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Overview of the Musculoskeletal System
1
Robert Cole and Adrien-Maxence Hespel 2
1 Department of Clinical Sciences, College of Veterinary Medicine, Auburn, AL, USA
2 College of Veterinary Medicine, University of Tennessee, Knoxville, TN, USA

32.1 Juvenile Bone Disease and present with short ears, short tail, and large feet.
Hindlimb abnormalities are often described as a waddling
32.1.1 Hereditary and Congenital gait and this rapidly deteriorates [8].
Musculoskeletal Disease
32.1.2.1 Radiographic Signs
Hereditary and congenital disease of the musculoskeletal Radiographic changes of mucopolysaccharidosis involve
system will usually manifest with clinical signs in the juve- both the axial and appendicular skeleton. The most severe
nile patient. Hereditary metabolic diseases include (but are changes are centered in areas of endochondral ossification
not limited to) storage diseases, osteochondrodysplasia, [7, 9]. These include marked epiphyseal dysplasia of the
congenital hypothyroidism, and hereditary rickets. long bones and vertebral endplates as characterized by
Congenital diseases will include spinal and extremity mal- smaller granular epiphysis and shorter vertebral bodies.
formations [1]. Joint laxity is also common, especially affecting the cox-
ofemoral joints. This laxity combined with the epiphyseal
32.1.2 Storage Diseases changes results in progressive degenerative joint disease
and bridging ventral spondylosis in the spine of older ani-
Lysosomal storage diseases are a rare, often heritable, con- mals [7, 9]. Finally there is shortening of the rostral skull
dition caused by a deficiency in (one or multiple) enzymes leading to a flattened maxilla and malformed or absent
in the lysosomes of cells, or by a failure of enzyme activity front sinuses.
(Figure 32.1) [1–6]. Although there are different types of
lysosomal storage diseases, the most frequently diagnosed
is mucopolysaccharidosis, in which there is a reduction or 32.1.3 Osteochondrodysplasia of Scottish
absence of glycosaminoglycan catabolism. Lysosomal deg- Fold Cats
radation of these mucopolysaccharides is needed for The Scottish fold cat is a pure-bred cat with forward-
normal growth [1, 4]. The lack of glycosaminoglycan deg- folded ears, an outward sign of generalized defective
radation results in the storage of these products in many cartilage formation. Scottish fold osteochondrodysplasia
tissues. The most common types recognized in feline is an inheritable disorder characterized by skeletal
patients are Type I and Type VI [1]. Type I was first recog- changes including short, thick tails and splayed feet [1,
nized in domestic shorthairs while Type VI has only been 10]. The disturbed osteochondral ossification leads to
reported in Siamese. The most pronounced clinical mani- abnormal longitudinal bone growth of the skeleton.
festations involve the musculoskeletal, ocular, neurologic, These cats will, as a result, have shortened and widened
hepatic, and cardiovascular systems [7]. Type I cats are digits as well as vertebrae most noticeable at the tail
characterized by facial dysmorphia with a large head, short base. The affected joints are abnormally stressed, lead-
ears, wide-spaced eyes, and larger than normal body size. ing to degenerative joint disease and new bone forma-
They often have hindlimb gait abnormalities and joint tion at the site of ligament attachment and joint capsule
pain. Type VI cats have hypertelorism and a flattened face insertion. In severe cases, ankyloses will result [1].

Feline Diagnostic Imaging, First Edition. Edited by Merrilee Holland and Judith Hudson.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.