Osteoporosis in swine

Lorenzett, Marina P.; Cecco, Bianca S.; Bianchi, Matheus V.; Cruz, Raquel A.S.; Linhares, Daniel C.L.; Guedes, Roberto M.C.; Driemeier, David; Pavarini, Saulo P.

doi:10.1590/1678-5150-PVB-7068

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Livestock Diseases • Pesq. Vet. Bras. 42 • 2022 • https://doi.org/10.1590/1678-5150-PVB-7068 linkcopy

Osteoporosis in swine

Osteoporose em suínos

Authorship SCIMAGO INSTITUTIONS RANKINGS

ABSTRACT:

Forty-six pigs presented muscle weakness, hind limb paresis and paralysis, weight loss, lateral recumbency, and death in a clinical course of 7 to 10 days. Two pigs were necropsied and exhibited bone fragility, bone callus formation, and multiple fractures in the limbs, ribs, and vertebrae. Microscopically, there was a diffuse and marked decrease in thickness and number of trabeculae. These were disconnected, with a “free-floating” appearance, while the cortex of the long bones was thinned, with an increase of the cortical porosity by enlargement of Haversian canals and endosteal erosion and decreased osteoblastic activity. Flame atomic absorption spectrometry in liver samples revealed significant zinc overload (>2300ppm) and copper deficiency (<33.1ppm). In this communication, we present the first pathologic description of an outbreak of osteoporosis in pigs, and we also provide a brief review of metabolic bone diseases in pigs.

INDEX TERMS:
Swine; bone diseases; bone fragility; metabolic disorder; zinc; copper

Authorship

person Marina P. Lorenzett

schoolSetor de Patologia Veterinária, Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul (UFRGS), Av. Bento Gonçalves 9090, prédio 42505, Porto Alegre, RS 91540-000, Brazil.Universidade Federal do Rio Grande do SulBrazilPorto Alegre, RS, BrazilSetor de Patologia Veterinária, Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul (UFRGS), Av. Bento Gonçalves 9090, prédio 42505, Porto Alegre, RS 91540-000, Brazil.

0000-0002-9551-3399

person Bianca S. Cecco

0000-0003-4827-4011

person Matheus V. Bianchi

0000-0002-3951-0038

person Raquel A.S. Cruz

schoolInstituto de Biociências, Universidade Federal do Mato Grosso do Sul (UFMS), Campo Grande, MS, Brazil.Universidade Federal do Mato Grosso do SulBrazilCampo Grande, MS, BrazilInstituto de Biociências, Universidade Federal do Mato Grosso do Sul (UFMS), Campo Grande, MS, Brazil.

0000-0002-5885-4178

person Daniel C.L. Linhares

schoolCollege of Veterinary Medicine, Iowa State University, Ames, IA, USA.Iowa State UniversityUSAAmes, IA, USACollege of Veterinary Medicine, Iowa State University, Ames, IA, USA.

person Roberto M.C. Guedes

schoolDepartamento de Clínica Veterinária e Cirurgia, Escola de Veterinária, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG, Brazil.Universidade Federal de Minas GeraisBrazilBelo Horizonte, MG, BrazilDepartamento de Clínica Veterinária e Cirurgia, Escola de Veterinária, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG, Brazil.

person David Driemeier

0000-0003-3766-0654

person Saulo P. Pavarini *

0000-0001-8980-6294

person*Corresponding author:
emailsauloppvet@yahoo.com.br

Conflict of interest statement.- The author’s declare no conflict of interest.

SCIMAGO INSTITUTIONS RANKINGS

Setor de Patologia Veterinária, Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul (UFRGS), Av. Bento Gonçalves 9090, prédio 42505, Porto Alegre, RS 91540-000, Brazil.Universidade Federal do Rio Grande do SulBrazilPorto Alegre, RS, BrazilSetor de Patologia Veterinária, Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul (UFRGS), Av. Bento Gonçalves 9090, prédio 42505, Porto Alegre, RS 91540-000, Brazil.

Instituto de Biociências, Universidade Federal do Mato Grosso do Sul (UFMS), Campo Grande, MS, Brazil.Universidade Federal do Mato Grosso do SulBrazilCampo Grande, MS, BrazilInstituto de Biociências, Universidade Federal do Mato Grosso do Sul (UFMS), Campo Grande, MS, Brazil.

College of Veterinary Medicine, Iowa State University, Ames, IA, USA.Iowa State UniversityUSAAmes, IA, USACollege of Veterinary Medicine, Iowa State University, Ames, IA, USA.

Departamento de Clínica Veterinária e Cirurgia, Escola de Veterinária, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG, Brazil.Universidade Federal de Minas GeraisBrazilBelo Horizonte, MG, BrazilDepartamento de Clínica Veterinária e Cirurgia, Escola de Veterinária, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG, Brazil.

Figures | Tables

Figures (2)
Tables (1)

Thumbnail

Fig.1-4. Gross features of osteoporosis in pigs associated with zinc overload and copper deficiency. (1) Several ribs present fractures near the costochondral junction and are surrounded by hemorrhage. (2) The femur exhibits a comminuted complete fracture and is surrounded by hemorrhage and edema (Pig 1). (3) Two vertebrae have complete transverse fractures, whereas other vertebrae are markedly shortened, indicating previous fractures. (4) The vertebrae show marked depletion of cancellous bone and formation of transverse reinforcement trabeculae.

Thumbnail

Fig.5-10. Microscopical features of osteoporosis in pigs associated with zinc overload and copper deficiency. (5) The bone trabeculae of the vertebrae are reduced, both in thickness and in number, and are disconnected, with the appearance of “free-floating trabeculae”. There is also a moderate decrease of hematopoietic cells. HE, obj.10x. (6) Normal bone (vertebrae) appearance of control pig shows trabeculae connected to each other and hematopoietic cells in regular numbers. HE, obj.10x. (7) The cortex of long bones is severely thinned, with an increase of the cortical porosity by the enlargement of Haversian canals and by endosteal erosion. HE, obj.20x. (8) Normal bone (vertebrae) appearance. HE, obj.20x. (9) A rib section shows a moderate decrease of osteoblasts, indicating reduced osteoblastic activity. HE, obj.20x. (10) Normal bone (rib) appearance shows regular osteoblastic activity. HE, obj.20x.

Thumbnail

Table 1. Metabolic disease in growing/adult pigs

imageFig.1-4. Gross features of osteoporosis in pigs associated with zinc overload and copper deficiency. (1) Several ribs present fractures near the costochondral junction and are surrounded by hemorrhage. (2) The femur exhibits a comminuted complete fracture and is surrounded by hemorrhage and edema (Pig 1). (3) Two vertebrae have complete transverse fractures, whereas other vertebrae are markedly shortened, indicating previous fractures. (4) The vertebrae show marked depletion of cancellous bone and formation of transverse reinforcement trabeculae. open_in_new

imageFig.5-10. Microscopical features of osteoporosis in pigs associated with zinc overload and copper deficiency. (5) The bone trabeculae of the vertebrae are reduced, both in thickness and in number, and are disconnected, with the appearance of “free-floating trabeculae”. There is also a moderate decrease of hematopoietic cells. HE, obj.10x. (6) Normal bone (vertebrae) appearance of control pig shows trabeculae connected to each other and hematopoietic cells in regular numbers. HE, obj.10x. (7) The cortex of long bones is severely thinned, with an increase of the cortical porosity by the enlargement of Haversian canals and by endosteal erosion. HE, obj.20x. (8) Normal bone (vertebrae) appearance. HE, obj.20x. (9) A rib section shows a moderate decrease of osteoblasts, indicating reduced osteoblastic activity. HE, obj.20x. (10) Normal bone (rib) appearance shows regular osteoblastic activity. HE, obj.20x. open_in_new

table_chartTable 1. Metabolic disease in growing/adult pigs

Disorder	Age of affected pigs	Cause	Lesion distribution	Gross features	Histopathology
Osteoporosis (Doige 1982, Craig et al. 2016)	Growing and adult pigs	Cu/Ca deficiency, starvation, vitamin A toxicity, increased stress	Vertebrae, ribs, long bones, flat bones of the skull	Reduced breaking strength of ribs. Marked depletion of cancellous bone in the metaphyses and epiphyses. Reduced cortex thickness	Bone trabeculae decreased in thickness and number, disconnected, “free-floating trabeculae”, increased porosity of the cortical bone due to enlargement of Haversian canal, low level of osteoblastic activity
Fibrous osteodystrophy (Thompson & Robinson 1989)	Growing and adult pigs	Ca and vitamin D deficiency, excess P	Skull bones, especially mandibles and maxilla. Also, scapula and vertebral column	Bilateral enlargement of the bones of the skull, movable teeth, jaw swelling. Soft, pumice-like bones, and decrease in bone density. Ribs may bend or snap with little effort	Increased osteoclastic bone resorption, marked fibroplasia, and increased osteoblastic activity with formation of immature woven bone, frequently poorly mineralized
Rickets (Pepper et al. 1978, Dittmer & Thompson 2011, Madson et al. 2012, Gris et al. 2020)	Growing pigs	Deficiency of Ca, P, vitamin D. Ca/P imbalance	Sites of rapid growth, metaphyseal and epiphyseal regions of long bones, and costochondral junctions of the large middle ribs	Weak bones that bend before breaking with a weak snap and have enlarged growth plates, giving a clinical appearance of swollen joints, increased volume of costochondral joints (rachitic rosary), kyphosis	Decreased mineralization of the growing bone, evident persistence of hypertrophic chondrocytes at sites of endochondral ossification
Osteomalacia (Craig et al. 2016)	Late finishing and adult pigs	Deficiency of Ca, P, vitamin D. Ca/P imbalance	Vertebrae, femur, pelvis, and ribs	Bones with reduced resistance to pressure and tension. In severe cases the marrow cavity is expanded, the cortex is thin, spongy, and soft	Decreased mineralization with the significant remodeling of the mature bone. Localized accumulation of osteoid at sites of mechanical stress

Cu = copper, Ca = calcium, P = phosphorus.

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[TFN1] Cu = copper, Ca = calcium, P = phosphorus.