma
    • - Sheets of malignant plasma cells with eccentric nuclei and stippled nuclear chromatin. Immunohisto-chemical studies show uniform reaction of the lesional cells for antibodies directed against kappa light chains, indicating a monoclonal neoplastic proliferation
    • Bence Jones proteins = light chain proteins found in 30-50% of patients (due to the RENAL failure)
    • - Even histo-pathologic and radiographic findings strongly suggest multiple myeloma, should screen serum or urine by protein electrophoresis
    • Bisphosphanates are prescribed to prevent pain from pathologic fractures. Bisphosphanates do not increase survival. BRONJ may occur. Prognosis is generally poor.
  52. Plasma-cytoma
    -Unifocal, monoclonal, neoplastic proliferation of plasma cells that usually arises within bone -IMPORTANT: may give rise to multiple myeloma!!!!!!
    • I: Single lymph node region or single extralymphatic organ or site
    • II: 2+ lymph node regions on the same side of the diaphragm or 1+ lymph node regions with extralymphatic site
    • III: Lymph node regions on both sides of the diaphragm possibly with extralymphatic organ or site, the spleen, or both
    • IV: Diffuse or disseminated involvement of one or more extralymphatic organs
  54. Oral mucosa resistance factors?
    • SSE (strat squam epi)
    • cytokines
    • high density capillaries
    • saliva (IgA, SLPI)
    • mucins, agglutins, PRP, , cystatins, etc
    • hypotonic effect
  55. meth mouth
    • xerostomia
    • grinding
    • poor OHI
    • diet, GI
    • contaminated ingredients acid, lye
  56. HIV screening guidlines
    • all health care setting (opt out)
    • annual check for high risk
    • separate consent should no longer be required
    • prevention counseling also should not be required as part of screening]
    • facilities with > 0.1 % HIV prevalence
  57. controlling methods of HIV spread
    • ARV pregnant
    • nPEP (non occupational)
    • PrEP (pre-exposure)
  58. rapid HIV test what fluid?
    • oral exudate not just saliva
    • must be confirmed with Western Blot
  59. Bleeding disorders Vascular Defects
    • Vascular purpuras: Excessive corticosteroids - Cushing's disease or exogenous
    • Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)
    • :Autosomal dominant inherited telangiectases of mucous membranes leading to bleeding from mucous membranes -e.g., epistaxis, gastrointestinal bleeds, gingival bleeds
    • Encephalotrigeminal Angiomatosis (Sturge Weber Angiomatosis)
    • Rare, nonhereditary disease involving hamartomatous
    • vascular proliferation in the tissues of brain and face
    • Capillary malformations are called “port wine stains”, CNS angiomas lead to mental retardation, hemiparesis,
    • seizures

    • Vitamin C. deficiency
    • ¡Results in impaired collagen synthesis
    • resulting in bleeding gums, perifollicular
    • hemorrhages