Osteoarthritis Z. Rozkydal Chrup •Synovial joint •The end of bones •Hyaline cartilage •Ligaments •Joint capsule •Synovial membrane •Synovial fluid •Hyaline cartilage •Chondrocytes • •Matrix – intercelullar mass: • •Fibrilar structure - collagen • •Proteoglycans • •Proteins of noncollagen nature • •Hyaluronic acid • •Water – 70 volume percent Chrup, barva norm •Hyaline cartilage •Chondrocytes- 2 percent of volume • •Localised in lacunes of matrix • •Isogenetic groups 2-8 cells •from one mother cell Hyal chrup Chrupavka norm •Hyaline cartilage - layers •Superficial • •Middle • •Deep • •Zone of calcifying •Catilage • •Bone Chrup, barva norm •Collagen •Collagen type II (3 alfa-1 chains- 90 %) • •Chains form fibrils •Fibrils form a three dimensional network •Paraler to the surface •In deep layers in columns • Hyal chrup •Proteoglycans- PG •They are high hydrophylic •- elasticity !! • •Large PG - glukosaminoglycans: •Chondroitin 6- sulfate •Keratansulfate •Chondroitin 4- sulfate • •Small PG: •Decorin, biglycan •Agrecan – binds on hyaluronic acid •Sulfatan glukosaminoglycan Chrup, barva norm •Noncollagen proteins •Fibronectin, chondronectin •Anchorin •Cytocins- interleukin-1, interleukin- 6 •Enzymes – metaloproteinase • (kolagenase, gelatinase) •Growth factors •Prostaglandins Chrup, barva norm Hyaluronic acid •Forms with proteoglycans intercelullar mass •Hydrophylic, maintains homeostasis •Responsible for lubrication of the joint •Promotes transport of nutritiens into the cartilage •Gives the cartilage elastic resistance •Gives rheologic properties to synovial fluid Chrup • •High volume of water gives •resistance in pressure • •Condrocytes are nourished •from synovial fluid • •Cartilage has no vessels and nerves - low regeneration - •The fluid is pushed by •movements into the cartilage - •Hyaline cartilage Chrup •Synovial membrane •It contains: •Cells A – macrophages •Cells B – produce hyaluronic acid •Cells C – mixed cells – properties of cells A and B Chrup •Network of vessels Chrup •Synovial fluid •Clear, slight yellowish •Viscous • •The amount of 0,13-3,5 ml •Intracelular pressure: -8 až - 12 ml H2O - •Proteins- only one third •of concentration in plasma Chrup •Synovial fluid •Cytology: 65/mm3 lymfocytes, monocytes, mononucluears • •Mucin = hyaluronic acid and N-acetylglucosamin • - gives viscosity • •No fibrinogen Diseases of joints •Osteoarthrosis deformans •Rheumatoid arthritis •Psoriatic arthritis •Gout •Ancylosing spondylitis •Septic arthritis • Dieseases of joints •Systemic arthritis (lupus erythematodes) •Haemofilia •Aseptic necrosis •Osteochondritis dissecans •Chondromatosis •Neurogenic arthropathy •Pigmented villonodular synovitis Osteoarthritis •Degenerative, slow and progressive disease • of hyaline cartilage of synovial joint • •All conditions changing the structure and function of hyaline membrane and surrounding tissues lead to osteoarthritis Chrup Osteoarthrosis deformans •Primary (after 40 years of age ) • •Secondary – the cause is known • •Osteoarthrosis •15 percent of the population • •50 percent of people above 65 years • •80 percent of people above 75 years •Primary O.A. • •Begins over 40 y. •Small joint in hands •Cervical and lumbar spine •Hip and knee joints Artroza 2 Hauser 15 •Secondary O.A. • •1. Mechanical factors (DDH, Perthes disease, • aseptic necrosis, slipped femoral epiphysis, • condition after fractures) •2. Metabolic disorders (ochronosis, gout, • chondrocalcinosis, Gaucher disease) •3. Hormonal disorders (acromegaly, diabetes m.) •4. Haemofilia •5. Inflamated disorders (septic artritis, R.A.) stková 10 •DDH- developmental dysplasia • of the hip joint •Obr. 6 •Condition after Perthes disease • •Obr. 8 O kočovský 1 •Idiopatic necrosis of the femoral head CLS - necrosis Jelínek •Obr. 7 Olšová 15 •Necrosis after femoral neck fracture •Obr. 9 •Rheumatoid artritis CLS - R CLS- R •Obr. 10 •Ancylosing spondylitis - hip joint Suchý 15 •Obr. 11 Weiterová 1 •Ancylosing spondylitis •Obr. 12 •Septic arthritis •Obr. 13 Gaža 15 •Risk factors • •Age over 50 years • •Obesity • •Mutation of gene for procollagen II (COL2A1) • •Autosomal gene for Heberden´s nodes •is dominant in female and recessive in male • •Female are involved twice oft than male •- after 55 years – postmenopausal defecit of • estrogens - O.A. is more often •Mechanical O.A. Výuka schéma artrózy •Obr. 14 Paleček ASK •Macroscopis changes • •Cartilage is matte, soft, yellowish, fibrilations •Obr. 15 tibie 4 + femur 4 Čechová ASK •Ulcers, defects •Obr. 16 •Obr. 17 Procházka ASK 1 •Subchondral bone is sclerotic •Obr. 18 •Obr. 19 Pribilová 1 •Macroscopic changes • •Subchondral cysts • •Osteophytes • •Narrowing of cartilage • •Hypertrophic synovial membrane • •Loose bodies • • •Obr. 20 Artroza1 •Condrocytes form clusters in 10-20 •Irregularities of the surface •lamina splendens is absent, fibrilations •Fissures, defects of cartilage •Collagen network is disturbed Chrup Chrup •Biochemical changes • •Higher amount of water •Synthesis of PG is higher •Loss of proteoglycans •Chondroitin 6 sulfate is lower •Ketaransulfate is lower •Condroitin 4 sulfate is higher Chrup •Clinical symptoms •Pain, mild, in weather changes, later is higher •Stiffness •Effusion, synovitis •Limping, difficultis in standing and walking •Muscle atrophy, joint contracture •Malalignment •Kellgren- Lawrence classification I- IV. O •I. II. III. IV. •1 Softening and swelling •2 Fragmentation and fissures up to 1,3 cm •3 Fragmentation and fissures above 1,3 cm •4 Erosions up to subchondral bone •Chondropathy Chondropathy I. st. S6R00001 •Chondromalatia- soft cartilage Chondropathy II. st. S6R00002 •Fissures in the cartilage Chondropathy III. st. •Fibrilation- „ crab meet“ Chondropathy IV. st. S6R00002 •Defects to subchondral bone •Change of life style •Low weightbearing •Loss of overweight •Crutches, sticks •Physioterapy •Physical therapy • •Conservative treatment •Conservative treatment • •Analgetics nonopioid (paracetamol) • •Analgetics opioid (tramadol, codein,) • •Nonsteroidal antiinflammatory drugs (NSAID) •Inhibitors of cyclooxygenase 1 COX - 1 inhibitors • •Ibuprofen •indometacin •piroxicam •naproxen •diclofenac •tiaprofenic acid • •NSAID •NSAID • Inhibitors of cyclooxygenase - 2 COX 2 inhibitors •Preferred: meloxicam (Movalis, Recoxa) • nimesulid (Aulin, Coxtral, Nimesil) • •Selective : celecoxib (Aclexa) • rofecoxib • •SYSADOA • •- Symptomatic, slow acting, antiinflamatory drugs • (chondroprotectives) • •Slowly acting •Long lasting efect •Stimulation of PG and collagen •Inhibition of catabolic enzymes • SYSADOA 1.systemic: glucosamin sulfate chondroitin sulfate diacerein ASU piascledine 2. local: hyaluronic acid •SYSADOA local •- viscosuplementation •Hyalgan • •Synvisc • •Synovial • •Monovisc • •Hyaline • •Renehavis Chrup Chrup •Local corticosteroids •Diprophos •Depo-Medrol • •They influence synovitis •Do not stop progression of O.A. •Synthetic activity of chondrocytes is lower •The amount of chondrocytes and PG is lower • •Recommended treatment •Paracetamol- up to 4 g per day • •NSA - + inhibitors of proton pump (omeprazol) • •Chondroprotectives • •Hyaluronic acid • •Local corticosteroids • •Pain department- in a case we can not do surgery a nelze • •PRP- platelets rich plasma • •ACP- autologous conditioned serum- Orthokine • •Mesenchymal stem cells ? • • •Other options •Operative treatment •Preventive surgery • - correct treatment of intraarticular fractures - correct treatment of ligament injuries - correct treatment of dislocations - correct treatment of menical lesions - treatment of chondromalatia •- removal of loose bodies • •Preventive surgery • - Correction of malalignment- osteotomy - Acetabuloplasty, shelf plasty •- Replacement of cruciate ligaments •- synovectomy, debridement, shaving •Operative treatment •Operative treatment •Resection arthroplasty – op. sec. Keller • op. sec. Girdlestone • •Arthrodesis • •Total joint replacement • •Options for localised chondral defects Shaving and drilling • - •- abraze subch Drilling - •Abrasion chondroplasty ER 6 •Curretage •Shaver ER 7 Perforation of subchondral bone - slight bleeding Steadman, J.R., 1999 Multipotent stem cells into the defecfts The aim- to create fibrocartilago •Microfractures ER 7 •Microfractures ER 8 ER 10 •Hangody, L., 1992 •Defects up to 2 - 4 cm2 • •Osteochondral autograft transfer- OAT •Mosaicplasty ER 12a ER 12b ER OAT 1 •OAT ER OAT 1 •4 years after surgery •ACI – autologous chondrocyte implantation •Transplantation of autologous chondrocytes •into defects of cartilage •Chondrocytes in suspension under periostal layer ER ACI 1 ER ACI 4 ER ACI 4 •Scaffolds- HyaloFast, Chondrotissue… • •Biodegradable • •Matrix for stem cells from bone marrow •after drilling or from serum •Hyalografts and chondrografts ER 16 •Collagen scaffolds •HyaloFast- scaffold •Polymer of HA • •No special fixation • •Scaffold serves for maintaining of stem cells from bone marrow • •Supports viable cells • • • • • •Fills the defects of hyaline cartilage C:\Users\Petra Kotalíková\Desktop\surgical_training__overview__01_250x.jpg C:\Users\Petra Kotalíková\Desktop\surgical_training__overview__02_250px0.jpg •Diferential diagnosis •Rheumatoid arthritis •Ancylosing spondylitis •Psoriatic arthritis •Septic arthritis •Haemofilic arthropathy •Gout •Chondrocalcinosis •Neurogenic arthropathy • Artropatie- Charcot rtg Artropatie Charcot •Neurogenic arthropathy •Obr. 30 •Obr. 31 •Neurogenic arthropathy Neur, R.A. •R.A. •Juvenilní R.A. • - Still´s disease R Gout Chrup Chondrocalcinosis • HPT 2 Chrup •Synovial chondromatosis • •Septic arthritis M 000 Boháček