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OSTEOPOROSIS
DR. Md Akbar Khan MS(ORTHO)
Asst. Prof of Orthopaedics
ACSR Govt Medical College, Nellore
 Jean Lobstein – coined the term & described its
pathoanatomy.
 Osteoporosis is a major public health problem,
which results in substantial morbidity,
mortality and high costs.
 Silent disease – patients unaware of ongoing
bone loss which is asymptomatic.
 Fracture may be the first symptom
INTRODUCTION
 Skeletal disorder characterized by low bone
mass & micro-architectural deterioration of
bone tissue which results in increased bone
fragility and fracture susceptibility.
 WHO definition – Bone density that falls 2.5
SD below the mean for young healthy adults
of same race & gender
DEFINITION
 Reduced bone mass
 Reduced mineralization
 Micro architectural deterioration of bone tissue
There is
 Subnormal osteoid production
 Excessive rate of de-ossification
 Subnormal osteoid mineralization
CHARACTERISTIC FEATURES
CHARACTERISTIC FEATURES
 Normal – BMD not more than 1 SD
 Osteopenia - 1 to 2.5 below SD
 Osteoporosis - 2.5 below SD
 Severe Osteoporosis – With fragility fractures
WHO GRADING
PRIMARY OSTEOPOROSIS

Type I - Postmenopausal osteoporosis

Type II - Senile osteoporosis

Idiopathic - Premenopausal and Younger
CLASSIFICATION
SECONDARY OSTEOPOROSIS
 Metabolic - Calcium & Vit. D deficiency
 Endocrine - Cushing syndrome, Hyperparathyroidism
 Renal disease
 Gastrointestinal - IBD, Malabsorption
 Hereditary connective tissue diseases - Marfan
syndrome, Homocystinuria.
 Bone marrow infiltration - Multiple Myeloma,
lymphoma, leukemia.
 Drugs - Phenytoin, Corticosteroid, heparin, lithium.
 Life style - Alcohol, smoking, inactivity,
immobilization,
 Miscellaneous - Rh. arthritis
CLASSIFICATION
Non-modifiable
 Peak bone mass
 Female sex
 Caucasian race
 Advanced age
 Family history
Potentially modifiable
 Cigarette smoking & Alcoholism
 Estrogen deficiency
 Low body weight
 Low calcium intake
 Lack of physical activity
CONTRIBUTING FACTORS
 Bone formation & bone resorption - (2 Process)
 Osteoclast (bone resorbing cells) & Osteoblast (bone
forming cells) - (2 Type of Cells)
 Parathormone & Vitamin D - (2 Biomolecules)
 Cortical & Trabecular bones - (2 Types of Bones)
 Investigations – Markers of bone formation &
resorption (2 Marker Investigations)
 Treatment – Drugs which enhance bone formation &
decrease resorption (2 Types of Drugs)
BALANCING ACT BETWEEN
Fragility fractures / Insufficiency fractures
 Outcome depends on
Bone density
Severity of fall
In three most common fractures
 Distal radius – Fall > Density
 Vertebral body – Density > Fall
 Hip fractures – Fall & Density play equal role
OSTEOPOROTIC FRACTURES
Risk Factors :
 Increased age
 Female gender
 Estrogen deficiency
 Inadequate calcium intake
 Low bone density (osteopenia)
 Low body weight
 History of fractures in adult life
 History of fractures in first-degree relative
 Smoking and alcohol use
 Lack of physical activity
OSTEOPOROTIC FRACTURES
 Osteoporosis is usually asymptomatic until
fracture occurs.
 May present as backache of varying degrees of
severity
 Spontaneous fracture
 Collapse of vertebrae
 Loss of height is common
 Thoracic kyphosis
CLINICAL MANIFESTATIONS
 Osteoporosis is usually asymptomatic until
fracture occurs.
 May present as backache of varying degrees of
severity
 Spontaneous fracture
 Collapse of vertebrae
 Loss of height is common
 Thoracic kyphoses
CLINICAL MANIFESTATIONS
 Hyperparathyroidism
 Paget’s disease
 Osteomalacia
 Osteogenesis imperfecta
 Multiple myeloma
 Renal Osteodystrophy
 Secondary tumors
DIFFERENTIAL DIAGNOSIS
 Serum calcium
↑  Hyperparathyroidism / Malignancy
↓  Malnutrition / Osteomalacia
 PTH
 ↑  Hyperparathyroidism
 ↓  Malignancy
 ↑ PTHrP  Malignancy
 TSH  To r/o Hyperthyroidism
 Urinary free Cortisol  Cushings disease
INVESTIGATIONS
 Urine Calcium
Low (<50mg/24 hrs)
 Osteomalacia, Malnutrition, Malabsorption
 High (300mg/24 hrs)
 ↑ renal calcium leak -Males with osteoporosis
 Absorptive hypercalciuria - Idiopathic
Granulomatous disease
 Malignancy and diseases with ↑ bone turnover
INVESTIGATIONS
 Serum & Urine immuno-electrophoresis
Multiple myeloma
 Urinary N – Telopeptide (NTX)
 Marker of bone resorption
 >40 n mol  high turnover
 25- hydroxy vitamin D & 1,25 hydroxy vitamin Dlevels
Liver Disease, Renal Osteodystrophy
 Monitor response to anti-osteoporotic treatments
INVESTIGATIONS
Ca PO4 ALP
Osteoporosis N N/↓ N
Hyperparathyroidism ↑ ↓ ↑
Paget’s disease N or ↑ N / ↑ ↑↑
Osteomalacia N/ ↓ ↓ ↑
Osteogenesis Imperfecta N N N/ ↑
Multiple Myeloma N/ ↑ N/ ↑ N
INVESTIGATIONS
 Post menopausal osteoporosis
Trabecular resorption & cortical resorption
 Senile osteoporosis
Endosteal resorption
 Hyperparathyroidism
Subperiosteal resorption
RADIOLOGY
 Principal tensile & compressive trabeculae on hip X Ray
Grade VI to Grade I
 Grade VI:
 Normal trabecular groups are visible
 Upper end of femur is occupied by cancellous bone
 Grade V:
 Both Trabeculae is accentuated
 Ward's triangle appears prominent
 Grade IV:
 principal tensile trabeculae are markedly reduced
 can be traced from lateral cortex to upper part of femoral neck
SINGH’S INDEX
 Grade III:
 There is break in continuity of principal tensile trabeculae
opposite greater trochanter
 Grade II:
 Only principal compressive trabeculae stand out prominently
 Remaining trabeculae have been essentially absorbed
 Grade I:
 Principal compressive trabeculae are markedly reduced in
number and are no longer prominent
 Grade 6 normal
 Grade 3 definite osteoporosis
 Grade 1 is severe osteoporosis
SINGH’S INDEX
SINGH’S INDEX
 Cod fish vertebra
 Kyphosis
 Collapse of vertebra
 Compression
Fractures
 Schmorl's nodules
 Kleer Koper Score
VERTEBRAL X RAY
 Assessed from lateral view of spine – T4 – L5
Normal – Grade 0
Biconcave deformity – Grade 1
Wedge deformity – Grade 2
Compression deformity – Grade 3
Kleer Koper Score
 Reconstructive CT
pictures show L 1,2,
and L3 fractures
with biconcave
deformities
COMPUTER TOMOGRAPHY
 Chronic benign
compression fractures
 Sagittal MRI scan
shows multiple
collapsed vertebrae
MRI SCAN
 Amount of bone matter per cubic centimeter of
bone
 Reported in Three terms – Gm/ mm3
,T score &
Z score
 Measured by
Dual Energy X Ray Absortiometry
Qualitative Ultrasound
Qualitative Computer Tomography
BONE MINERAL DENSITY
Recommendation for bone density measurements:
 Estrogen-deficient women at clinical risk.
 Individual with vertebral abnormalities - plain film
 More than 3 months of steroid treatment
 Primary hyperparathyroidism
 Monitoring of drug therapy
 Women who have multiple risk factors
 Postmenopausal women who is not on estrogen
replacement.
 Pt. with strong Family History of osteoporosis.
 All women age>65.
BONE MINERAL DENSITY
 X ray photons of different energy
 Sites recommended by WHO
Total proximal femur
Femoral neck
Lumbar spine
Radius with evidence of
OA / surgery at
other 3 sites
DUAL ENERGY X RAY ABSORTIOMETRY
 Results expressed in T & Z scores
DUAL ENERGY X RAY ABSORTIOMETRY
 Emits ultrasonic waves
 Attenuation of waves which predict strength
of bone
 Measured in calcaneum
 At present outdated due to errors
QUALITATIVE ULTRASOUND
 Mainly for spine
 Specifically analysis trabecular bone
 Less precise than DEXA
 More radiation
 Costlier than DEXA
QUALITATIVE COMPUTER TOMOGRAPHY
 Key to management is prevention.
 Prevention of osteoporosis is a misnomer
 It is actually prevention of fractures by the time
the patient already have osteoporosis
 Increasing public awareness about importance
and risks involved helps
 Altering personal and dietary habits
 Regular physical activity(3-4 hrs/week)
 Peri-menopause & postmenopause: calcium+
oestrogen – weight bearing exercises.
PRIMARY PREVENTION
 Use handrails on stairs, Bathroom
 Keep rooms free of clutter
 Keep floors clean but not slippery
 Wear supportive, low-heeled shoes.
 Don’t walk in socks; floppy slippers
 Install ceiling lighting in bedrooms
 Use rubber matt in shower/tub
 Check posture in mirror often
 Conservative
 Surgical
MANAGEMENT
 Calcium – 1 to 1.5 gm/day
 Vitamin D – 400 to 800 IU/day
 Weight bearing and gravity resistant exercises
 Avoid alcohol, cigarette
 Moderate phosphate intake
 Prophylactic agents
 Alendronate – 35mg
 Raloxifine – 60mg
PROPHYLAXIS
 Anti resoptive class of Drugs
Calcium/Vitamin D
Bisphosphonates
Calcitonin
Selective Estrogen Receptor Modulators (SERMS)
 Anabolic Drugs
Parathyroid Hormone
Sodium fluoride & Strontium Renelate
 Other Agents
Vitamin K2-7 fortified calcitriol & Denosumab
MEDICALTREATMENT
Mechanism of action
 Binds to the surface of hydroxyapatite crystals
and inhibits its resorption
 First line of treatment in postmenopausal
osteoporosis
Side effects
 Gastrointestinal intolerance
 Esophagitis
 Bone pain
BISPHOSPHONATES
 Once a week (oral)
Alendronate –35mg (prevention) & 70 mg treatment
Risedronate - 35mg (prevention) & 50 mg treatment
 Once a month (oral)
Ibandronate - 150 mg
 Once In 3 months (Intravenous)
 Ibandronate - 3 mg / 3 ml over 15 – 30 sec
 Once in a year(Intravenous)
Zolendronate -5 mg / 100 ml infusion over 15–20 min
BISPHOSPHONATES
 Salmon Calcitonin Nasal Spray
For postmenopausal osteoporosis
200 IU once a day intranasal, alternating nostrils
Side effects – nasal mucosal irritation
 SERM’S (Raloxifene)
For postmenopausal osteoporosis - 150 mg
 Recombinant Human PTH ( Teriparatide)
 Produced genetically engineered E. Coli
Injection - 750 micrograms
Calcium & Vitamin D supplements to correct imbalance
Other Agents
 Sodium Fluoride & Strontium Renelate
Increase bone mass by inhibiting osteoclasts
Stimulate osteoblasts
 Vitamin K2-7 fortified calcitriol & calcium
combinations
 Denosumab
 monoclonal antibody binds with RANK Ligand
Inhibits bone resorption
Other Agents
 GOALS
Improve quality of life
Give a stable fixation
Early mobilization & weight bearing
SURGICAL TREATMENT
 BASIC PRINCIPLES
Biological fixation
Load sharing implants
Impaction & compression
Wide buttress plates
Long splintage
Augmentation of implants
Replacement arthroplasty
SURGICAL TREATMENT
 Without opening fracture site & without
disturbing biomechanics
 Use of longer plate with less no of screws –
greater stability
BIOLOGICAL FIXATION
 Interlocking nails , tension band constructs
 Moved from conventional plating, DCP & LC-
DCP to Interlocking nails & LCP
 These bones have poor holding power of screws
 Bones are like tough spring
 Interlocking nails & LCP locking the screws to
plates creating angular stable devices,
diminishing screw holding power of bone
LOAD SHARING IMPLANTS
TERMS:
Fixed Position
Fixed Angle
Locking Screw
Locking Plate
LOCKING PLATES
LOCKING SCREW-PLATE CONSTRUCTS
Locking head screw
Threaded plate hole
PULLOUT OF LOCKING SCREWS
Creates Fixed Angle Generates
Friction/Compression
4.4mm Core Dia. 3.5mm Core Dia.
5.0 mm Locking Screw 4.5 mm Cortical Screw
 Enhances stability
 In comminuted fractures – controlled impaction
&compression is advisable-DHS with wt. bearing
 LCP plates are used in metaphyseal fractures,
upper tibial fractures, & supracondylar fractures
& proximal humerus with specialized plates
IMPACTION & COMPRESSION
 Bone cement
 Bone graft
 Bone subsitutes
Hydroxyapatite
Tricalcium phosphate Hydroxyapatite
Tricalcium phosphate
 Biodegradable bone cement
Calcium phosphate – Norian skeletal repair system
Glass isometric cement
AUGMENTATION OF IMPLANTS
 If no other option
REPLACEMENT ARTHROPLASTY
 Contoured plates
Proximal humeral plates
Distal femoral plates
Proximal tibial plates
Distal tibial plates
 LISS plates
Proximal tibia distal femur with zig & minimally
invasive techniques
SPECIAL PLATES
Osteoporosis Treatment and Prevention
Osteoporosis Treatment and Prevention

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Osteoporosis Treatment and Prevention

  • 1. OSTEOPOROSIS DR. Md Akbar Khan MS(ORTHO) Asst. Prof of Orthopaedics ACSR Govt Medical College, Nellore
  • 2.  Jean Lobstein – coined the term & described its pathoanatomy.  Osteoporosis is a major public health problem, which results in substantial morbidity, mortality and high costs.  Silent disease – patients unaware of ongoing bone loss which is asymptomatic.  Fracture may be the first symptom INTRODUCTION
  • 3.  Skeletal disorder characterized by low bone mass & micro-architectural deterioration of bone tissue which results in increased bone fragility and fracture susceptibility.  WHO definition – Bone density that falls 2.5 SD below the mean for young healthy adults of same race & gender DEFINITION
  • 4.  Reduced bone mass  Reduced mineralization  Micro architectural deterioration of bone tissue There is  Subnormal osteoid production  Excessive rate of de-ossification  Subnormal osteoid mineralization CHARACTERISTIC FEATURES
  • 6.  Normal – BMD not more than 1 SD  Osteopenia - 1 to 2.5 below SD  Osteoporosis - 2.5 below SD  Severe Osteoporosis – With fragility fractures WHO GRADING
  • 7. PRIMARY OSTEOPOROSIS  Type I - Postmenopausal osteoporosis  Type II - Senile osteoporosis  Idiopathic - Premenopausal and Younger CLASSIFICATION
  • 8. SECONDARY OSTEOPOROSIS  Metabolic - Calcium & Vit. D deficiency  Endocrine - Cushing syndrome, Hyperparathyroidism  Renal disease  Gastrointestinal - IBD, Malabsorption  Hereditary connective tissue diseases - Marfan syndrome, Homocystinuria.  Bone marrow infiltration - Multiple Myeloma, lymphoma, leukemia.  Drugs - Phenytoin, Corticosteroid, heparin, lithium.  Life style - Alcohol, smoking, inactivity, immobilization,  Miscellaneous - Rh. arthritis CLASSIFICATION
  • 9. Non-modifiable  Peak bone mass  Female sex  Caucasian race  Advanced age  Family history Potentially modifiable  Cigarette smoking & Alcoholism  Estrogen deficiency  Low body weight  Low calcium intake  Lack of physical activity CONTRIBUTING FACTORS
  • 10.  Bone formation & bone resorption - (2 Process)  Osteoclast (bone resorbing cells) & Osteoblast (bone forming cells) - (2 Type of Cells)  Parathormone & Vitamin D - (2 Biomolecules)  Cortical & Trabecular bones - (2 Types of Bones)  Investigations – Markers of bone formation & resorption (2 Marker Investigations)  Treatment – Drugs which enhance bone formation & decrease resorption (2 Types of Drugs) BALANCING ACT BETWEEN
  • 11. Fragility fractures / Insufficiency fractures  Outcome depends on Bone density Severity of fall In three most common fractures  Distal radius – Fall > Density  Vertebral body – Density > Fall  Hip fractures – Fall & Density play equal role OSTEOPOROTIC FRACTURES
  • 12. Risk Factors :  Increased age  Female gender  Estrogen deficiency  Inadequate calcium intake  Low bone density (osteopenia)  Low body weight  History of fractures in adult life  History of fractures in first-degree relative  Smoking and alcohol use  Lack of physical activity OSTEOPOROTIC FRACTURES
  • 13.  Osteoporosis is usually asymptomatic until fracture occurs.  May present as backache of varying degrees of severity  Spontaneous fracture  Collapse of vertebrae  Loss of height is common  Thoracic kyphosis CLINICAL MANIFESTATIONS
  • 14.  Osteoporosis is usually asymptomatic until fracture occurs.  May present as backache of varying degrees of severity  Spontaneous fracture  Collapse of vertebrae  Loss of height is common  Thoracic kyphoses CLINICAL MANIFESTATIONS
  • 15.  Hyperparathyroidism  Paget’s disease  Osteomalacia  Osteogenesis imperfecta  Multiple myeloma  Renal Osteodystrophy  Secondary tumors DIFFERENTIAL DIAGNOSIS
  • 16.  Serum calcium ↑  Hyperparathyroidism / Malignancy ↓  Malnutrition / Osteomalacia  PTH  ↑  Hyperparathyroidism  ↓  Malignancy  ↑ PTHrP  Malignancy  TSH  To r/o Hyperthyroidism  Urinary free Cortisol  Cushings disease INVESTIGATIONS
  • 17.  Urine Calcium Low (<50mg/24 hrs)  Osteomalacia, Malnutrition, Malabsorption  High (300mg/24 hrs)  ↑ renal calcium leak -Males with osteoporosis  Absorptive hypercalciuria - Idiopathic Granulomatous disease  Malignancy and diseases with ↑ bone turnover INVESTIGATIONS
  • 18.  Serum & Urine immuno-electrophoresis Multiple myeloma  Urinary N – Telopeptide (NTX)  Marker of bone resorption  >40 n mol  high turnover  25- hydroxy vitamin D & 1,25 hydroxy vitamin Dlevels Liver Disease, Renal Osteodystrophy  Monitor response to anti-osteoporotic treatments INVESTIGATIONS
  • 19. Ca PO4 ALP Osteoporosis N N/↓ N Hyperparathyroidism ↑ ↓ ↑ Paget’s disease N or ↑ N / ↑ ↑↑ Osteomalacia N/ ↓ ↓ ↑ Osteogenesis Imperfecta N N N/ ↑ Multiple Myeloma N/ ↑ N/ ↑ N INVESTIGATIONS
  • 20.  Post menopausal osteoporosis Trabecular resorption & cortical resorption  Senile osteoporosis Endosteal resorption  Hyperparathyroidism Subperiosteal resorption RADIOLOGY
  • 21.  Principal tensile & compressive trabeculae on hip X Ray Grade VI to Grade I  Grade VI:  Normal trabecular groups are visible  Upper end of femur is occupied by cancellous bone  Grade V:  Both Trabeculae is accentuated  Ward's triangle appears prominent  Grade IV:  principal tensile trabeculae are markedly reduced  can be traced from lateral cortex to upper part of femoral neck SINGH’S INDEX
  • 22.  Grade III:  There is break in continuity of principal tensile trabeculae opposite greater trochanter  Grade II:  Only principal compressive trabeculae stand out prominently  Remaining trabeculae have been essentially absorbed  Grade I:  Principal compressive trabeculae are markedly reduced in number and are no longer prominent  Grade 6 normal  Grade 3 definite osteoporosis  Grade 1 is severe osteoporosis SINGH’S INDEX
  • 24.  Cod fish vertebra  Kyphosis  Collapse of vertebra  Compression Fractures  Schmorl's nodules  Kleer Koper Score VERTEBRAL X RAY
  • 25.  Assessed from lateral view of spine – T4 – L5 Normal – Grade 0 Biconcave deformity – Grade 1 Wedge deformity – Grade 2 Compression deformity – Grade 3 Kleer Koper Score
  • 26.  Reconstructive CT pictures show L 1,2, and L3 fractures with biconcave deformities COMPUTER TOMOGRAPHY
  • 27.  Chronic benign compression fractures  Sagittal MRI scan shows multiple collapsed vertebrae MRI SCAN
  • 28.  Amount of bone matter per cubic centimeter of bone  Reported in Three terms – Gm/ mm3 ,T score & Z score  Measured by Dual Energy X Ray Absortiometry Qualitative Ultrasound Qualitative Computer Tomography BONE MINERAL DENSITY
  • 29. Recommendation for bone density measurements:  Estrogen-deficient women at clinical risk.  Individual with vertebral abnormalities - plain film  More than 3 months of steroid treatment  Primary hyperparathyroidism  Monitoring of drug therapy  Women who have multiple risk factors  Postmenopausal women who is not on estrogen replacement.  Pt. with strong Family History of osteoporosis.  All women age>65. BONE MINERAL DENSITY
  • 30.  X ray photons of different energy  Sites recommended by WHO Total proximal femur Femoral neck Lumbar spine Radius with evidence of OA / surgery at other 3 sites DUAL ENERGY X RAY ABSORTIOMETRY
  • 31.  Results expressed in T & Z scores DUAL ENERGY X RAY ABSORTIOMETRY
  • 32.  Emits ultrasonic waves  Attenuation of waves which predict strength of bone  Measured in calcaneum  At present outdated due to errors QUALITATIVE ULTRASOUND
  • 33.  Mainly for spine  Specifically analysis trabecular bone  Less precise than DEXA  More radiation  Costlier than DEXA QUALITATIVE COMPUTER TOMOGRAPHY
  • 34.  Key to management is prevention.  Prevention of osteoporosis is a misnomer  It is actually prevention of fractures by the time the patient already have osteoporosis  Increasing public awareness about importance and risks involved helps  Altering personal and dietary habits  Regular physical activity(3-4 hrs/week)  Peri-menopause & postmenopause: calcium+ oestrogen – weight bearing exercises. PRIMARY PREVENTION
  • 35.  Use handrails on stairs, Bathroom  Keep rooms free of clutter  Keep floors clean but not slippery  Wear supportive, low-heeled shoes.  Don’t walk in socks; floppy slippers  Install ceiling lighting in bedrooms  Use rubber matt in shower/tub  Check posture in mirror often
  • 37.  Calcium – 1 to 1.5 gm/day  Vitamin D – 400 to 800 IU/day  Weight bearing and gravity resistant exercises  Avoid alcohol, cigarette  Moderate phosphate intake  Prophylactic agents  Alendronate – 35mg  Raloxifine – 60mg PROPHYLAXIS
  • 38.  Anti resoptive class of Drugs Calcium/Vitamin D Bisphosphonates Calcitonin Selective Estrogen Receptor Modulators (SERMS)  Anabolic Drugs Parathyroid Hormone Sodium fluoride & Strontium Renelate  Other Agents Vitamin K2-7 fortified calcitriol & Denosumab MEDICALTREATMENT
  • 39. Mechanism of action  Binds to the surface of hydroxyapatite crystals and inhibits its resorption  First line of treatment in postmenopausal osteoporosis Side effects  Gastrointestinal intolerance  Esophagitis  Bone pain BISPHOSPHONATES
  • 40.  Once a week (oral) Alendronate –35mg (prevention) & 70 mg treatment Risedronate - 35mg (prevention) & 50 mg treatment  Once a month (oral) Ibandronate - 150 mg  Once In 3 months (Intravenous)  Ibandronate - 3 mg / 3 ml over 15 – 30 sec  Once in a year(Intravenous) Zolendronate -5 mg / 100 ml infusion over 15–20 min BISPHOSPHONATES
  • 41.  Salmon Calcitonin Nasal Spray For postmenopausal osteoporosis 200 IU once a day intranasal, alternating nostrils Side effects – nasal mucosal irritation  SERM’S (Raloxifene) For postmenopausal osteoporosis - 150 mg  Recombinant Human PTH ( Teriparatide)  Produced genetically engineered E. Coli Injection - 750 micrograms Calcium & Vitamin D supplements to correct imbalance Other Agents
  • 42.  Sodium Fluoride & Strontium Renelate Increase bone mass by inhibiting osteoclasts Stimulate osteoblasts  Vitamin K2-7 fortified calcitriol & calcium combinations  Denosumab  monoclonal antibody binds with RANK Ligand Inhibits bone resorption Other Agents
  • 43.
  • 44.  GOALS Improve quality of life Give a stable fixation Early mobilization & weight bearing SURGICAL TREATMENT
  • 45.  BASIC PRINCIPLES Biological fixation Load sharing implants Impaction & compression Wide buttress plates Long splintage Augmentation of implants Replacement arthroplasty SURGICAL TREATMENT
  • 46.  Without opening fracture site & without disturbing biomechanics  Use of longer plate with less no of screws – greater stability BIOLOGICAL FIXATION
  • 47.  Interlocking nails , tension band constructs  Moved from conventional plating, DCP & LC- DCP to Interlocking nails & LCP  These bones have poor holding power of screws  Bones are like tough spring  Interlocking nails & LCP locking the screws to plates creating angular stable devices, diminishing screw holding power of bone LOAD SHARING IMPLANTS
  • 48. TERMS: Fixed Position Fixed Angle Locking Screw Locking Plate LOCKING PLATES
  • 49. LOCKING SCREW-PLATE CONSTRUCTS Locking head screw Threaded plate hole
  • 51. Creates Fixed Angle Generates Friction/Compression 4.4mm Core Dia. 3.5mm Core Dia. 5.0 mm Locking Screw 4.5 mm Cortical Screw
  • 52.
  • 53.  Enhances stability  In comminuted fractures – controlled impaction &compression is advisable-DHS with wt. bearing  LCP plates are used in metaphyseal fractures, upper tibial fractures, & supracondylar fractures & proximal humerus with specialized plates IMPACTION & COMPRESSION
  • 54.  Bone cement  Bone graft  Bone subsitutes Hydroxyapatite Tricalcium phosphate Hydroxyapatite Tricalcium phosphate  Biodegradable bone cement Calcium phosphate – Norian skeletal repair system Glass isometric cement AUGMENTATION OF IMPLANTS
  • 55.
  • 56.  If no other option REPLACEMENT ARTHROPLASTY
  • 57.  Contoured plates Proximal humeral plates Distal femoral plates Proximal tibial plates Distal tibial plates  LISS plates Proximal tibia distal femur with zig & minimally invasive techniques SPECIAL PLATES

Editor's Notes

  1. Maintaining a home environment that reduces the risk of falling is important. The next two slides list helpful considerations that patients should be made aware of. Use handrails on stairs, in bathroom Keep rooms free of clutter Keep floor surfaces clean but not slippery Wear supportive, low-heeled shoes. Do not walk in socks or floppy slippers Use 100 watt bulbs in all rooms Install ceiling lighting in bedrooms Use rubber matt in shower/tub Keep a flashlight at bedside Check posture in mirror often
  2. The quickest and easiest way to comprehend internal locking constructs is by using the external fixator as an analogy. A internal locking construct is very similar to a “low profile” internal ex-fix. The main difference between the two is that the internal locking construct is positioned closer to the bone surface to increase position holding strength, and to also offset the bending moments and stress an ex-fix is typically exposed to when in use. In addition to this analogy, we should bring to your attention terms such as ‘fixed position constructs,’ “fixed angle devices”, “locking screw and locking plate constructs”, all of these are frequently used to describe internal fixators. Incidentally fixed angle devices are not a new concept. Can anyone name a few? Blade plates, Dynamic hip screws Dynamic condylar screws With all this in mind, often the question arises…. Is an internal fixator any better than conventional plating? What are the benefits?
  3. Liegt die herkömmliche Platte im Bereich der Schrauben nicht gut am Knochen an, kann es zum belastungsbedingten Abkippen kommen
  4. To achieve fixed angles, a locking screw for an internal fixator incorporates one critical design feature, threads on the head of the screw. This is the main difference between standard cortex screws and locking screws. These threads screw into a matching thread on a plate when inserted. However, other enhancements are also evident in specific locking screw designs, namely a larger core diameter (for resisting bending loads), a tighter thread pitch and a radial preload similar to that of the AO self drilling and tapping Schanz screw used in external fixators. Locking screws can be both bicortical and unicortical. however screws which are used in a unicortical manner, can feature self-drilling and self tapping tips.