Bone Pathology (Oral Pathology)

Bone Pathology (Oral Pathology)

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Chronic osteomyelitis

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Date created

Mar 1, 2020

Cards (25)

Section 1

(25 cards)

Chronic osteomyelitis

Front

i. Etiology: unresolved acute osteomyelitis or may arise w/o acute process ii. Population: iii. Location: iv. Clinical: pain, swelling and sometimes pus discharge -pt. is systemically well -Bone deposition may exceed resorption resulting in hyperostosis v. Radiograph: ill-defined radiolucency, moth eaten with radio-opaque bony sequestrum -May involve large areas in long-standing cases -Lab tests may be indicative of infection or may be normal

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Focal chronic sclerosing osteomyelitis

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i. Etiology: low grade chronic infection ii. Population: before age 20, but can occur later in life and after extraction of offending tooth; Focal radiopacity osteomyelitis more common in ASAINS iii. Location: apex of tooth with deep dental caries or deep restoration iv. Clinical: bone sclerosis (increased radio density) and response of bone to low grade infection -Tx. endo or extraction, no abx v. Radiograph: focal radiopacity intermixed with radiolucency

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Chondroma

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i. Etiology: benign neoplasm of cartilage ii. Population: iii. Location: rare in jaws; premaxilla and condyles when present. Benign chondroma in jaws is less common than well-differentiated chondrosarcoma iv. Clinical: non-painful firm to hard, smooth surfaced or lobulated submucosal mass -Overlying mucosa is normal v. Radiograph: irregular radiolucency or "mottled" radiopacity.

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Inflammation of bone

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AKA Osteomyelitis -usually a bacterial infection that involves all three components--marrow, cortex and periosteum, may occur in any bone -In jaws, occurs with an odontogenic infection -Acute or chronic--may be localized (focal) or diffuse -"alveolar abscess" used for infections of alveolar bone only while "osteomyelitis" is used for infections that also include the cortical bone and periosteum -May be difficult to differentiate clinically, in acute form, pus is formed that spreads through all three components of the bone, cutting off the blood supply and leading to necrosis of the bone

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Polyostotic Fibrous Dysplasia

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i. Etiology: hormones--Albriht's syndrome; Jaffe's is not hormone induced ii. Population: females iii. Location: long bones and jawbones iv. Clinical: 20% of Fibrous Dysplasia cases, 2 sub-types 1. Jaffe's--polystotic FB and "cafe au last" spots on skin 2. Albright's syndrome--polyostotic FD, cafe au last spots, precocious puberty v. Radiograph: similar to monostotic FD

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Torus Mandibularis

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i. Etiology: unknown, maybe autosomal dominant, maybe bruxism and other occlusal related mechanical irritation. ii. Population: occurs by age 30 but may continue to grow slowly, no sex predilection. Malaysian pts. 1.7% of mandibular tori iii. Location: bilateral but asymmetric on mandible iv. Clinical: bony outgrowth on the lingual surface of the mandible above the mylohyoid ridge -resembles torus palatinus

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Central Ossifying Fibroma (COF)

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i. Etiology: true tumor of bone ii. Population: young adults, mean age 35, females 5:1 iii. Location: mandible 90% iv. Clinical: slow growing lesion causing expansion and displacement of teeth v. Radiograph: passes through 3 stages: radiolucent, mixed radiolucent/radiopaque, and radiopaque with the peripheral radiolucency -Presence of radiolucent rim (capsule) helps differentiate COF from fibrous dysplasia--FD is diffuse, has no capsule and blends in with the surrounding bone. -Characteristic downward expansion of inferior border of mandible

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Exostosis

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i. Etiology: caused by local mechanical irritation, sometimes associated with maxillary or mandibular tori ii. Population: iii. Location: bilateral molar region, maxilla iv. Clinical: present as protuberances of thickened cortical bone arising from cortical plate along the buccal and posterior alveolar ridge -asymptomatic unless overlying mucosa is injured v. Radiograph: radio-opaque mass

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Central giant cell granuloma (CGCG)

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i. Etiology: unknown but possibly low-pressure hemorrhage into bone followed by incomplete healing ii. Population: females, 60% cases occur in children and adults below 30 iii. Location: Anterior mandible, may cross midline iv. Clinical: considered a reactive lesion of bone, classified as non-aggressive and aggressive -non-aggressive form is more common v. Radiograph: irregular radiolucency with indistinct margins and coarse trabecular of bone extending into the lucency -Needle aspiration may produce blood vi. Treatment: all pts. should be tested for PHT levels to exclude hyperparathyroidism -If CGCG presents a brown tumor, manage underlying condition; if not hyperparathyroidism, enucleation and curettage -recurrence is common

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*Bisphosphonates (BSPs) induced jaw osteonecrosis (BON)

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Bisphosphonates (BSPs) are used for treatment of osteoporosis (Fosamax) and multiple myeloma and cancer metastasis to bone (Aredia and Zometa). -Contain nitrogen -Synthetic analog of inorganic pyrophonate known for anti-osteoclast activity--induces bone necrosis -Only 1% of orally ingested BSPs are deposited in bone compared to 50% of IV BSPs -Stays in bone for many years, if not entire life -Ex. pt. was on Fosamax for 10 years, they would recycle Fosamax at 25% of original dose for many years (half life of Fosamax is 12 years) w/o any new doses -Bone metabolism remains suppressed -Regular dose of 10 mg/day suppresses bone forming surface by 60-90% -Long term Fosamax use is controversial--some say increased bone strength and decreased fracture rate

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Osteoma

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i. Etiology: common neoplasm of bone, slow growing ii. Population: males 2x iii. Location: peripheral or central along inferior border of mandible, paranasal sinuses and on cranial base iv. Clinical: peripheral osteomas may be composed of dense cortical bone and are called compact or "ivory" esteems or they may have peripheral cortex surrounding cancellous bone -Central esteems are composed of dense compact bone and are not separated from the surrounding bone by a capsule, may be difficult to differentiate from enostoses -Soft tissue osteomas are rare but may be seen within the tongue and buccal mucosa -Gardner's syndrome--multiple osteomas in jaw, long bones, multiple impacted supernumerary teeth, permanent teeth, odontomas, multiple polyposis of oval mass of lg. intestine (premalignant) and skin cysts or tumors -May be sessile or pedunculate and occur v. Radiograph: one or more round to oval masses of radiopaque material -Starts as radiopaque, does not go through the stages of central ossifying fibroma of radiolucent to radiopaque. *No radiolucent rim at periphery

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Torus Palatinus

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i. Etiology: unknown but possibly hereditary (autosomal dominant) ii. Population: 11-30, rare before 10. Females. 25% of the population, more common in East and SE Asians and Eskimos iii. Location: midline of hard palate iv. Clinical: Bony outgrowth at midline of the hard palate covered by normal/sometimes thin mucosa smooth surfaced but may have multi lobular appearance. Slow growing, painless except if traumatized. -No tx necessary unless it interferes with function or is symptomatic such as in recurrent ulceration of the overlying mucosa -Should be excised if creating difficulty with prostheses

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Osteosclerosis (hyperostosis)

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i. Etiology: idiopathic, inflammatory condition of bone such as local or diffuse chronic sclerosis osteomyelitis, developmental, mechanical, et al. ii. Population: iii. Location: iv. Clinical: Very dense bone -Late periapical cemental dysplasia may produce a similar clinical and radiographic picture -Osteosarcoma rarely produces significant amounts of dense bone but metastatic prostate carcinoma may induce hyperostotic change sin the surrounding bone -Hyperostotic bone is brittle and poorly vascular which predisposes to both fracture and infection -Pts. with osteoporosis may be severely anemic due to obliteration of cancellous bone reducing blood cell production -No tx., treat the underlying disease, due to poor vascularity, surgery on the lesion should be avoided

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Acute Osteomyelitis

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i. Etiology: secondary to odontogenic infection, trauma, or surgery ii. Population: any age iii. Location: mandible iv. Clinical: pain, swelling of infected area, regional acute lymphadenitis and elevated temperature -Peripheral blood count has increased neutrophils -less than one month in duration -Formation and spread of pus is so rapid that bone resorption may not occur prior to signs and symptoms, thus no radiographic radiolucency v. Radiograph: No evidence of bone necrosis until 1-2 weeks then a diffuse decrease in radio density of the trabecular leading to radiolucent areas ("moth eaten" appearance)

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Giant Cell Lesions

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Several lesions of bone that contain significant aggregates of giant cells histologically -Central giant cell granuloma, hyperparathyroidism, aneurysmal bone cyst, cherubim and fibrous dysplasia -Diagnosis based on histological, radiographic and clinical grounds as histology is not specific

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Monostotic fibrous dysplasia

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i. Etiology: unknown ii. Population: males=females, children/young adults and completes growth by 30 iii. Location: jaws, maxilla iv. Clinical: monostotoic form constitutes approx. 80% of all fibrous dysplasia case -one type in maxilla may be more aggressive, involves craniofacial complex--craniofacial fibrous dysplasia -asymptomatic swelling of maxilla/mandible -May involve other bones including zygoma, sphenoid et al. -Unilateral and displaces teeth, but otherwise firmly seated -Growth is usually slow, possibly fast esp. during puberty v. Radiograph: ground glass appearance where fine radiopacity is noted -mandibular lesions are more deceiving--more variability vi. Treatment: surgical recontouring of affected bone in some cases, performed after cessation of growth due to high incidence of secondary procedures/multiple procedures frequent -Tendency for increased growth of the lesion following surgical intervention

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Diffuse chronic sclerosing osteomyelitis

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i. Etiology: Marx believed it is an infection of actinomycosis and E cordoned origin ii. Population: adults around 30-40/can be in children, females (2x)/some say equal gender, no race predilection iii. Location: posterior mandible iv. Clinical: adult type is proliferative rxn of bone to low grade infection such as periodontitis -Treat with NSAIDS or abx (some say abx don't work) with hyperbaric oxygen, surgery if those don't work -years of pain, sometimes getting more intense v. Radiograph: diffuse, irregular aggregate of bone with indistinct borders, may mimic Paget's disease

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Chondrosarcoma

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i. Etiology: malignant neoplasm of cartilage ii. Population: males slightly, 50s iii. Location: maxilla, bucal/lingual expansion iv. Clinical: uncommon, esp. in jaws. But, more common than benign chondroma in the jaws *low tendency for metastasis -Prognosis is better than osteosarcoma *Most common symptoms is swelling with buccal and lingual expansion, asymptomatic v. Radiograph: Snowflake or punctate calcific foci within a diffuse radiolucency

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Hyperparathyroidism

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i. Etiology: excessive production of parathyroid hormone (needed for calcium release) a. Primary: parathyroid adenoma or hyperplasia and rarely adenocarcinoma b. Secondary: chronic renal disease (renal osteodystrophy) where ions are lost through renal failure and demand for calcium production comes as a secondary factor ii. Population: middle age females (3x) iii. Location: small bones such as jaws and small finger bones iv. Clinical: PTH stimulates osteoclasts to resorb bone and release calcium into blood, when too much PTH, too much bone resorption -multiple bone lesions indistinguishable from CGCG, called "brown tumor" bc chocolate color of soft tissue in bone -stones, bones, moans and groans -Hypercalcemia possible with hypophosphatemia v. Radiograph: generalized loss of density with loss of lamina dura and irregular radiolucent lesions -"ground glass" appearance

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Benign Fibro-Osseous Lesions

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-variety of diseases with similar histology including fibrous dysplasia, periodical cemntal dysplasia, cemntifying/ossifying fibroma etc -Characterized by the presence of a mixture of bone and fibrous tissues -Diagnosis is based on histological, radiographic and clinical grounds as histology is not specific

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Osteosarcoma

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i. Etiology: most common primary malignant tumor of bone ii. Population: males, 30-33 in jaws (18-23 for long bones) iii. Location: mandible=maxilla, long bones iv. Clinical: SERIOUS disease. -Painless sore, possible paresthesia if sensory nerve canal or foramina are involved. -Early disease, surface of the lesion is smooth or 'lobulated' and covered with normal mucosa -With progression, margins poorly defined with fixation of surrounding soft tissues. -Ulceration of soft tissue covering may occur -Teeth in region of tumor may be mobile or displaced and spacing may occur v. Radiograph: similar to osteomyelitis. radiolucent, mixed radiolucent/radiopaque varies to dense sclerosis -Usually destructive ill-defined and sometimes have sunburst or sun ray appearance -Widened PDL *Treatment: chemotherapy and surgical excision of primary tumor

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Aneurysmal bone cyst

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i. Etiology: unknown, possibly high-pressure hemorrhage (CGCG is due to low-pressure hemorrhage) ii. Population: before age 20, slight female predominance iii. Location: not common in jaws, mandible iv. Clinical: pain and swelling, aspiration may yield blood v. Radiograph: similar to CGCG but may be honeycombed or multilocular -expansion and thinning leading to ballooning or "blow out" distention of bone are highly suggestive

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Cherubism

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i. Etiology: benign hereditary autosomal dominant ii. Population: average age 7, as early as 1 iii. Location: bilateral maxilla/mandible iv. Clinical: slows and regresses after puberty -broad face due to mandibular expansion -appearance is responsible for term 'cherubim' -diplopia not present v. Radiograph: bilateral radiolucency may be multilocular and involve all four quadrants

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Gardner's syndrome

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i. Etiology: autosomal dominant with complete penetrance and variable expressivity, chromosome 5 gene ii. Population: diagnosed before puberty but transformation ~30 y/o iii. Location: jaws and sinuses, frontal sinus, GI iv. Clinical: intestinal polyposis with 100% transformation rate in late age -May appear before puberty but transformation does not take place until ~30, where 50% of pts. develop cancer of polyps -Up to 60% of GS pts. develop multiple epidermoid cysts *Oral: multiple osteomas of jaws and sinuses, including frontal sinuses -46% have multiple osteomas and 90% may have 1+ -GS osteomas are not expansile -Multiple odontomas, super numerary teeth and multiple epidermoid cysts

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Paget's Disease of Bone (osteitis deformans)

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i. Etiology: unknown, possibly inflammatory, vascular or viral, maybe EBV, maybe prion disease ii. Population: over 40,, men, UK iii. Location: cranium and maxilla iv. Clinical: 3 phases: bone resorption, vascular and sclerosing -found in elderly people at autopsy -chronic, slowly developing disease causing pain, headache, deafness, blindness, facial paralysis et al. -enlarging bone impinges on peripheral nerves -enlarging bone affects denture fitting or development of spacing in dental arch -Separation of teeth and hypercementosis are common -Increase in alkaline phosphatase -INCREASE OSTEOSARCOMA v. Radiograph: appears as an osteolytic lesion (ground glass) progressing to irregular sclerotic masses with "cotton-wool" appearance -Softening of bones leads to pbowing of the legs and development of a "simian gait"

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