Outline of Veterinary Skeletal Pathology

Table of Contents Table of Contents Chapter 1, Page 1 Ch 1, p 2 



Outline of Veterinary Skeletal Pathology

Chapter 1 - Bone, Basic Principles

A. Structure and Composition. The shapes of individual bone are genetically determined, but biomechanical forces induced by muscle pull, gravity, and joint function modify the structure in health and disease.
1. Microanatomy. Osseous tissue is a special type of connective tissue. There are three cell types in both compact and cancellous bone:
a. Osteoblasts (figs. Ia-1, Ia-2) are derived from local osteoprogenitor mesenchymal cells and
(1) contain abundant endoplasmic reticulum
(2) have a prominent Golgi apparatus
(3) are responsible for synthesizing osteoid (figs. Ia-2, Ia-3), the unmineralized bone matrix.
b. Osteocytes (figs. Ia-4, Ia-5) are osteoblasts that become embedded in bone matrix as it is being deposited. The cells are found within bone lacunae, and they communicate with each other and the overlying tissue by canaliculi through which they extend tenuous cytoplasmic processes.
c. Osteoclasts (figs. Ia-5, Ia-6) are multinucleated giant cells formed from blood born mononuclear cells.
(1) they are bone resorbing cells found on bone or mineralized cartilage surfaces where they create a special microenvironment by sealing a portion of their cytoplasm to the bone surface.
(2) Here they create an acid environment that assists in removing mineral, and they digest the bone matrix creating a resorption (Howship's) lacunae, which appear as pits along the bone surface.
d. Bone matrix is composed of the following:
(1) type I collagen (figs. Ia-7, Ia-8) is the major fibrous protein in bone and is synthesized by osteoblasts as a procollagen molecule. After cleavage of the procollagen molecule, the soluble tropocollagen undergoes fibrilogenesis.
(2) noncollagenous proteins are synthesized by osteoblasts and play a major role in bone biology. They include bone phosphoporteins, osteonectin, osteopontin, osteocalcin (bone gla-protein), bone proteoglycan, bone morphogenetic protein, bone sialoprotein (fig. Ia-9) and bone proteolipid.
(3) glycosaminoglycans are added as post-transcriptional modifications of collagen or noncollagenous proteins and are thought to help regulate osteoid mineralization.

2. Macroanatomy
a. The skeleton consists of two macroscopic types of bone:
(1) cortical bone or compact bone (figs. Ia-10, Ia-11) makes up the bone cortex that predominates in the long bones of the extremities.
(2) cancellous bone (fig. Ia-10) or trabecular bone predominates in flat bones, and is present in the metaphyses of long bones.
b. Anatomical components of a long bone are:
(1) the epiphysis or the bone's end usually contains a secondary ossification center (fig. Ia-10).
(2) physeal plate (fig. Ia-12) is the cartilaginous region that separates the epiphysis from the metaphysis. Other bone growth areas occur adjacent to articular cartilage (articular-epiphyseal complex cartilage, AE complex (fig. Ia-13) or at bony outgrowths (apophyses).
(3) metaphysis (fig. Ia-12) is the region of transformation of cartilage to bone.
(a) osteoclasts resorb bone on the exterior of the metaphysis to produce a concave surface, cut-back or funnel zone (fig. Ia-14).
(b) osteoblasts add bone between trabeculae of the metaphyseal interior, a process called compaction (fig. Ia-14).
(4) diaphysis (fig. Ia-10) or bone shaft is covered on its external surface by the periosteum and on the internal surface by the endosteum (fig. Ia-15).
c. Bone envelopes (fig. Ia-15) are bone surfaces that have different behavioral and functional properties.
(1)The three bone envelopes are called:
(i) the periosteal envelope which covers the outside surface of bone;
(ii) the endosteal envelope which is divided between the endocortical and trabecular;
(iii) the Haversian envelope that includes Volkmann's canal surfaces.
(2) Properties:
(i) in the normal situation, the turnover sites on the endosteal envelope and the Haversian systems on the inner third (paramedullary) of the cortex are in negative balance;
(ii)Negative balance means that the depth of osteoclastic erosion is greater than the thickness of lamellar bone deposited during formation;
(iii) the sites on the periosteal surfaces are in slightly positive balance, and the outside dimension of bone continues to expand ever so slightly, even in old animals;
(iv) the balance is neutral in the Haversian systems of the external two-thirds of the diaphyseal compacta.

B. Bone development, growth and maturation
1. Development.
a. Long bones increase in length by endochondral ossification.
b. Flat bones (scapula and many bones of the skull) develop by the process of intramembranous bone formation.

2. Growth and maturation.
a. Woven bone (fig. Ia-16) is the initial bone produced during growth, and the collagen fibers are laid down in a disorganized or "basket-weave" pattern. This type of bone also occurs in reactive processes.
b. Mature or lamellar bone (fig. Ia-16) has "plywood-like" orientation of the collagen fibrils that increases structural strength.
c. Bone modeling (fig. Ia-13) is the architectural change (size, structural orientation, contour) that occurs during growth because of coordinated efforts of osteoblasts laying down bone and osteoclasts resorbing bone on separate bone surfaces. In adults, bone modeling activity is greatly diminished.
d. Bone remodeling (fig. Ia-17) is the process by which microscopic packages, which form the basic multicellular unit (BMU) (fig. Ia-17), remove old bone (osteoclastic resorption) and replace it with new bone (osteoblastic formation) without altering the bone's gross structure (fig. Ia-18).
(1) when remodeling activity increases, osteoclastic resorption temporarily increases bone porosity (increased remodeling space).
(2) this process is responsible for the replacement of woven bone with lamellar bone during development.

C. Effects of Mechanical Usage may be seen as differences in bone structure between normal and paralyzed individuals.
1. Growth.
a. Increased mechanical usage increases bone modeling and decreases bone remodeling.
b. The amount of compacta within the cortex increases.
c. The expansion of the marrow cavity is retarded (modeling).
d. The rate of disappearance of spongiosa from the metaphysis decreases (remodeling).
e. This leads to an increased external diameter of the bone, an increase in the cortical bone's cross section, and a dense metaphyseal spongiosa.

2. Adult. Increased mechanical usage conserves the amount of bone that is already present by decreasing remodeling. The age-related expansion of the marrow cavity at the endosteum of the cortex is retarded.


3. Disuse releases the inhibition on bone remodeling, and remodeling activity increases (fig. Ia-19).
a. In the growing animal, bone modeling is depressed. The net result is retardation in the accumulation of compact bone of the cortex, an increased loss in the amount of metaphyseal spongiosa, and a resultant increase in the diameter of the marrow cavity.
b. The outside diameter and the bone cross-sectional area of the bone are reduced.
c. There is less compacta, and the marrow cavity is enlarged.

D. Response to injury.
1. Bone Fracture
a. Types.
(1) simple
(2) comminuted
(3) impacted
(4) infraction
(5) greenstick
(6) stress
(7) pathological
b. Repair stages.
(1) regional acceleratory phenomenon (RAP)(fig. Ia-20) is a general metabolic shift that occurs in the injured region where normal physiologic processes are accelerated.
(2) hematoma. Following fracture, mechanical disruption of blood vessels leads to hemorrhage, and interruption in the blood supply results in necrosis of osteocytes of cortical bone. This extends a variable distance from the fracture site (figs. Ia-21, Ia-22, Ia-23).
(3) inflammation and fibroplasia. An initial inflammatory response follows injury, and there is organization of the initial hematoma and formation of granulation tissue (figs. Ia-24, Ia-25, Ia-26, Ia-27). This process may progress to fibrosis in the case of a nonunion (fig. Ia-28).
(4) during the reparative phase, bone growth and mineralization occur as an external and internal fracture callus is formed.
(a) the retracted periosteum and endosteum are sites where mesenchymal cells migrate into the granulation tissue.
(b) these differentiate to form fibrous tissue or cartilage, and bone is formed by endochondral ossification (figs. Ia-29, Ia-30, Ia-31, Ia-32).
(5) bone remodeling, based on the basic multicellular unit, replaces the injured and necrotic original cortical bone (figs. Ia-33, Ia-34).
(a) remodeling replaces the newly produced woven bone of the callus with lamellar bone.
(b) the size of the callus is diminished with each remodeling cycle (negative bone balance).
(6) bone modeling is the process by which resorption and formation drifts tend to straighten crooked bones (figs. Ia-35, Ia-36). It is of much greater intensity in neonates than in juvenile animals.

2. General Reaction of Bone to Injury. The ways bone responds to injury are limited and similar to those seen during fracture repair.
a. Regional Acceleratory Phenomenon (RAP).
(1) occurs following:
(a) numerous diseases
(b) trauma
(c) denervation
(d) burns
(e) bone infections
(f) neoplasms
(2) the accelerated processes include:
(a) bone tissue perfusion
(b) modeling and remodeling processes
(3) a RAP can be seen as areas of bisphosphonate accumulation,"hot spots", in bone scintigraphy (fig. Ia-37) or as regions of increased bone turnover with fluorochrome bone markers (fig. Ia-38).
(4) the RAP is responsible for the multiple cement lines or mosaic pattern that characterizes certain disease states (fig. Ia-39)
(5) the RAP can often accelerate longitudinal bone growth following fracture, denervation, tumor, or a surgical procedure such as periosteal stripping.
b. Bone Necrosis is most commonly seen following fracture or in association with bone inflammation or bone neoplasms.
(1) aseptic bone necrosis occurs in:
(a) Legg-Calve-Perthes disease of immature, small-breed dogs (See chapter 3)
(b) severe anemia, ischemia due to vascular occlusion
(c) thrombosis or following pancreatic release of lipolytic enzymes.
(2) necrotic bone is characterized histologically by death and disappearance of osteocytes from their lacunae and empty vascular channels (fig. Ia-40).
(3) necrotic bone may be removed completely by the remodeling process, or it may become a sequestrum (isolated), surrounded by reactive bone (involucrum)(fig. Ia-41).
(4) the process of simultaneous removal and replacement of necrotic bone has been called "creeping substitution" (fig. Ia-42).
c. Inflammation and Fibrous Repair of bone is similar to that seen in other organs except that its localization is determined by the vascular supply.
d. Growth and Mineralization.
(1) under pathological conditions woven bone is usually produced (fig. Ia-43); and later this is replaced by lamellar bone during remodeling.
(2) juxtaposed bone (fig. Ia-42) is the deposition of unusually basophilic woven bone on pre-existing viable or necrotic bone. It indicates a sudden disruption of normal surface bone remodeling processes by an overpowering insult or inciting agent.
(3) neoplasia can be considered cell growth where proliferation occurs without adequate control.
e. Modeling.
(1) bone modeling occurs principally during growth, but it continues to a small extent throughout life. Bone modeling-dependent reactions lead to insufficient or excess accumulations of bone.
(2) examples are nutritional osteopenia in young animals and angular limb deformities in foals (discussion to follow).
(3) modeling drifts can be reactivated in adults during the formation of marginal osteophytes that occur in degenerative joint disease (fig. Ia-44). The resorption of bone around a metastatic tumor in bone can be considered a modeling activity.
f. Remodeling is a common pathway by which diverse influences can affect bone structure.
(1) it is the process by which microdamage, induced by biomechanical activity, can be repaired.
(2) it is responsible for maintaining mineral homeostasis when the capacity of the bone surface-canalicular system is over extended.
(3) remodeling-dependent reactions to injury occur in growing animals as the spongiosa is remodeled and in the adult after modeling has slowed.
(4) these include losses or gains in the amount of bone, improper distribution, or bone of abnormal quality.
(5) metabolic bone diseases in adult animals have their major effect on the remodeling sequence. See discussion.

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