ࡱ> KMHIJM hbjbj== WWv^lzzzzzzz3333|4|5|5|5|5|5[6[6[6$ z[6W6[6[6[6I?zz|5|5II?I?I?[6z|5z|5I?[6I?r I?IV zz|5p5 `ϴS;:031=*v<_0_[>_I?zzzzRheumatoid Arthritis PATHOLOGICAL FEATURES: Symmetric peripheral joint pain & swelling, particularly of the hands, Synovial inflammation leads to granulation tissue (pannus) ( erosion of odontoid, rheumatoid nodules may appear (20% of the time); Scleromalacia (Sclera perforation); Sjogrens Syndrome (Atrophy of lacrimal glands) RADIOGRAPHIC FEATURES: 1st radiographic changes on hands & feet (most commonly), bilateral symmetrical distribution (20% Unilateral), periarticular osteopenia (1st due to hyperemia then disuse and steroid treatment), marginal erosions (no sclerotic borders), uniform loss of joint space, Joint deformity (arthritis mutilans), large pseudo-cysts (geodes) ( pannus invasion of marrow spaces causing cyst-like cavities (Loves the carpals, PIPs, ulnar styloid process (MCPs) (May see ulnar deviation of the hands & fibular deviation of the feet (May cause increased ADI, most common cause of bilateral protrusio acetabuli, narrowed IVDs and Fat pad sign (intra-articular effusion seen on lateral view) (Later changes could include deformities, dislocation, articular bony destruction, bony fusion, and complete destruction of joint space (Woman dominance 3:1 (40-50 yrs old) (Cervical spine is affected 50-80% of the time (loss of disk space & endplate erosions) (Prominent bilateral symmetrical findings at the GH and AC jts (Feltys SYN = Hepatosplenomegaly, RA and leukopenia (Caplans SYN = RA and pneumoconiosis Features associated with a poor prognosis: (Rheumatoid Nodules (commonly on the arm extensors) (Exacerbation of disease for > 1 year (Onset earlier than 30 years old (Extra-articular manifestations Degenerative Joint Disease (Spine) Cartilaginous Jts(Discovertebral Jx) ( AKA Intervertebral Osteochondrosis (IVOC)/DDD; Spondylosis Deformans Uncovertebral Jts ( AKA Neurocentral AKA Lushka C2/3-C6/7-only Cervical, degenerate like a true jt. Some people have at C7/T1 Synovial Jts ( Apophyseal (facet) Occiput/C1-L5-S1, jts guide motion of motion segment- not major weight bearing jt., degenerate same as all other Synovial jts Costovertebral (Rib head/V.Body) ; Costotransverse (Rib tubercle/TP) Fibrous Jts (Enthesis)( DISH- Diffuse Idiopathic Skeletal Hyperostosis; OPLL (Deg of Lig Flav, Supra & Inter spinous ligs) DISH is more common DISH and OPLL are cousins and are arthropathies not arthritis dont destroy art cart, dont result in jt space narrowing *IVOC and Spondylosis Def usually occur together but not always *IVOC & Lig Flava are highly correlated Intervertebral Osteochondrosis (IVOC)Spondylosis DeformansOsteoArthritis (OA)SiteNucleus PulposaAnnular FibersFacet / CostoIVDMod ( Sev Decrease in disc height Vacuum Phenom. Normal to slight decrease in disc height NormalFacet, Costo & Lushka Normal NormalJt space narrowing; subchondral sclerosis; osteophytosisVertebral BodySubchondral sclerosis on both endplates; Schmorls nodes Osteophytosis Normal*Enthesospondylophytes / Enthesophytes / Spondylophytes / Osteophytes  *PLL tightly adheres to the IVD, corner or body as well as a couple mm up. Where ALL does not firmly attach to the disk, attaches a couple mm up the body. Dehydration of disk ( 1st step to IVOC / DDD / Central Nuclear DD QUICK AND DIRTY MRI & CT Hx T1-fat is bright H+ more loosely bound than in water T2- nucleus is bright white (water), longer times to develop image No other imaging allows us to see water content of disc, Proton density Signal get Gold standard for spinal disc disease Looks for H+ ions (so high water would be lit up) Low signal- ligs, tendons, cortical bone, and annulus CT developed, history Godfrey Houndsfield- done with profits from Beatles (EMI), done in 1960s another was given credit to someone else in 1980s, motion x-ray, British electrical engineer, now in 4th generation, America dentist developed it into full body imaging, the first were only head scanners, first in early 1970s, by late 1970s it was full body, can be done at any plane, manipulate for IVOC Sequelae of IVOC Lumbar L5 (most common) ( L1 1) Disk Dehydration (Desiccation) plane film not sensitive starts at NP ( AF (Longitudinal fissures Vac Phen) 2) Narrowing usually uniform ( facet reposition ( Subluxation 3) Subchondral sclerosing (variable) Hyaline cart end plate degeneration, may get Schmorls nodes Vacuum Sign of Kneuttson / Vac Phen thought to be nitrogen gas, fissures act as suction and suck gas out of remaining water, normally in lumbar, can see in middle of disc - Variable finding (sometimes in Extension and not in neutral) - Long narrow Dense (black) Horizontal ( IVOC - Smaller round black spots at anterior corners (peripheral) ( Spondylosis Def (Disruption of sharpey fibers) Vacuum Sign Locations: DiseaseLocationIVOCNP & AFSpondylosis DefAF (peripheral)Cart / Schmorls Node (Rare) (Related to IVOC)IVD w/in Vert BodyIntraspinal Discal Herniation (Related to IVOC)IVD w/in Spinal Canal Or Epidural spaceOA *Synovial Jt( normal finding *Fibrous Jt ( pathologicalApophyseal JtAVN *Poor prognosis (not common)Vertebral Body IVOC Minimal ( Mild ( Moderate ( Severe ( Advanced * Happens in the most mobile sections of the spine (Cerv & Lumbar) C5 (#1) ( C6 ( C4 ( (dropoff) C3 ( (dropoff) C7 ( C2 (rare) Lumbar - Most common to least 5, 4, 3, 2, 1, lots of variation Tend to narrow uniformly but not always CONTOUR LINES: 1) Prevertebral (parallel) 2) Posterior Body (Georges) 3) Anterior Body 4) Spinolaminar (most valid) 5) Posterior spinous *Break in same direction = Intra-Segmental Integrity Top vertebra always moves ( Gravity pulls down (Analyze by looking at motion segment) Lumbars (L1, L2) retro not as severe because facets are steeper, more so in cervicals, leads to spinal stenosis Spinal Stenosis (more dangerous in cervicals ( cord is thicker) SYMPTOMS ( No linear relationship SI (IVOC) ( lower 2/3 most frequently Hemispherical Spondylo Sclerosis: (unique form of subchondral sclerosis) Domed shape - L4 disk level most common ( Vert Body Osteosclerosis (Huge density change) Pattern surrounding IVOC Differential: Blastic Met (has no pattern), Infectious (similar focal lesion) SPONDYLOSIS DEFORMANS ( Osteophytes Anterior most of the time Posterior (infrequent) evidence of a fraying herniation Osteophyte formation: (happens a few mm from anterior corner) 1) Normal 2) Sharpey fibers Anteriorly disrupted (vacuum arises) from disc bulging and pushing on ALL 3) Pressure on Enthesis of ALL ( Traction enthesophytes 4) CLAW spondylophytes ( Jagged protrusions 5) Joining of Adjacent Osteophytes (Rare) ( Acquired block *All levels demonstrate osteophytes (Thoracic shows signs earliest) Osteophytes = Horizontal Syndesmophytes = Vertical Thoracic Spine ( Anterior and right lateral osteophytes Not in left ( Pulsations?? Osteophytes ( Cortex, Medullary cavity & Cartilage cap (this is why osteophytes are larger than they appear on films) You see what you look for, you recognize what you know Lecture Two: IVOC =Central Nuclear DD Spond Defrom = Peripheral angular DD Pure Spondylosis can happen at any area of spine- IVOC can happen more frequently in cervical and lumbar spine. When scoliosis is present IVOC and Spond Def are usually present on the concave side (thats why scoliosis increases in adults) Destroyers of bone = Tumors and Infections ( Mets and M. Myeloma (differentiate from infection by noting that MM begins at the Vertebral body and spreads to the periphery = pedicle) If the etiology were congenital there would be hypertrophy in adjacent structures BIG 6 (Cancers that metastasize to bone)= Lung, Breast, Prostate, Kidney, Ewings, Neuroblastoma BIG 3 = Lung, Prostate & Breast 1)Breast --(70% of mets to bone in females) Silent cancer- first symptom is mets-Usually Lytic 2)Lung Silent cancer- first symptom is mets- can be grossly destructive 2)Prostate--(60% of mets to bone in males- more commonly Blastic. Unlikely to be silent and then pop up with mets- b/c squeezes urethra- get up 4 times in middle of night to whiz and then cant go when they get there. Lushka Joint AKA Oncovertebral AKA Neurocentral C2/3 C6/7 (C7/T1) C4/5 & C5/6 = most common Disk Degeneration occurs first then Lushka Jt follows (Linearly) *Osteophytes are predominate finding at uncinate process Osteophytes project Post (need oblique view to see), Lat (more significant)& Ant *Cervical IVFs are 45 AnteroLateral in cervical spine *Osteophytes are larger than what appear on film due to their Cartilage Cap, which extends further than can be visualized Narrowing of Cervical IVF: Facets narrow IVF from Posterior Lushka narrow IVF from Anterior (much more common) MODIC classification of MRI changes: Type I Decreased signal on T1, and increased signal on T2. Represents marrow edema. Associated with an acute process. Histological examination shows disruption and fissuring of the endplate and vascularized fibrous tissues within the adjacent marrow Type II - the most common type Increased signal on T1, and isointense or slightly hyperintense signal on T2. Represents fatty degeneration of subchondral marrow. Associated with a chronic process. Histological examination shows endplate disruption with yellow marrow replacement in the adjacent vertebral body. Type I changes convert to Type II changes with time, while Type II changes seem to remain stable. Type III Decreased signal on both T1 and T2. Correlate with extensive bony sclerosis on plain radiographs. Histological examination shows dense woven bone; hence, no marrow to produce MRI signal. Facet Arthrosis: *Dominate in Cervical and Lumbar Progression: 1) Narrowing 2) Sclerosis 3) Osteophytosis *Facet Jt degeneration w/o disk degeneration ( Unusual Locations of Facet Degeneration that do not follow disk degeneration ( C2/3 (most common), C3/4, C3/T1 Presents Uniformly quite often SUP ( INF??? Synovial cysts ( herniations of synovium around Syn. Jt. ( Range from completely asymptomatic to complete Nerve Root occlusion Pillar view ( demonstrates facet arthrosis = LC view with 20 caudad tube tilt. FYI-Bumpy, smooth contour in AP view = normal Lumbar Oblique ( best view for viewing lumbar facet arthrosis although AP works Facet Osteophytes in Lumbars can impinge nerves in 3 areas IVF stenosis ( Superior osteophytes Lateral Recess (just medial to pedicles) where exiting nerve root sits ( Inferior osteophytes Central Canal CostoVertebral Arthrosis Costovertebral (R.Head/V.Body) T11 & T12 (more rare) Costotransverse (R.Tubercle/TP) T9 & T10 (Young people & asymptomatic - will see every day) Can be associated with pain referral syndromes: Roberts Syndrome ( pain referral syndrome (epigastric pain: Xiphoid ( umbilicus- mimics GI issues) Maignes Syndrome ( facet arthrosis pain referral pattern (lower thoracic spine [facet] refers to lower Lumbar spine) SI Joint DJD *Dominates in lower 2/3 of joint Already very narrow jt so hard to tell if jt space is narrowed. Sacral and iliac subchondral sclerosis and osteophytes if seen. (Easier to see with CT than with plane film). Irregular Articular surfaces found in DJD Pubic Symphysis (females after many births) SI AC Temporal Mandibular JT FYI ( 20% of RA ends in 2 DJD Osteo Condensans Ilii ( Sclerotic changes in females in only Ilium not sacrum Complications of Spinal Degenerative Arthritis Alignment abnormalities (intervertebral) Senile kyphosis Intervertebral Disc Displacement Spinal Stenosis (IVF &/or Central canal) Alignment abnormalities lead to Spinal Stenosis Lumbar Contour lines Anterior body Posterior body * Body pedicle junction ( more consistent Spondylolisthesis The Wiltse Classification (Antero) Types 2 & 3 are by far the most common Type 1 Dysplastic ( Anomalous facet development (L5-S1) Type 2 Isthmic ( (Rare in cervical, Common in Lumbar) Lysis of Pars - Chronic stress Fx (L5 Crawling to walking) Elongated Pars - Subtype A that heals (Not thought to be developmental) Acute Pars Fx (Gymnasts, Athletes) *Irregular margin Type 3 Degenerative ( DJD of facets (most common) Type 4 Traumatic ( Fx other than Pars or dislocation of one or more facets 1) Articular process Fx 2) Pedicle Fx Type 5 Pathological ( Intrinsic bone destruction (Rarest); Bone softening (Osteomalacia, Pagets, Osteoporosis, Fibrous Dysplasia) *Bone above always move in relation to the bone below ( Segments above Antero segment are in line with it ( segment below looks Retro Type 1 ( Hypoplastic or aplastic. Not too common but not rare Type 2 A ( Breaks will be smoother, maybe sclerotic. Isthmic at L5 often have facet syndrome at L4/L5 that causes pain. Something has to happen to post arch in order for segment to move forward. Lat Lumbar- If you dont see lucency, but you see sclerosis and excess bone formation= Type 3 Flexion/Extension Lumbar views show instability ( e"4mm are unstable (does not respond well to conservative care) Type 3  is usually the only Wilste classification found in the cervical spine (w/the rare exception of type 2), OA of facets, can create one motion segment spinal stenosis. KEY distinction from isthmic. *Inverted Napoleon Hat Sign when an axial view of a vertebra can be seen on an AP x-ray ( Pronounced spondylolisthesis where vertebra translates so far that it falls off its supporting vertebra below 3 methods for measuring Spondylolisthesis- Meyerdings- measurements are vague- low grade, mid grade, high grade of each Grade. Percentage- specific Absolute measure in mm Use percent or absolute. L4 on L5 is the most common level Acute pars defect=spondylolytic spondylolisthesis. 3 Fs ( Female, Forties, L4 (most common occurrence for Spondylo) Retrolisthesis ( Not part of Wilste classification Due to DDD ( narrowing causes facet dislocation / subluxation = (discogenic retrolisthesis) *Cervical more common ( Flatter facets Retro = Narrowing = Spinal stenosis (especially in the cervicals) *Look at contour lines of every motion segment for disruption of Superior segment to Inferior segment If contour lines all break in same direction intra-segmental integrity is maintained (NO BREAK) but no intersegmental integrity Senile Kyphosis Special form of disk degeneration Occurs at Anterior body Multiple continuous segments Increased kyphosis @& & B& Discal Displacement Anterior Displacement ( Spondylosis Deformans Posterior Displacement ( Interspinal Disk Degeneration Superior Displacement ( Cartilagenous (Schmorls Node) Inferior Displacement ( Cartilagenous (Schmorls Node) Spinal Stenosis Trigger Measurements: Cervical spine C3-C7 ( > 13mm sagittal (normal); 11-13mm (gray area); 10mm or less (plain film stenosis) Pavlovs ratio ( > 0.82 (Sagittal canal: Body) on a 72 LC film Congenital Pedicogenic stenosis (short pedicles) Acquired Discogenic Retro or Degenerative Antero C1 & C2 ( Spinal canal is much larger (stenosis is very rare) Retrodental ( > 18mm (normal) Interpedicular (Lumbar)( > 20mm (normal) <20mm (AKA Coronal stenosis) Medial cortex to Medial cortex (Achondroplasia-dwarfism) Eisensteins Line ( highest point on Superior process to lowest part on Inferior process (Determines where lumbar spinolaminar line is) Sagittal dimensions from posterior body to this line ( > 15mm (normal); 13-15mm(gray area); 12 or less (plain film spinal stenosis) Causes of Spinal Stenosis: Alignment abnormalities Lig Flava ( Disk degeneration causes buckling of Lig Flava Discal herniation Osteophytes from facets (Inferior growth) Secondary Spinal DJD Ochronotic Arthropathy: (homogentisic acid oxydase deficit) Calcification and Ossification of IVD = Ochronosis (An inborn error of metabolism in a patient with alkaptonuria (leave urine on counter & it turns black). This disease is due to a deficiency of homogentisic acid oxidase and has a pigmentation deposit in cartilage. Spinal Abnormalities: (Osteoporosis of vertebral bodies. (Calcification of IVDs (Flat, linear, plate like, wafer like from NP ( AF (only totally unique finding) CPPD is spotty (Disc space narrowing with vacuum phenomenon (Small or absent osteophytes (Loss of lumbar lordosis Extraspinal Abnormalities: (Involvement of SI joints, pubic symphysis, large peripheral joints (Bony sclerosis (Fragmentation w/intra-articular osseous bodies (Tendinous calcification, ossification & rupture (Usual involvement of hands, wrists, feet, elbow, ankles Hemochromatosis - Deposits of iron into all body tissues (Men 20:1; 40-60yrs old (Diagnostic triad = Cirrhosis, Diabetes and bronze colored skin (Bronze Diabetes) (Primary form genetic defect of GI absorption (Secondary form arises from alcoholic cirrhosis, multiple transfusions, anemia and over ingestion (Osteopenia, chondrocalcinosis and periarticular calcification (Uniform jt space loss, osteophytosis, subchondral cysts (geodes) and sclerosis Wilsons disease- Deposits of copper in various tissues (Autosomal recessive genetic disorder (Copper deposits in Basal Ganglia (hepatolenticular degeneration), liver cirrhosis and cornea (Kayser-Fleischer rings) (Key signs of arthropathy osteopenia, chondrocalcinosis, cysts and irregular cortex (Spine squaring of the vertebral bodies and Schmorls nodes Acromegaly (Growth hormone secreted after fusion of growth plates due to an eosinophilic adenoma (Prominent forehead, thickened tongue and broad, large hands (Bitemporal hemianopia, headache and carpal tunnel syndrome are primary signs (Heel pad sign > 20 mm (Sella turcica enlargement, sinus overgrowth, lengthening of mandible (Hand & foot: widened shafts, bony protuberances, spade-like deformity of tufts, widened joint spaces (due to cartilaginous overgrowth) (Spine Increased vertebral dimensions in sagittal and transverse planes but no change in height as well as posterior vertebral body scalloping (Premature degeneration and exaggerated osteophytes and widening IVD heights (Increased ADI >6mm, widening of facet jt space and hyperostosis of SPs Werners Syndrome: Prematured aging (acquired) Visible coronary artery calcification on plain film CPPD Deposition Disease: (#1 cause of cartilage calcification) Reasonably common > 50 yrs old 3 subclinical entities: Pseudogout (inflammatory) - inflammatory Chondrocalcinosis Pyrophosphate arthropathy (DJD) - degenerative CPPD Calcium Pyrophosphate Dihydrate crystal deposition disease (Pseudo-Gout) (Simulates arthropathies Gout, RA, DJD and Neurotrophic arthropathy (Factors that have high correlation to deposition Age, genetics and presence of a co-existing disease like gout, HPT and diabetes (Chronic progressive jt pain, intermittent swelling, reduced ROM and crepitus (Predominately in peripheral joints - knees, wrists, ankles, hips and elbows (Czechoslovakian, Chilean and Dutch genetic links (Potential sites for calcification Synovium, Hyaline & Fibrocartilage, Capsular ligaments, Tendon or ligament and blood vessels (Found in both fibrous and hyaline cartilage adjacent to chondrocytes (Most common tendinous deposits - Achilles, triceps, quadriceps and supraspinatus Chondrocalcinosis: calcification involving hyaline and fibrocartilage (Hyaline Cartilage Elbow, GH, Hip, Knee and wrist (Thin, linear, parallel to jt cortex) (Fibrocartilage AC & SC jts, Annulus fibrosus, Hip & Shoulder labrums, Knee Menisci, Symphysis Pubis, TFCC (wrist) [Thick, irregular and shaggy] Pyrophosphate arthropathy loss of joint space, subchondral sclerosis, Geodes, loose bodies, osteophytes, fragmentation and collapse of articular cortex. (Pyrophosphate Arthropathy vs. DJD Unusual articular distribution in joints w/o Hx of trauma or surgery Unusual intra-articular distribution radiocarpal, trapezioscaphoid, talocalcaneal, and patellofemoral compartments Prominent subchondral cysts Large Geodes Severe, destructive subchondral bone changes fragmentation and collapse Variable osteophyte formation large or absent, despite severe joint changes (Knee most common joint for clinical and radiologic changes to be visible; chondrocalcinosis of menisci and hyaline cartilage of femur seen, Medial femorotibial compartment most commonly involved; Isolated patellofemoral compartment involvement is highly indicative of CPPD (Wrist Calcification of the TFCC at ulnarcarpal joint; Terry Thomas sign scapholunate dislocation SLAC (scapholunate advanced collapse) deformity diminished radiocarpal joint space, scapholunate dissociation and rotary subluxation of the scaphoid allows the capitate to migrate proximally Trapezioscaphoid joint severe degenerative signs Radioulnar compartment lack of articular changes (unlike RA) DISH spinal & extraspinal ligamentous calcification (predominately ALL) (AKA Forestiers disease (13-32% of DISH patients have Type 2 Diabetes mellitus (Males 5th-6th decades (Morning stiffness, ! ROM & low-grade musculoskeletal pain (Dysphagia (20%); ossific masses in Achilles and quadriceps tendons (Carrot stick fractures in C-spine (C5-C7) ( from seemingly trivial injuries (Treated with conservative care and NSAID s (Anterolateral aspect of at least 4 contiguous segments (IVD space is preserved (Absence of apophyseal or SI ankylosing or significant sclerosing (Costovertebral/transverse may be bridged (20%) (Most commonly found in the Thoracic spine (Only found on right side due to pulsation-inhibition effect (aorta) (Extraspinal sites pelvis, patella, calcaneous, foot and elbow (Differential Dx DJD, AS, Psoriasis and Reiters (DISH vs. AS ( DISH = hyperostosis of iliac crest, iliolumbar ligament, supra-acetabular region, trochanters, ischial tubes and Pubic Symphysis AS = none of those & demonstrates ankylosing OPLL- (Ossified Posterior Longitudinal Ligament Syndrome) (May result in compression myelopathy of the spinal cord (High incidence in Japan (symptomatic) and Europe and NA (asymptomatic) (Most common site Cervical spine (candle wax appearance) (Progressive difficulty walking (myelopathy); Paresthesia & reduced tactile sensations (Spinal pain is usually absent but when present it is musculoskeletal in nature (Usually presents in a three to four segment ossification, but may only be one (Distinct absence of posterior disk protrusion (Diagnostic sign dense-linear radiopaque strip 1-5mm in thickness, paralleling posterior aspect of vertebral bodies (Adjacent disk space and apophyseal joints are normal (Occurs with DISH in 50% of patients Neurotrophic Arthropathy/Charcot's Disease (Destructive articular disease secondary to loss or impairment in Joint Proprioception (joint anesthesia) (Most common location is the Lumbar spine (#1 cause is Diabetes (L-spine, hip, knee, ankles & feet=Charcots feet), #2 cause is NeuroSyphilis (T &L-spine, hip, knee, ankle, foot) #3 Syringomyelia (C & L-spine, shoulders, elbow, wrist and hand) (Altered gait patterns, loss of deep tendon reflexes and pain insensitivity (Neurologically initiated increased interosseous blood flow stimulates osteoclast action (Hypertrophic Pattern: (6 'Ds': Debris, Density, Destruction, Dislocation, Disorganization, Distension) ( found in weight bearing joints (L-spine, hip, knee, ankle) (Atrophic Pattern: (tapered configuration) Distinct lack of Hypertrophic features ( found in non-weight bearing joints (shoulder, elbow, and wrist as well as hip and foot) (Jigsaw vertebra extensive fragmentation of vertebral body (Tumbling Building Block spine Vertebral malalignments with Anterior, Posterior and Lateral displacements (Knee distinctively hypertrophic in nature, found in medial compartment in early stages Completely screwed up joint- can be mimicked by: Anderson lesion- fracture through previous spinal ankylosis (in spine)- focused hypermobility- end plates start breaking down- carrot stick fracture (fx of ankylosis) Infection Pseudo- Charcots *s+I^ac"4Jgiy!"*9IZgh ӿӷӬӬӷӬӬӬӬӿӿӬӿӬӬӿӬӬӿӝӝ jCJ OJQJmHnHuB*CJ OJQJphCJ H*OJQJ jCJ OJQJ6CJ OJQJ] CJ OJQJ>*CJ OJQJ56CJ OJQJ&56>*CJ OJQJehr>I!g H } ? e ; < = > $a$h H I } ~  = ? @ e f < O P Q m n ƴƠ{ssbs! 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