Ananda yulian Riana sari aditya Diana rahmalia Eman sulaeman

BONE EPIPHYSEAL PLATE SYNOVIAL JOINTS SKELETAL MUSCLE

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)

When an area of bone is completely deprived of its blood suply, its reaction is local death (avascular necrosis of bone).

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.

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)

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

The periosteum and endosteum react to bony injury with localized increased in bone deposition to form callus.

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

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

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.

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.

Synovial joint the smooth and reciprocally shaped cartilagious

sensitive

stretching

Increased fluid pressure

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

Limited healing
Ro: width/thickness Rheumatoid atritis Infections Ankylosing Prolonged immobilization of synovial joint Continous compression of articular cartillage Intra-articular Injections of Hydrocortison

Slowly
Aging

Pheripheral proliferation

Change in the intercellular cement substance of the matrix &subsequent uncovering of the collagen Premature aging of cartilage fibril Previous destruction of cartilage

Pheriperal perichondrium

Rest and motion

R>M

1970( continuous passive motion) Stimulate differentiation of pluropontential mesenchymal cells in subchondral bone, tendon and ligament

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

Fibrous joint capsule and ligament provide stability and undesired movement
Abnormal conditions: undully strecthed and elongated (joint laxity) Becoming tight and shortened (joint contracture)

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

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.

When a given muscle is repeatedly exercised against resistance stronger and larger (work hypertrophy)

Occlusion of arteries supplying muscle whether by persistent traumatic vascular spasm, thrombosis, embolism, or a compartement syndrome, result in ischemic necrosis of the muscle.

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.

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.