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 •cartilage • •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- HA •HA + proteoglycans + collagen - 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 make 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 is high •Chondroitin 6 sulfate - less •Ketaransulfate- less •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 Combined drugs + collagen •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. •Juvenile R.A. • - Still´s disease R Gout Chrup Chrup Chondrocalcinosis • HPT 2 Chrup •Synovial chondromatosis • •Septic arthritis M 000 Boháček