Lecture 17: Bone Pathology II Flashcards
What wrong and what cause
congenital cortical hyperosteosis (diaphyseal dysplasia)
Cause: autosomal recessive hereditary disease of newborn pigs
what are the signs of congenital cortical hyperosteosis
thickening of 1 or both forelimbs
Congenital cortical hyperostosis involved abnormal __ formation involving major lone bones. __ and __ bones most severely affected
periosteal bone formation, radius and ulna
piglets with congenital cortical hyperostosis are either __ or __ within first few days of life
stillborn, die
what are chondrodysplasias
primary lesions in the growth cartilage on physis and articular epiphyseal cartilage complex
what is disproportionate dwarfism and what is cause
chondrodysplasia that results in short legs with normal sized heads
Cause: mutation in fibroblast growth factor 4 (FGF4) that cause inappropriate activate of one or more FGFR (3) causing downregulation of chondrocytes proliferation
what is primordial dwarfism
limb length is proportional to head, caused by endocrine disorder- pituitary dwarfism or malnutrition
FGFR3 receptor is expressed by __ and __, not __ and acts as a __ chondrocyte proliferation
resting and proliferating chondrocytes, not hypertrophic chondrocytes, acts as inhibitor of chondrocyte proliferation and terminal differentiation
what is spider lamb syndrome and cause
chondrodyplasia in sheep
Point mutation in FGFR3, removing FGFR3 induced inhibition of chondrocyte proliferation
what breeds are affected by spider lamb syndrome
suffolks and Hampshire
what is pathogenesis of spider lamb syndrome
point mutation in FGFR3–> decreased FGFR3 inhibition of chondrocytes entering hypertrophic phase—> increased length of long bones and presence of multiple secondary ossification centers in epiphyses—> variation in shape, size and orientation of bones
what wrong and cause
spider lamb sheep syndrome
Notice multiple secondary ossification centers
Cause: point mutation in FGFR3
what are osteochondroses
lesions in growth cartilage of young animals, characterized by focal or multifocal failure or delay of endochondral ossification
what is osteochondrosis latent
well demarcated area of necrosis in epiphyseal cartilaged centered on necrotic blood vessels (only visible microscopically)
what is osteochondrosis manifest a
retained necrotic epiphyseal cartilage that is appreciated grossly
what is OCD
lesion at articular epiphyseal cartilage complex that forms a cleft in the necrotic cartilage with subsequent fracture of articular cartilage resulting in cartilaginous or osteochondral flap
identify the different osteochondroses seen in 1-3
- Osteochondrosis latent
- Osteochondrosis manifests
- Osteochondrosis dissects
what are joint mice
cartilage or osteochondral flaps that have fractured/detached from articular surface
how do bone cysts form
osteochondrosis—> necrosis—> cavitation—> subchondral cyst
what wrong
OCD with joint mice
what is rickets and osteomalacia and cause
failure of mineralization with subsequent bone deformities and fractures
Cause: vitamin D or phosphorus deficiency
what is pathogenesis of rickets and osteomalacia
vitamin D deficiency—> hypocalcemia—> stimulates PTH—> renal phosphorus loss enhanced further reducing deposition of calcium in bone—> causing bone pain, pathological fractures, and deformities such as scoliosis and kyphosis
what animals get rickets and what does it affect
growing animals, failure of endochondral ossification, affects bones and epiphyseal cartilage
who gets osteomalacia and what does it affect
adults, soft bone- affects bone only
how would you characterize this lesion, what wrong and what cause
Rachistic rosary- due to rickets- irregular growth plates due to failure of endochondral ossification
what could have caused this in 1yr old steer
Rickets- phosphorus or vitamin D deficiency- pale blue is cartilage extending into bone
what are some causes of fibrous osteodystrophy
- Primary parathyroid adenoma, hyperplasia, carcinoma
- Secondary hyperparathyroidism- renal or nutritional
- Pseudo hyperparathyroidism
Fibrous osteodystrophy is characterized by
widespread osteoclastic resorption of bone and replacement by primitive fibro-osseous tissue resulting in weakened bones
how does increased PTH, renal disease and nutritional deficiency of ca2+ lead to fibrous osteodystrophy/ pathogenesis
stimulation of osteogenic and osteoclast bone resorption—> decrease bone mineralization and replacement by fibro-osseus CT—> weakened bone structure
what could have caused this swelling of mandible and maxilla
fibrous osteodystrophy—> osteoclast activity—> resorption of bone and replaced by fibro-osseous tissue
what is osteitis
inflammation of bone