REVIEW OF SKELETAL

SYSTEM
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 SKELETAL SYSTEM
• Function:
• Protection
• Hematopoiesis
• Mineral homeostasis
• Calcium
• Phosphorus
• Carbonate
• Magnesium

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 STRUCTURE

• Bone is a connective tissue:

• Matrix
• Collagen fibers for flexibility and tensile
strength
• Calcium for rigidity
• Hydroxyapatite Ca5(PO4)3OH

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• Cells:
• Osteoblast
• Form organic components of matrix
• Osteocyte
• Osteoblasts
• From monocytes
• Secrete citric and lactic acids
• Collagenases and other enzymes
• Stimulated by Paratyroid Hormone
• Inhibited by Calcitonin

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 TYPES OF BONE

• Dense or Compact (85%)

• Osteon (Haversian System)
• Central (Haversian) canal
• Lamellae
• Lacunae with osteocytes
• Canaliculi

• Spongy (cancellous) bone (15%)

• Trabeculae

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 PERIOSTEUM

• Outer layer is dense, Irreguler CT with nerves and blood

vessels
• Inner layer
• Osteoblasts
• Anchored to bone by collagen fibers that penetrate into bone

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 JOINTS

• Degree of movement
• Synarthrosis – immovable joint
• Amphiarthrosis – slightly movable joint
• Diarthrosis – freely movable joint

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• Synovial joints
• Joint capsule
• Fibrous CT
• Tendons and ligaments
• Nerves, blood and lymph vessels
• Synovial membrane
• Loose fibrous CT
• Many blood vessels – good repair
• Joint (synovial) Cavity

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• Synovial fluid
• Plasma filtrate
• Synovial cells and leukocytes phagocytize
debris and microbes
• Articular cartilage
• Reduce friction
• Distribute force

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 BONE PATHOPHYSIOLOGY
• Inherited conditions:
• Osteogenesis imperfecta
• Inherited defect in collagen synthesis
• Osteopenia and brittle bones
• Often- defective tooth formation, blue sclera,
faulty hearing, other defects
• Inheritance can be dominant, recessive or by new
mutation
• Several degrees of severity ( I,II,III,IV)
• Biphosphate treatment can improve bone mass in
all types of the disorder
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• Achondroplasia
• Involves a defect in normal cartilage development
• Epiphyseal plates close early in long bones; individual has short arms
and legs, but normal spine and skull
• Dominant inheritance, but frequent new mutations
• Other organs develop normally
• Individuals live a normal lifespan

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 ACQUIRED DISORDERS
• Osteoporosis – “porous bone”
• Most common metabolic bone disease in North America
• Can be attributed to genetics, diet or hormones
• Most osteoporosis is idiopathic osteoporosis
• Bone loss due to an identifiable cause is secondary osteoporosis
• Bone tissue is mineralized normally, but over time the structural integrity
of bone is lost and it becomes thinner and weaker, and more prone to
fractures.

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• Key features: bone fracture and the associated pain.
• WHO defines osteoporosis by bone density:
• Normal bone > 833 mg/cm2
• Osteopenia 833 to 648 mg/cm2
• Osteoporosis < 648 mg/cm2
• Can be generalized, involving major portions of the axial
skeleton
• Can be regional, involving one segment of the appendicular
skeleton

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• Remodeling is constant
• Teen years more bone is laid down than reabsorbed
• Peak bone mass or maximum density reached at around 30 years of age
• After age 30, bone is reabsorbed faster than it is laid down (loss of
about 0.7% /year)
• In women, bone loss is most rapid in the first years after menopause, but
continues throughout postmenopausal years
• Est. 55% of people over 50 have osteoporosis or low bone mass.

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• Men also lose bone density, but start out with more bone mass
so takes longer.
• By age 90 about 17% of males have had a hip fracture, vs. 32
% of females
• Vertebral fractures also occur → kyphosis
• Most common in whites, but affects all races.
• African Americans have about half the fracture rates of whites
(higher peak bone mass)

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 RISK FACTORS
• Family history
• White race
• Increased age
• Female sex
• Small stature
• Fair or pale skin
• Thin build
• Early menopause (natural or surgical)
• Late menarche

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 RISK FACTORS CONT.
• Nulliparity
• Obesity
• Weight below a healthy range
• Acidosis
• Low dietary calcium and vitamin D
• High caffeine intake
• Sedentary life style
• Smoker
• Excessive alcohol consumption
• Liver, kidney disease, rheumatoid arthritis, etc.

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• Often progresses silently for decades until fracture occurs
• Bones can fracture spontaneously
• Most severe in spine, wrist and hips
• Estrogens and androgens may be factors in both sexes
• Testosterone is converted into estrogen in peripheral tissues and
decreases bone loss
• Rapid bone loss is osteoclast mediated
• Slow bone loss is osteoblast mediated

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 CLINICAL MANIFESTATIONS
• Pain and bone deformity
• Kyphosis caused by vertebral collapse
• Fractures of long bones
• Fatal complications include fat or pulmonary embolism,
pneumonia, hemorrhage and shock
• 20 % die as a result of surgical complications

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 TREATMENT
• No known cure
• Slow bone loss and promote bone deposition
• Calcium and vitamin D supplements
• Nasal or subcutaneous calcitonin
• Hormone replacement therapy
• Biophosphates – inhibit osteoclasts
• Dual x-ray absorptiometry for diagnosis
• PREVENTION

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 PREVENTION
• Intake of calcium, vitamin D, magnesium and possibly boron
• Regular, weight-bearing exercise
• Avoid tobacco and glucocorticoids
• No alcoholism
• Hormone replacement?
• Parathyroid hormone?
• Testosterone for men and possibly women

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 RICKETS AND OSTEOMALACIA
• Inadequate mineral deposition in essentially normal organic
matrix
• Softened bone:
• Subject to malformation and distortion –pain

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 RICKETS
• Dietary vitamin D deficiency causes inadequate mineralization
of the developing skeleton in infants and children
• Rarely seen in Western nations
• Poverty
• Ignorance
• Bones are soft and easily deformed
• Tendency to fractures
• Therapy: supply vitamin D and calcium

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WWW.TALKORIGINS.ORG/FAQS/HOMS/RICK
ETS.HTML
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 OSTEOMALACIA
• Rarely due to vitamin D deficiency
• Usually GI malabsorption, renal defect or chronic kidney or
liver diseases.
• Elderly often affected due to inadequate diet or lack of outdoor
activity
• May accompany and complicate osteoporosis.

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 JOINT DISORDERS
• Osteoarthritis
• Most common joint disease in North America
• Minimal inflammatory component
• Differentiated from inflammatory disease by:
• Absence of synovial membrane inflammation
• Lack of systemic signs and symptoms
• Normal synovial fluid
• Much of the pain and loss of mobility associated with aging.

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 OSTEOARTHRITIS
• Incidence increases with age: 85% of people age 65 have some joint
degeneration
• Incidence similar, but women more severely affected
• Exceptional stress on joints: gymnasts, etc.
• Biochemical defect in cartilage
• Malformed joint, obesity and postural defects
• Genetic component
• Torn ACL or meniscectomy

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 OSTEOARTHRITIS
• When associated with known risk factors it is secondary OA
• No risk factors – idiopathic OA
• Pathological characteristics:
• Erosion of the articular cartilage
• Sclerosis of subchondral bone
• Formation of bone spurs or osteophytes

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 OSTEOARTHRITIS
• Begins in articular cartilage
• Yellow-grey or brownish gray
• Thin, irregular, frayed
• Cracks or fissures develop (fibrillation)
• Fluid filled cysts may form
• Microfractures of subchondral bone
• Formation of fibrocartilage repair plugs
• Bone surface exposed
• Bone responds by becoming dense and hard

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 OSTEOARTHRITIS
• Synovial membrane is indirectly affected
• Fragments of fibrocartilage cause inflammation –pain
• Fibrous repair of joint capsule restricts motion
• Osteophytes form – pain and loss of motion
• Joint mice

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 OSTEOARTHRITIS
• Affects one or more weight-bearing joints
• Hand, wrist, lower cervical spine, lumbar spine and sacroiliac, hip, knees,
ankles, feet
• Aches and stiffness
• Symptoms increase with activity; diminish with rest
• Usually no swelling or redness of adjacent tissues
• Sometimes nocturnal pain – may be referred

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 OSTEOARTHRITIS
Primary signs and symptoms of joint disease are:
pain, stiffness, enlargement or swelling, tenderness, limited
range of motion, muscle wasting, partial dislocation, and
deformity, crepitus

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 OSTEOARTHRITIS
• Evaluation made through clinical assessment and radiologic
studies, CT scan, arthroscopy and MRI
• Treatment:
• Glucosamine may decrease pain and slow or stop progression
– 1500 mg/day
• Chondroitin sulfate – questionable absorption

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 OSTEOARTHRITIS
• Analgesics and antiinflammatory drugs (NSAIDs)
• Injections of corticosteroids or sodium hyaluronate (to
improve lubrication)
• Range of motion exercises
• Reduce aggravating factors
• Weight loss
• Use of cane, crutches or walker
• Surgical removal of bone spurs, and other
• Replacement of joint

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 OSTEOSARCOMA

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08/25/20
 DEFINITION

• Osteosarcoma is an aggressive malignant neoplasm arising

from primitive transformed cells of mesenchymal origin (and
thus a sarcoma) that exhibit osteoblastic differentiation and
produce malignant osteoid.
• It is the most common histological form of primary bone
cancer in age 12-25yrs.

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 EPIDEMIOLOGY

• Male more than female

• at any age but
75% of cases appear at age 12-25yrs

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 RISK FACTORS:

•Radiation exposure

•Patients who survive after taking therapy for

another Cancer.

•Retinoblastoma(malignant tumor arising from retina

of eye).

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 SITES OF PREDLECTION:

• Osteosarcoma :It originates more frequently in the

metaphyseal region of tubular long bones, with 42% occurring
in the femur

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SKELETAL DISTRIBUTION : MOST
COMMON AT KNEE REGION

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OSTEOSARCOMA

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 CLINICAL PRESENTATION

• Painful mass arising from bone

• Metastasize early

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 OSTEOSARCOMA :
IT IS FORMED OF SPINDLE SHAPED CELLS SHOWING MALIGNANT
CRITERIA IN FORM OF PLEOMORPHISM,HYPERCHROMASIA,
ABNORMAL MITOSIS, GIANT CELLS . IN BETWEEN SPINDLE CELLS
THERE IS MALIGNANT OSTEOID.

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 TNM GRADING
• T categories of bone cancer
• T0: There is no evidence of a main (primary) tumor.
• T1: The tumor is 8 cm (around 3 inches) across or less.
• T2: The tumor is larger than 8 cm across.
• T3: The tumor has “skipped” to another site or sites within the same bone.
• N categories of bone cancer
• N0: The cancer has not spread to regional (nearby) lymph nodes.
• N1: The cancer has spread to nearby lymph nodes.
• M categories of bone cancer
• M0: There is no spread (metastasis) to distant organs.
• M1a: The cancer has spread only to the lung.
• M1b: The cancer has spread to other distant sites in the body.

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 THE STAGE
• Stage IA
T1, N0, M0, G1 or G2 (or GX): The tumor is 8 cm across or less and is low grade (or the grade can’t be
assessed). It has not spread to nearby lymph nodes or to distant parts of the body.
• Stage IB
T2-T3, N0, M0, G1 or G2 (or GX): The tumor is larger than 8 cm across or has “skipped” to other sites in
the same bone. It is low grade (or the grade can’t be assessed). It has not spread to nearby lymph nodes or
to distant parts of the body.
• Stage IIA
T1, N0, M0, G3 or G4: The tumor is 8 cm across or less and is high grade. It has not spread to nearby lymph
nodes or to distant parts of the body.
• Stage IIB
T2, N0, M0, G3 or G4: The tumor is larger than 8 cm across and is high grade. It has not spread to nearby
lymph nodes or to distant parts of the body.
• Stage III
T3, N0, M0, G3 or G4: The tumor has “skipped” to other sites in the same bone. It is high grade. It has not
spread to nearby lymph nodes or to distant parts of the body.
• Stage IVA
Any T, N0, M1a, any G: The tumor has spread only to the lungs. It has not spread to the lymph nodes or to
other distant sites. (It can be any size or grade.)
• Stage IVB (if either of these applies)
Any T, N1, any M, any G: The tumor has spread to lymph nodes. It can be any size or grade, and might or
might not have spread to other distant sites.
Any T, any N, M1b, any G: The tumor has spread to distant sites other than the lung. It can be any size or
grade.

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ANATOMIC DESCRIPTION - TYPE

• Type is the overall

fracture pattern
• Examples are:
• Simple
• Spiral
• segmental
 ANATOMIC DESCRIPTION -
COMMUNITION
• Comminution is the measure of the number of pieces of
broken bone that there are.
• Examples are: non-comminuted or mildly comminuted or
severely comminuted
ANATOMIC DESCRIPTION - LOCATION

• Location is the anatomic location of the fracture usually

described by giving the bone involved and location on the
bone
• Examples are: distal radial shaft, proximal 1/3 humeral shaft,
intra-articular distal tibial
 ANATOMIC DESCRIPTION -
DISPLACEMENT
• Displacement is the amount the pieces of a fracture have
moved from their normal location
• Can be displaced or non-displaced
• Subdivided into 3 sub-categories: translation, angulation, and
shortening
DISPLACEMENT - TRANSLATION

• Translation is
sideways motion of
the fracture - usually
described as a
percentage of
movement when
compared to the
diameter of the bone.
 DISPLACEMENT - ANGULATION

• Angulation is the
amount of bend at a
fracture described in
degrees. Described
with respect to the apex
of the angle or with
respect to direction of
distal fragment.
 DISPLACEMENT - SHORTENING

• Shortening is the
amount a fracture is
collapsed expressed in
centimeters.
Sometimes called
bayonette apposition.
 WHY CLASSIFY FRACTURES?

• Classification or description of fractures is only used when the

classification or description is useful in providing treatment or
outcomes
 OPEN FRACTURES - GRADE 1

• wound less than 1 cm w/ minimal soft tissue injury

• wound bed is clean
• bone injury is simple w/ minimal comminution
• w/ IM nailing, average time to union is 21-28 weeks
 OPEN FRACTURES - GRADE 2

• wound is greater than 1 cm w/ moderate soft tissue injury

• wound bed is moderately contaminated
• fracture contains moderate comminution
• w/ IM nailing, average time to union is 26-28 weeks
 OPEN FRACTURES - GRADE 3A

• wound greater than 10 cm w/ crushed tissue and

contamination
• soft tissue coverage of bone is usually possible
• w/ IM nailing, average time to union is 30-35 weeks
 OPEN FRACTURES - GRADE 3B

• wound greater than 10 cm w/ crushed tissue and

contamination
• soft tissue is inadequate and requires regional or free flap
• w/ IM nailing, average time to union is 30-35 weeks
 OPEN FRACTURES - GRADE 3C

• is fracture in which there is a major vascular injury requiring

repair for limb salvage
• fractures can be classified using the MESS
• in some cases it will be necessary to consider BKA following
tibial fracture
 FRACTURE HEALING

• Reparative process of self-healing (union) occurs in the

following stages:
1. Fracture hematoma (d/t bleeding, edema)
2. Granulation tissue → osteoid (3 – 14 days
post injury)
3. Callus formation (minerals deposited in
osteoid)
 FRACTURE HEALING

• Reparative process of self-healing (union) occurs in the

following stages:
4. Ossification (3 wks – 6 mos)
5. Consolidation (distance between fragments
decreases → closes).
6. Remodeling (union completed; remodels to
original shape, strength)
BONE HEALING

Fig. 61-7