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MUSCULOSKELETAL TISSUES RESPONSE

TO DISEASES AND INJURY


INTRODUCTION

BONE
EPIPHYSEAL PLATE
SYNOVIAL JOINTS
SKELETAL MUSCLE
I. BONE
There are just 4 basic ways in which bone can react to
abnormal conditions:
1. Local death
2. Alteration of bone deposition
3. Alteration of bone resorption
4. Mechanical failure (fracture)
1. Local Death

When an area of bone is completely deprived of its blood


suply, its reaction is local death (avascular necrosis of bone).
2. Bone deposition greater than
bone resorption
A. Generalized Reactions
1. Osteopetrosis (Marble bones)
Bone deposition is normal but bone resorption is
defective.
2. Acromegaly
Bone deposition is increase by excessive
intramembranous ossification from the
periosteum.
2. Bone deposition greater than
bone resorption
B. Localized Reactions:
1. Work Hypertrophy
The bone react to the extra stresses and strain of
increased function by increased bone deposition.
Varus deformity of the foot the fifth
metatarsal hypertrophies.
2. Degenerative Osteoarthritis
Subchondral sclerosis
3. Fractures
The periosteum and endosteum react to bony injury with
localized increased in bone deposition to form callus.
4. Infection
The periosteum reacts to infection by deposition of new
bone.
5. Osteosclerotic Neoplasm
Osteoid osteoma (benign neoplasm)
Osteosarcoma (malignant neoplasm)
3. Bone deposition less than bone
resorption
A. Generalized Reactions
1. Osteoporosis
Bone deposition is decreased because of decreased
formation of matrix and resorption is increased.
Examples: osteogenesis imperfecta, disuse
osteoporosis, steroid induced osteoporosis,
postmenopausal osteoporosis.
2. Rickets in Children and Osteomalacia in Adults
Although the osteoblastic formation of matrix is normal,
there is decreased calcification (hypocalcification) of
the matrix with a resultant decreased in the
amount of calcified bone.
B. Localized Reactions
1. Disuse Atrophy (disuse osteoporosis)
Decreased bone deposition whereas the bone resorption
continues unchanged.
2. Rheumatoid Arthritis
The bone reacts to the periarticular soft tissue
inflammation of RA by decreased bone deposition and
possibly increased bone resorption.
Decreased in functiondisuse atrophy
4. Mechanical Failure of Bone
(Fractures)
The periosteum and endosteum react to bony injury with
localized increased in bone deposition to form callus.
II. EPIPHYSEAL PLATES
Normal growth requires:
1. intact structure and a normal blood supply
2. intermittent pressures normal physical activity.
There are just 3 ways in which an epiphyseal plate can react:
1. increased growth
2. decreased growth
3. torsional growth
1. Increased in Growth
A. Generalized
1. Arachnodactyly (Hyperchondroplasia) (Marfan`s
Syndrome)
There is excessive cartilaginous growth
(hyperchondroplasia) in all epiphyseal plates.
2. Pituitary Gigantism
Excessive growth hormone from an eosinophilic adenoma
of the anterior pituitary gland.
B. Localized
1. Chronic Inflammation
The prolonged hyperemia stimulates local
growth, such as chronic osteomyelitis and
rheumatoid arthritis.
2. Displaced Fracture of the shaft of a Long Bone
The nutrient artery to the shaft of a long bone is
disrupted a temporary compensatory hyperemia
at the epiphyseal ends.
3. Congenital Arteriovenous Malformations
The continuing hyperemia stimulation the
epipheseal plates.
2. Decreased in Growth
A. Generalized
1. Achondroplasia
There is deficient cartilaginous growth
2. Pituitary Dwarfism (Lorain type)
Deficient growth hormone
3. Rickets
Hypocalcification of the preosseus cartilage of the
epiphyseal plate in the zone of calcifying cartilage.
B. Localized
1. Disuse Retardation
2. Physical Injury
Fracture local cessation of growth
3. Thermal Injury
Epiphyseal plate is sometimes destroyed either by
local cold (frostbite) or by local heat (burns).
4. Ischemia
5. Infection
Chondrolytic action of pus destroy epiphyseal plate.
3. Torsional Growth
When a growing long bone and its epiphyseal plate are
subjected to either continual or intermittent twisting forces,
the bone gradually becomes twisted.
The torsional deformity in the long bones occurs through
torsional growth in the involved epiphyseal plate and can
ussualy be reversed by applying corrective torsional force in
the opposite direction.
III. SYNOVIAL JOINTS
Synovial joint the smooth and reciprocally shaped
cartilagious
sensitive

stretching

Increased fluid pressure


Reaction of articular cartillage
Blood vessels, lymphatic,nerve

Abnormal condition in 3 ways

Destruction Degeneration Pheripheral


proliferation
Limited healing Slowly
Ro: Aging
width/thickness
Change in the intercellular cement
substance of the matrix
&subsequent uncovering of the
Abnormal condition in 3 ways

Destruction Degeneration
Pheripheral
proliferation
Slowly
Limited healing
Aging Pheriperal
Ro:
width/thickness perichondrium
Rheumatoid atritis Change in the
intercellular
Infections
cement
Ankylosing substance of
Prolonged immobilization the matrix
of synovial joint &subsequent
Continous compression uncovering of
of articular cartillage the collagen
Premature
fibril aging of cartilage
Intra-articular Injections
of Hydrocortison Previous destruction of
cartilage
Possibility of healing and
regeneration of articulation

Rest and motion R>M

1970( continuous passive motion)


Stimulate differentiation of pluropontential
mesenchymal cells in subchondral bone, tendon and
ligament
Reaction of Synovial Membrane
Nutrition and lubrication

Abnormality 3ways

An effusion
Hypertrophy
By forming adhesions between itself and the
articular cartilage
Joint effusion:
a. serous: mild sprain
b. inflammatory exudate: synovitis and RA
c. grossly purulent: septic arthritis
d. hemorrhagic: severe injury or hemophilia
Reaction of joint capsule and
ligament

Fibrous joint capsule and ligament provide stability and


undesired movement

Abnormal conditions:
undully strecthed and elongated (joint laxity)
Becoming tight and shortened (joint contracture)
IV. SKELETAL MUSCLE
The skeletal muscle reacts to many disorders and injuries in a
limited number of ways including:
1. atrophy
2. hypertrophy
3. necrosis
4. contracture
5. regeneration
1. Disuse Atrophy

Skeletal muscle that is not used normally, reacts by becoming


weaker and smaller.
Disorders of the anterior horn cell (poliomyelitis), the
peripheral nerve fiber (polyneuritis), the myoneural junction
(myasthenia gravis)disuse atrophy.
2. Work Hypertrophy

When a given muscle is repeatedly exercised against


resistance stronger and larger (work hypertrophy)
3. Ischemic Necrosis

Occlusion of arteries supplying muscle whether by persistent


traumatic vascular spasm, thrombosis, embolism, or a
compartement syndrome, result in ischemic necrosis of the
muscle.
4. Contracture
If muscle remains in a shortened state for a prolonged period
persistent shortening (muscle contracture).
Polymyositis, muscular dystrophy, and cerebral palsy.
Muscle fibers of a necrotic muscle are subsequently replaced
by dense fibrous scar tissue (fibrous contracture) joint
deformities.
5. Regeneration

Injured muscle fibers may regenerate (sarcolemma, muscle


cells, satellite cells).
Partial loss of innervation in a skeletal muscle gain a new
motor nerve fiber from the remaining intact nerve fibers.
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