Outline of Veterinary Skeletal Pathology

Ch 1, p 1 Ch 1, p 1 Chapter 2, Page 1 Ch 2, p 2 

Outline of Veterinary Skeletal Pathology

Chapter 2 - Bone - Pathologic Conditions

A. Abnormalities of Bone Growth and Development.
1. General.
a. Causes. Genetic abnormalities, biomechanics, environment, hormones, and nutrition.
b. Definitions.
(1) malformations are structural defects that occur during the embryonic period because of a localized error of development (fig. Ib1-1).
(2) deformities occur as alterations in the size, shape, or structure of bone that was previously normal; these usually arise late in embryonic life or after birth (fig. Ib1-2).

2. Skeletal Dysplasia.
a. (Osteo)chondrodysplasia frequently results in disproportionately short stature.
(1) this is because interstitial expansion of cartilage that is responsible for longitudinal growth is affected more than appositional growth that affects bone width (fig. Ib1-3).
(2) classification based on limb involvement.
(a) rhizomelic- major area of shortening is in the proximal segments of the limbs.
(b) mesomelic- major shortening involves the middle segments of the limbs.
(c) acromelic- Those that primarily affect the digits.
(3) classification based on microscopic anatomy.
(a) hypochondroplasia represents those diseases in which the physeal plate appears well organized and in which regular endochondral ossification occurs.
(i) example- Snorter dwarfism in cattle (figs. Ib1-3, Ib1-4, Ib1-5).
(b) dyschondroplasia represents those diseases characterized by differing forms of disorganization of endochondral ossification (figs. Ib1-6, Ib1-7, Ib1-8).
(i) example- Dexter "bull dog" calves (see bone diseases in cattle).
b. Mucopolysaccharidoses are inherited diseases that usually lead to cellular accumulation of mucopolysaccharides.
(1) there is abnormal catabolism caused by deficient activity of certain lysosomal enzymes.
(2) mucopolysaccharidosis VI (Maroteaux-Lamy syndrome) and VII (Sly syndrome) are seen in cats and dogs and may cause abnormal cartilage and bone development (fig. Ib1-9).
c. Multiple Cartilaginous Exostoses (osteochondroma) (fig. Ib1-10)
(1) protuberances composed of bone and cartilage that arise from bones, at or near epiphyseal cartilage.
(2) the cartilagenous mass is progressively replaced from the base by spongy bone (fig. Ib1-11).
(3) they are seen in man, horse, dog, cat and laboratory animals.
(4) inheritance in man and horse is due to a single autosomal dominant gene.
d. Fibrous Dysplasia is a fibrous replacement of bone containing regularly spaced woven bone trabeculae.
(1) formed by direct conversion of fibro-osseous tissue to bone (osseous metaplasia)(fig. Ib1-12).
(2) lesions may be present in single (monostotic) or multiple (polyostotic) bones.
e. Osteogenesis Imperfecta is a heterogenous group of diseases in which bone collagen is thought to be abnormal.
(1) there is increased bone fragility (figs. Ib1-13, Ib1-14).
(2) there is poor collagen formation in the bone trabeculae, or the bone is composed of woven bone and is hypercellular (figs. Ib1-15, Ib1-16)(see discussion).
f. Osteopetrosis is an autosomal recessive condition in which osteoclasts are abnormal in either their differentiation or function (see discussion).
(1) there is a failure to resorb the primary spongiosa.
(2) the medullary cavity of the diaphysis is filled with cancellous bone (fig. Ib1-17).
(3) clinical features. Two forms are seen in the canine.
(a) the benign (juvenile) form occurs in young adult dogs that are presented to the veterinarian with spontaneous bone fracture or anemia. The external shape of the bone appears normal but the marrow cavity is filled with cancellous bone (figs. Ib1-18, Ib1-19).
(b) the malignant form is seen in many species, and affected animals usually die shortly after birth (fig. Ib1-20).

B. Metabolic Bone Disease. These conditions interfere with normal bone growth and development in the young or with normal bone remodeling in the adult.
1. Definitions. Common lesions (morphologic diagnoses) found in metabolic bone disease.
a. Osteopenia- a general term for reduction in bone mass.
b. Osteosclerosis- too much mineralized trabecular bone.
c. Osteomalacia- defective mineralization of bone matrix.
d. Fibrous osteodystrophy- increased osteoclastic resorption of cortical and trabecular bone with peritrabecular fibrosis.
e. Osteoporosis- reduction in the amount of normally mineralized bone, below what is normal for the animal's age, sex, and species.
f. Abnormal endochondral ossification- usually characterized by inability of the growth-plate cartilage matrix to mineralize properly and by the unusual persistence of hypertrophic cartilage cells.

2. Diseases
a. Rickets.
(1) definition. Abnormal endochondral ossification that is characterized by increased depth of the hypertrophic-cartilage cell zone of the physis and excess osteoid.
(a) it is due to failure to deposit adequate quantities of mineral in the cartilage and bones of growing animals.
(b) osteomalacia is a similar condition in adults where trabecular or Haversian canal bone-forming surfaces have excessively thick osteoid.
(2) pathology.
(a) macroscopic appearance. There is enlargement of the ends of the long bones and costochondral articulations (rachitic rosary) (fig. Ib2-1); bones of the limbs may become permanently bent (valgus deformity or "bow legs"); bones are abnormally soft and can often be cut with a knife; and physeal cartilages are abnormally thick.
(b) microscopic appearance.
(i) Increased depth of the zone of hypertrophic cartilage cells of the physis adjacent to the primary spongiosa of the metaphysis (fig. Ib2-2).
(ii) Disorderly arrangement of the hypertrophic cartilage, as well as a crookedness and irregularity of this zone within the physis from one side of the bone to the other (figs. Ib2-3, Ib2-4).
(iii) Disorderly penetration of the zone of hypertrophic cartilage by blood vessels (fig. Ib2-5).
(iv) Defective calcification and failure of normal degeneration of the cells of hypertrophic cartilage (fig. Ib2-5).
(v) A great excess of uncalcified osteoid in the metaphysis (fig. Ib2-6).
(vi) The marrow areas of the spongiosa tend to be fibrosed with a corresponding reduction of myeloid cells. If secondary hyperparathyroidism in response to hypocalcemia is of sufficient degree, bone resorption and fibrous replacement become features of rickets, and the microscopic appearance, especially in the diaphysis, tends toward that of fibrous osteodystrophy (see next page).

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