MUSCULOSKELET

AL TISSUES
RESPONSE TO
DISEASES AND
INJURY

INTRODUCTION

BONE

EPIPHYSEAL PLATE

SYNOVIAL JOINTS

SKELETAL MUSCLE

A. 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).
the resultan segment of dead bone an
abnormal condition in itself and incites
further reaction from the surrounding living
tissue
Bone that remains alive can react
abnormal condition (an alternation
deposition or resorption, or both)

to
of

2. Alternation of bone
deposition
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.

Marble Bones

This show an
example of a
generalized
increase in
bone.
Increased
radiographic
density in all
bones

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
metatarsal
hypertrophies.
2. Degenerative Osteoarthritis
Subchondral sclerosis

foot the fifth

Work Hypertrophy of Bones

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. Alternation of 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.

Osteopenia

This is an example of generalized decrease in bone osteoporosis

(Osteopenia).
Decreased radiographic density in all bone

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.The plate to have an 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.

Arachnodactyly, hyperchondroplasia,
Marfans Syndrome

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.

Achondroplasia

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

In a normal Synovial joint the smooth and reciprocally shaped
cartilaginous, painless movement

The joint capsule

sensitiv
e
stretching
Increased fluid pressure

Reaction of articular
cartillage

Limited healing
Ro: width/thickness

Change in the intercellular cement substance

of the matrix &subsequent uncovering
of the collagen fibril

- Rheumatoid arthritis
- Infections
- Ankylosing
- Prolonged immobilization
of synovial joint
- Continous compression
of articular cartillage
- Intra-articular Injections of Hydrocortison

Change in the intercellular

cement substance of
the matrix
&subsequent
uncovering
of the collagen fibril
Premature aging of cartilage
Previous destruction of cartilage
Incongruity

Possibility of healing
and regeneration of articulation

Rest &
Motion

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 &

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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