Gonococcus.
Chondrocalcinosis, which involves CPPD deposition.
Lipoma, which is the most common soft tissue tumor in adults.
Parvovirus B19, Rubella, EBV, Hepatitis B and C.
Degeneration of cartilage leading to structural and functional failure of synovial joints.
The presence of Home-Wright Rosettes.
20s to 40s.
Multiple hereditary exostosis syndrome, an autosomal dominant disease.
It indicates the last page of a document or report.
Asymptomatic Hyperuricemia, Acute Arthritis, Asymptomatic Intercritical Period, and Chronic Tophaceous Gout.
Crystallization of monosodium urate (MSU) within and around the joints.
70% water, 10% Type II collagen, 8% proteoglycans, and chondrocytes.
Malaise, fatigue, and generalized pain.
They lack hallmarks of cancer.
<5 cm, circumscribed, slightly infiltrative with richly cellular fibroblasts.
Pain and swelling.
Benign hyaline cartilage.
A malignant tumor that produces cartilage.
80-90% 5-year survival rate.
It evolves from repetitive precipitation of monosodium urate (MSU) and leads to hyperplastic, fibrotic synovium and cartilage destruction.
Well-differentiated, Myxoid, and Pleomorphic.
They invade the cortex, periosteum, and soft tissue, frequently exhibiting hemorrhage and necrosis.
Purpura, cutaneous ulcers, and nail bed infarction.
Osteochondroma, with 85% being solitary.
It has multiloculated blood-filled cystic spaces.
Germline loss of function in EXT1 or EXT2 genes.
Soft gray, infiltrative mass with sheets of primitive round and spindle-shaped cells.
Dual line of differentiation of tumor cells.
Younger than 20 years old.
Degradation of articular cartilage proteoglycans allowing crystallization around chondrocytes.
A condition with skeletal features of polyostotic fibrous dysplasia and intramuscular myxomas in adults.
Endogenous (gout, pseudogout) and exogenous (steroid ester crystals, talcum).
They are cleaved, yielding fissures and clefts.
Monostotic occurs in one bone and stops enlarging at growth plate closure, while Polyostotic occurs in multiple bones and typically at an earlier age.
Direct extension, lymphatic or hematogenous spread, and intraspinal seeding.
Hyperuricemia (plasma levels above 6.8 mg/dl).
50% of the risk of developing RA is related to these alleles.
Neoplastic cells are primitive osteoblast precursors, with the bulk being non-neoplastic osteoclasts.
In the deep dermis, subcutis, or muscle.
Irregular, nodular thickening of palmar fascia causing flexion contracture.
Alveolar, Embryonal, and Pleomorphic.
H. influenza.
Dislodged pieces of cartilage that tumble into the joint.
Liposarcoma, typically occurring in individuals aged 40-60.
They initiate the immune response and produce inflammatory cytokines.
Firm, non-tender nodules that occur in 25% of individuals with RA.
Joint effusion and juxta-articular osteopenia with erosions.
Multiple osteochondromas become apparent during childhood.
Large, infiltrative masses that recur but do not metastasize.
They are cured by simple excision.
In their 40s or older.
Tophi, which are large aggregations of urate crystals surrounded by an intense inflammatory reaction.
Well circumscribed, intramedullary lesions that vary in size, tan-white and gritty, composed of woven bone and fibroblastic proliferation.
Borrelia burgdorferi.
Prominent osteophytes at the DIP, more common in women.
Metastatic tumors.
Acute arthritis, chronic tophaceous arthritis, tophi in various sites, and gouty nephropathy.
Multinucleated osteoclast-type giant cells.
In the epiphysis, mostly around the knee (distal femur, proximal tibia).
Oligoarthritis is more common, systemic disease is more frequent, and large joints are more affected.
Men, who are affected three times more often than women.
Pencil in a cup deformity.
Conventional chondrosarcoma, which is hyaline cartilage producing.
S. aureus.
Chronic progressive monoarticular infection.
A self-limited fibroblastic and myofibroblastic proliferation that occurs in young adults, often following trauma.
It has been most firmly implicated in the pathogenesis of RA.
Vasculitis.
Small joints, generally in a symmetrical pattern.
40%-60%.
Generally occurs during the first 2 decades of life.
In bones of endochondral origin, near the growth plate of long tubular bones.
Sharply demarcated radiolucencies with a thin rim of sclerosis.
Bacteria enters the joints via hematogenous spread from distant sites.
Calcified matrix appears as foci of flocculent densities.
A malignant bone tumor characterized by primitive round cells.
Destructive lytic tumor with permeative margins.
Deep achy pain that worsens with use.
A chronic inflammatory disorder of autoimmune origin affecting joints.
1. Chondrocyte injury, 2. Early OA with chondrocyte proliferation, 3. Late OA with marked loss of cartilage.
Prevalence increases beyond age 50.
MYH9-USP6 fusion gene.
Presence of 4 of the following: morning stiffness, arthritis in 3 or more joints, arthritis of hand joints, symmetric arthritis, rheumatoid nodules, serum RF, typical radio findings.
Pathologic changes in the ligamentous attachments and involvement of sacroiliac joints.
Arthritis, non-gonococcal urethritis or cervicitis, and conjunctivitis.
Infections by Yersinia, Salmonella, Shigella, and Campylobacter.
Uterus.
Wide surgical excision and possibly chemotherapy.
A mass of edematous synovium, inflammatory cells, and granulation tissue that erodes articular cartilage.
75%.
Swan-Neck and Boutonniere deformities.
Late adolescence and early adulthood.
Common in children, often found in the metaphysis of long bones.
Somatic gain-of-function mutation in the GNAS1 gene.
Painless, firm masses with eosinophilic spindle cells.
Low back pain and spinal immobility.
Rhabdomyosarcoma.
Monostotic, polyostotic, Mazabraud Syndrome, and McCune Albright Syndrome.
SS18-SSX1,2,4 gene.
(11;22)(q24;q12) translocation, fusing EWS and FLI1.
