osteoarthritis_and_osteoporosisppt-.ppt

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Osteoarthritis Osteoarthritis dr M Arman Nasution SpPD dr M Arman Nasution SpPD

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  • Osteoarthritisdr M Arman Nasution SpPD

  • Osteoarthritis

    Osteoarthritis is a non-inflammatory, degenerative condition of joints Characterized by degeneration of articular cartilage and formation of new bone i.e. osteophytes.

  • Common in weight-bearing joints such as hip and knee.Also seen in spine and hands.Both male and females are affected.But more common in older women i.e. above 50 yrs,particularly in postmenopausal age.

  • Risk factors Obesity esp OA knee

    Abnormal mechanical loading eg.meniscectomy, instability

    Inherited type II collagen defects in premature polyarticular OA

    Inheritance in nodal OA

    Occupation eg farmers

    Infection:Non-gonococcal septic arthritis

    Hereditary

    Poor posture

    Injured joints

  • Ageing process in joint cartilage

    Defective lubricating mechanism

    Incompletely treated congenital dislocation of hip

  • Classification of OA

  • Primary OAMore common than secondary OACause UnknownCommon-in elders where there is no previous pathology.Its mainly due to wear and tear changes occuring in old ages mainly in weight bearing joints.

  • Secondary OADue to a predisposing cause such as:1.Injury to the joint2.Previous infection3.RA4.CDH5.Deformity6.Obesity7.hyperthyriodism

  • Types of OANodal Generalised OA Crystal Associated OA OA of Premature Onset

  • Nodal Generalised OA Heberdens nodes Bouchards nodes CMC of thumb Halluxvalgus/rigidus Knees & hips Apophyseal joints

  • Crystal Associated OACalcium pyrophosphatedihydrate occursmainly in elderlywomen, and principallyaffects the knee

  • OA of Premature Onset Previous meniscectomy Haemochromatosis

  • Pathology

    OA is a degenerative condition primarily affecting the articular cartilage. 1.articular cartilage2.Bone3.Synovial membrane4.capsule5.Ligament6.muscle

  • Articular CartilageCartilage is the 1st structure to be affected.Erosion occurs,often central & frequently in wt. bearing areas.Fibrillation,which causes softening,splitting and fragmentation of the cartilage,occur in both wt. bearing & non-wt. bearing areas.Collagen fibres split and there is disorganisation of the proteoglycon collagen relationship such as H2O is attracted into cartilage, which causes futher softening and flaking.these flakes of cartilage break off and may be impacted b/w the jt.surfaces causing locking and inflammation.

  • Right: Early OA with area of cartilage loss in the center.

    Left: More advanced changes with extensive cartilage loss and exposed underlying bone

  • Arthroscopic appearances in OA of the knee joint: fibrillated surface of the cartilage on the medial femoral condyle

  • Bone(Eburnation)Bone surface become hard & polished as there is loss of protection from the cartilage.Cystic cavities form in the subchondral bone because eburnated bone is brittle and microfractures occur.Venous congestion in the subchondral bone.

  • Gross superior view of a femoral head from a patient with radiographic stage I OA. This shows an area of complete cartilage loss, with polishing or eburnation of the underlying bone.

  • Osteophytes form at the margin of the articular surface,which may get projected into the jt. Or into capsule & ligament,bone of the wt.-bearing jt.There is alteration in the shape of the femoral head which becomes flat and mushroom shaped.Tibial condyles become flatened.

  • Osteophyte at margin of articular surface

  • Synovial MembraneSynovial membrane undergo hypertrophy and become oedematous (which can lead to cold effusions).Reduction of synovial fluid secretion results in loss of nutrition and lubricating action of articular cartilage. CapsuleIt undergoes fibrous degeneration and there are low-grade chronic inflammatory changes

  • LigamentUndergoes fibrous degernationThere is low grade chronic inflammatory changes and acc.to the aspect joint become contracted or elongated. Muscles Undergoes atrophy,as pt. is not able to use the jt. Because of pain which further limits movts. and function.

  • Clinical features of OAPainStiffnessMuscle spasmRestricted movement Deformity Muscle weakness or wastingJoint enlargement and instabilityCrepitus Joint Effusion

  • Clinical features 1Pain and tendernessUsually slow onset of discomfort, with gradual and intermittent increasePain is more on wt. bearing due to stress on the synovial membrane & later on due to bone surface,which r rich in nerve endings coming in contact.-initially relieved by rest but later on disturb sleep.-Diffuse/ sharp and stabbing local pain

  • Clinical features Pain and tenderness (cont)

    Types of pain

    Mechanical: increases with use of the joint

    Inflammatory phases

    Rest pain later on in 50%

    Night pain in 30% later on

  • Clinical features 2Movement abnormalitiesGelling: stiffness after periods of inactivity, passes over within minutes (approx 15min.) of using joint againCoarse crepitus: palpate/hear (due to flaked cartilage & eburnated bone ends)

    Reduced ROM: capsular thickening and bony changes in joint,ms. Spasm or soft tissue contracture.

  • Clinical features 3DeformitiesSoft tissue swelling: mild synovitis small effusionsOsteophytesJoint laxityAsymmetrical joint destruction leading to angulation

  • Osteoarthritis of the DIP joints. This patient has the typical clinical findings of advanced OA of the DIP joints, including large firm swellings (Heberdens nodes), some of which are tender and red due to associated inflammation of the periarticular tissues as well as the joint.

  • Knee joint effusion

  • A patient with typical OA of the knees. In the normal standing posture there is a mild varus angulation of the knee joints due to symmetrical OA of the medial tibiofemoral compartments.

  • Pseudolaxity due to cartilage loss. The joint is not loaded in the first photograph

  • Unstable distal interphalangeal joints in OA. The examiner is able to push the joint from side to side due to gross instability, a common finding in late interphalangeal joint OA.

  • Radiographic Classification

    Stage 1Bony spur onlyStage 2Narrowing of jt. Space,less than half of the normal jt. spaceStage 3Narrowing of jt. Space,more than half of the normal jt. spaceStage 4Obliteration of jt. spaceStage 5Subluxation or sec.lateral arthrosis

  • Distribution of OA of the hip joint. OA can maximally affect the superior pole, inferior pole, posterior part or other segments of the hip joint. Superior pole involvement, with a tendency for the head of the femur to sublux superolaterally, is the commonest pattern. Involvement of the whole joint (concentric OA) is relatively uncommon.

  • Special InvestigationsBlood tests: Normal

    Radiological features:Cartilage lossSubchondral sclerosisCystsOsteophytes

  • Treatment PrinciplesEducationPhysiotherapyExercise programPain relief modalitiesAids and appliancesMedical TreatmentSurgical Treatment

  • EducationNonsystemic nature of diseasePrevent overloading of joint. Obesity!!Appropriate use of treatment modalitiesImportance of exercise programAids, apliances, bracesMedial treatmentsSurgical treatments

  • ExerciseWill not wear the joint out

    Important for cartilage nutrition

    Some evidence that lack of exercise leads to progression of OA

  • ExerciseEncourage full range low impact movements eg swimming, cyclingAvoidProlonged loadingActivities that cause painContact sportsHigh impact sports eg running

  • Quadriceps exercises for knee OA. Quadriceps exercises are of proven value for pain relief and improving function, and everyone with knee OA should be taught the correct techniques and encouraged to make these exercises a lifetime habit. There is a weight on the ankle.

  • Use of transcutaneous nerve stimulation (TENS) as an adjunct to other therapy for pain relief at the knee joint. The use of acupuncture, TENS and other local techniques to aid pain relief in difficult cases of OA is often worthwhile.

  • Aids and appliancesBraces / splintsSpecial shoes/insolesMobility aidsAids: dressing, reaching, tap openers, kitchen aidsTaping of patella in patello femoral OA

  • Use of a cane, stick or other walking aid. This patient, who has hip OA, has found that she can reduce the pain in her damaged left hip by leaning on the stick in the right hand as she walks. The reduction in loading can be huge, and the effect on symptoms and confidence with walking very beneficial.

  • The use of shoes and insoles to reduce impact loading on lower limb joints. Modern sports shoes (trainers) often have appropriate insoles. Alternatively, special heel or shoe insoles of sorbithane or viscoelastic materials can be used. They may help relieve pain as well as reducing the peak impact load on the joints during walking.

  • Medical TreatmentSimple analgesics: paracetamol, low dose ibuprofenNSAIDs/Coxibs PRN regularIntra-articular corticosteroidsTopical treatment eg NSAID creams, capsaicinChondroprotective agents

  • A patient with OA of the carpometacarpal joint of the left thumb undergoing arthrocentesis for injection of a depot corticosteroid preparation. The operator is distracting the patients thumb to open up the joint space.

  • Joint replacement surgeryIndications: pain affecting work, sleep, walking and leisure activities

    Complicationssepsislooseninglifespan of materials (mechanical failure)

  • DRAFT Aclasta Brand BookOsteoporosis: Challenges to meet

  • Bone and its componentBone HomeostasisBone remodelingDefinition and classification of osteoporosisPrevalenceRisk Factors and presentationDiagnosisConsequencesManagement principleTreatment goal

    Osteoporosis: Challenges to meet| BICC | 27th July, 2010

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Organic Component:protein collagen & specialized cells called osteoclasts, osteoblasts, and osteocytes

    Inorganic component:Mainly as calcium phosphate, in the form of Hydroxyapatite

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Bone Homeostasis: the situation when the body requires and achieves an equal amount of bone resorption and bone formation

    the amount of bone eroded by osteoclasts is equal to theamount of bone produced by osteoblasts, thereby producing a stable net mass of bone in the body

    Homeostasis

  • The combined processes of breaking down bone and building new bone are called Bone Remodeling.

    It is the bodys way of maintaining bone homeostasis.

    5 Stages: Initiation, Resorption, Reversal, Bone formation and Completion of remodeling. Osteoporosis: Challenges to meet| BICC | 27th July, 2010

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Osteoclast precursor cells are attracted to a bone site and penetrate the bone lining cells. These osteoclast precursor cells then form activated osteoclasts that align themselves in direct contact with mineralized bone matrix.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010The osteoclasts erode a cavity by removing mineral and organic components from the bone. The osteoclasts eventually die. This completes the resorption phase.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Cells of unknown origin prepare the bone surface for new bone formation by smoothing the surface of the cavity and depositing a thin layer of a cement-like substance.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Cells of unknown origin prepare the bone surface for new bone formation by smoothing the surface of the cavity and depositing a thin layer of a cement-like substance.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010The lining cells rest on the bone surface until the next cycle of bone remodeling begins.

    Some osteoblasts become osteocytes.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010

  • Challenges of OsteoporosisOsteoporosis: Challenges to meet| BICC | 27th July, 2010

  • National Osteoporosis Foundation: a disease characterized by low bone mass an micro-architectural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures.

    World Health Organization (1994) :bone mineral density T-score greater than 2.5 standard deviations from the mean peak adult bone mass (ie. a woman in her 30s).

    Osteoporosis: Challenges to meet| BICC | 27th July, 2010

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010

  • Losing bone with years

  • Osteoporosis, the silent thief of your boneOsteoporosis: Challenges to meet| BICC | 27th July, 2010

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Worldwide, over age of 501 in 3 women / 1 in 8 men have osteoporosis.

    80 % of those suffering from osteoporosis are women.Affects 75 million persons in the US, Europe and Japan.

    Over 50% of women aged 50 years or older and 20% of men will suffer an osteoporosis-related fracture within their remaining lifetime

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Being female Older age Family history of osteoporosis or broken bones Being small and thin History of broken bones Low sex hormonesLow estrogen levels in women, including menopause Missing periods (amenorrhea) Low levels of testosterone and estrogen in men

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010DietLow calcium intake Low vitamin D intake Excessive intake of protein, sodium and caffeine Inactive lifestyle Smoking , Alcohol abuse Certain medications steroid , anticonvulsants etcCertain diseasesanorexia nervosa, rheumatoid arthritis, gastrointestinal diseases and others

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010People may not know that they have osteoporosis until they break a bone. Vertebral (spinal) fractures may initially be felt or seen in the form of Persistent, unexplained back painLoss of heightSpinal deformities such as kyphosis or stooped posture.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Bone mineral density (BMD) tests can measure bone density in various sites of the body.

    BMD test is done to diagnose and predict fracture risk and to monitor therapy.

    For patients on pharmacotherapy, it is typically performed 2 years after initiating therapy and every 2 years thereafter; however, more frequent testing may be warranted in certain clinical situations.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Dual-energy X-ray Absorptiometry (DXA) Scan

    Gold-standard for BMD measurement.Measures central or axial skeletal sites: spine and hip.May measure other sites: total body and forearm.Validated in many clinical trials.Available in Bangladesh.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Dual-energy X-ray Absorptiometry (DXA) Scan

    ClassificationT-scoreNormal-1 or greaterOsteopeniaBetween -1 and -2.5Osteoporosis-2.5 or lessSevere Osteoporosis-2.5 or less and fragility fracture

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010FRACTURE , The most serious complication of Osteoporosis that leads to

    Increased morbidityIncreased mortalityDecreased quality of life

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010

    Decreased fracture riskLife style modificationTherapeutic Intervention Minimizing risk factorsSlowing/stopping bone loss Minimizing factors that Contribute to fallMaintaining or increasing bone density and strengthMaintaining or improving bone microarchitecture

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Supplements such as which maintain bone mass Calcium, Vitamin D

    Anti-resorptive agents which inhibit bone resorption Bisphosphonates

    Anabolic agents, which stimulate bone formation and, in turn, increase bone mass.

  • Osteoporosis: Challenges to meet| BICC | 27th July, 2010Prevent further bone lossIncrease or at least stabilize bone densityPrevent further fractures Relieve deformity (e.g., kyphoplasty)Relieve painIncrease level of physical functioningIncrease quality of life

  • Ass Wr Wb

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