The well-developed endoplasmic reticulum of osteoblasts readers them well

suited to the synthesis of protein and the production of cartilage. By contrast,

osteoclasts are well endowed with lysosomes, suggesting their abilities for
catalytic and hydrolytic breakdown. Both types of cells share a rich complement
of mitochon-dria, indicative of high levels of metabolic activity in both cell types.

Osteocytes demonstrate a limited ability to synthesize collage and resorb

bone, although certainly not to the magnitude that osteoblasts and osteoclasts can
perform these respective functions. The osteocyte also exerts some influence over
bone mineralization. Contrary to earlier notions of osteocyte function, this cell is
not inert or dormant (Gamble, 1988). The management of various metabolic bone
diseases and disuse bconditions may become more exact as more is learned about
the osteocyte.

PHYSIOLOGIC PROCESSES IN THE SKELETAL SYSTEM

Five physiologic processes that occur within the skeletal system have been
identified. Each of these basic processes serves a defined purpose for bone.

Growth
Growth is a process that results in an increase in a tissues volume. The process is
modulated by the endocrine system and influenced by genetic (phenotype) and
environmental (climate, nutrition) factors. Growth is the process that allows the
individual to achieve adult body size.

Being a tubular structure, bone achieves circumferential growth by bone

formation (osteoblastic activity) on the outer surface, whereas bone resorption
(osteoclastic activity) accurs on the inner surface. During the process, bone cortex
becomes thicker and stronger. Longitudinal growth, is achieved through the
epiphyseal growth plate, whereby new bone tissue is laid down on existing bone
tissue. Longitudinal growth usually continues in girls until age 15 and boys until
16. However, bone maturation and shaping continue until age 21 in both sexes.
 Bone formation begins during the second month of fetal life. Long bones in
the fetus begin growing when diaphyseal perichondrium (the outer covering of
cartilage cells) converts to an osteoblastic layer of tissue (now periosteum). This
periosteum gradually becomes vascularized, and bone tissue is laid down along
this outer layer, creating a primary ossification center. Hence, this bone nucleus
represented by the ossification center gradually expands. For the most part, this
same process occurs near either end of the developing cartilaginous bone. At
birth, what remains is a shaft of bone covered at both ends by a large mass of
cartilage cells, which will differentiate into cartilage, epiphysis, and epiphyseal
growth plate.

Modeling
Modeling refers to the architectural patterning or organizing of tissue that occurs
simulationeous with growth, thus influencing the shape of a bone. This process is
influenced by the type and nature of forces applied to the bone because from
follows function. A slight deformation in bone initiates electric events (which are
too low in intensity for the body to sense) that mediate osteoblastic activity. The
bone produced is structured to resist forces causing the original deformation.
Modeling occurs beginning in embryonic life and lasting through adult life and
serves a biomechanical purpose. Bone may model in responsetoabnormal
environmental forces (e.g.,osteogenesis imperfect Pagets disease, vitamin-
deficiency rickets). The inherent factors here are genetic and fibrous tissue as
well, these same phenomena explain such abnormal conditions as clubfoot, genu
varum and genu valgum, achondroplasia, and scoliosis in the case of cartilage, and
osteogenesis imperfect and structural changes in the hand of a person with an
inflammatory arthritic disease in the case of fibrous tissue.

Remodeling
Remodeling refers to the turnover of bone in mecroscopic packer mediated via
special functional units (also microscopic) so that, qualitatively and quantitatively,
bone remains unchanged. That is, the composition and total mass of the involved
bone are unaffected along microscopically circumscribed areas of simultaneous
resorption and formation. Thus, these two processes obviously must occur in
balance with each other. Remodeling likely represents the mode of repair for
microscopic bone damage, uch as microsfracture. In a sense, the follow-up or
fine-tuning of the modeling process is accomplished through remodeling so that
the physiologic and mechanical integrity of bone can the pathophysiology of adult
acquired (involutional-type II) osteoporosis and osteoalacia.

Repair
Repair is the process that heals gross physical injury to restore function. Repair
represents the macroscopic version of remodeling, a microscopic activity. As is
true in other tissues, repair in bone also server to isolate or confine local threats to
tissue integrity, such as infection, foreign bodies, and various tumors.

Blood-Bone Exchange
Blood-bone exchange is the movement of certain ions, largely electrolyte and
acid-base substances, between blood and the bone tissue via the interstitial fluids.
Hypercalcemia or hypocalcemia can be modulated by bone tissue. Levels of other
ions (e.g., phosphate, sodium) in the blood may be subject to the influence of bone
as well, but to a lesser extent. Bone may also possess limited activity as a buffer
for the body fluids by providing a source of, or reservoir for, hydrogen ions (H + )
when acid-base fluctuations occur. The osteocyte probably plays the major roie
among the various cells in the freeing or depositing of ionic substances.

Besides these physiologic process, another special and unique aspect of the
biochemical nature of bone can be used for intraosseous fluid resuscitation. Bone
marrow contains a dense meshwork of sinusoids that drain into large central
medullary venous channels. These channels exit the bone through emissary and
nutrient veins. Because of this rich network of vascular supply, a technique called
intraosseous infusion may be used to infuse drugs and solutions as rapidly as
those delivered through intravenous access. This technique may be implemented
in emergent situations where venous access cannot be readily obtained.
Resuscitating fluids, as well as antibiotics and drugs,may be administered via the
intraosseous route. This method is used in pediatric and adult patient, but it may
be used only for short-term periods.

BONE ETABOLISM
The knowledge base necessary to practice contemporary orthopaedic nursing
comprehensively is incomplete without some discussion of bone metabolism. This
is particularly relevant at a time when new development of patients with
metabolic bone disease. (For detailed discussion of metabolic bone disease, see
Chapter 15.) Patient care outcomes are enhanced when the nurse has an
understanding of basic bone metabolism and can use this knowledge when
providing patient care.

Bone metabolism is modulated by a variety of systemic hormones. The

complex process of bone replication directly affects the quality of bone matrix.
Bone metabolism is regulated by hormones, polypeptides streroids,and thyroid
hormone. Local biochemical agents, such as growth hormone and prostaglandins,
also affect bone remodeling (Table 6-2).

1,25-Dihydroxyvitamin D (Vitamin D)
Strictly speaking, vitamin D does not fit the description of a vitamin at all.
Instead, it is more appropriately defined as a steroid hormone. The metabolic
pathway for the production of vitamin D is summarized here.
The precursor to vitamin D is often called cholecalciferol (occasionally
designated vitamin D3 ). Cholecalciferol is available from two sources: the diet
and the skin. Dietary sources include dairy products, liver, and fish. In skin
exposed to sunlight, ultraviolet light (a component of sunlight) converts a
derivative of cholesterol into cholecalciferol (a process known as ultraviolet
photolysis).

Cholecalciferol then undergoes two conversions, one in the liver and one in
the kidney, resulting in the biologically active form of vitamin D, known as
calcitriol. To say that vitamin D is now in its biologically active form means that
it can now act as a hormone on its target organs-specifically, the intestine and
skeleton.

Calcitriol exerts its main effect on the intestinal tract, where it promotes
calcium absorption. It also exerts two effects on bone. The first and probably most
familiar is to facilitate mineralization of osteoid. When thin process fails, rickets
and osteomalacia result. The second is to work with parathyroid hormone (PTH)
in the efficient mobilization of calcium from bone. Calcitriol is necessary for
proper PTH function.

Vitamin D is a potent stimulator of osteoclastic bone resorption. Its effect on

calcium is seen in those tissue that metabolize calcium (bone, kidney,and
intestine).

Table 6-2. Biochemical and Physiologic Factors Affecting Bone and Muscle in
the Aging Musculoskeletal System

STIMULATION (FORMATION)
Anabolic steroids
Bone marrow cells
Calcitonin
Chondroitin sulfate
Cytokines and growth factors
Demineralized bone matrix
Electromagnetic fields
Exercise (load bearing)
Growth factor/ hormone
Hyaluronidase
Hyperbaric oxygenation
Insulin
Thyroid hormone
Vitamins A and D
RETARDATION (RESORPTION)
Anemia
Anticoagulants
Diabetes mellitus
Delayed stabilization after fracture
Denervation (secondary to muscle atrophy and loss of type II fast-twitch fibers)
Glucocorticoids
Hypoxemia
Loss of estrogen/ testosterone
Prostaglandins/ leukotrienes

DUAL REGULATION (FORMATION AND RESORPTION)

Hormones
Peptide
Calcitonin
CGRP (calcitonin gene-related pepride)
Parathyroid hormone
Steroid
Vitamins A and D
Estrogen
Testosterone
Thyroid
Glucocorticoid (protein synthesis)