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Skeletal Deformities and Their Causes: Introduction
Skeletal Deformities and Their Causes: Introduction M. E. Cook1 Animal Sciences Department, University of Wisconsin-Madison, 1675 Observatory Drive, Madison, Wisconsin 53706 ment is essential for continuous progress in solving current skeletal diseases. Although this research will be of great benefit to the poultry industry, the use of poultry models has proven valuable in studying human bone disease.
ABSTRACT Much has been done to characterize skeletal deformities in poultry and to identify the causes of these deformities. However, skeletal problems in poultry continue to cost poultry producers over $100 million per year. A basic understanding of bone growth and develop-
2000 Poultry Science 79:982–984
INTRODUCTION
SKELETAL PROBLEMS IN POULTRY
In 1997, approximately 200 million pullets, 7.5 billion broilers, and 300 million turkeys were raised in the US. In addition, 300 million layers were maintained in production (Schoeff and Lobo, 1998). Although skeletal problems typically are not a major problem in light breeds of chickens (pullets and layers), with the exception of cage layer fatigue, losses due to skeletal problems in broilers and turkeys are significant. Morris, in a survey conducted in 1993, estimates that losses caused by skeletal defects in broilers due to mortality, culling, and condemnation represented about 3.2% (Sullivan, 1994). These estimated losses have cost the broiler industry an estimated $120 million per year, or $.016 per broiler raised in the US.
The committee classified 12 types of skeletal abnormalities in poultry. These skeletal problems have both unique and overlapping pathologies and causes. Many of the pathological skeletal deformities are still commonplace and do not appear to be linked to defined causes. Long bone distortions (valgus or varus) are still commonplace, although the causes of these deformities in nutrient adequate diets are generally unknown. Valgus deformities result in a “knock-kneed” appearance (Randall and Miles, 1981). The tarsometatarsus deviates out laterally when placed in line with the tibiotarsus. Valgus deviations are the most common form of long bone distortion; however, they are rarely severe. Varus deviations result in a bow-legged appearance (Randall and Mills, 1981) in which the tarsometatarsus deviates inward when placed in line with the tibiotarsus. Although varus deviations are less common, they can result in more severe walking difficulty in poultry than valgus deviations. One observation that we and others have made, after observing thousands of chickens, is that the severity of the deviation is greatest in the right leg. This observation merits additional study. Tibial dyschondroplasia (TD) is another skeletal disease with many underlying causes that have yet to be defined (Orth and Cook, 1994). Tibial dyschondroplasia appears to be the result of an uncoupling of growth plate chondrocyte proliferation during bone elongation and endochondrial ossification. The resulting lesion is a mass of uncalcified cartilage in the proximal end of long bones (primarily the tibiotarsus, but not exclusively). Basic research is still needed to define the cellular and molecular pro-
NORTH CENTRAL-187 In the mid 1980s, a North Central Regional Committee (NC-187) was formed to address the issue of skeletal problems in poultry. Although this committee has now terminated, it summarized its findings in a symposium in 1994 (introductory paper, Sullivan, 1994). This committee provided the framework upon which many scientists have dedicated their studies to skeletal problems in poultry. A number of the speakers at this symposium, as well as the organizers (N. C. Rath and R. M. Leach), were longterm members of this committee. One of the missions of the committee was to develop and characterize a list of skeletal problems, their common names, clinical signs, and causes (Sullivan, 1994). In addition, the committee developed proposed research to answer many questions regarding skeletal problems in poultry.
Received for publication December 15, 1999. Accepted for publication February 29, 2000. 1 To whom correspondence should be addressed: mcook@facstaff. wisc.edu.
Abbreviation Key: NC-187 = North Central Regional Committee; TD = tibial dyschondroplasia.
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Downloaded from http://ps.oxfordjournals.org/ at Washington University, Law School Library on July 2, 2014
(Key words: skeletal disease, chicken, turkey, health, economics)
SYMPOSIUM: SKELETAL BIOLOGY AND RELATED PROBLEMS IN POULTRY
CAUSES OF SKELETAL DEFORMITIES Since the 1930s, numerous causes of skeletal deformities in poultry have been identified. Nutrients (toxicities, deficiencies, and imbalances), genetics, pathogens, mycotoxins, and management practices have all been shown to directly affect normal skeletal growth and development. Deficiencies of vitamins A and D, biotin, niacin, pantothenic acid, pyridoxine, choline, folic acid, calcium, phosphorus, manganese, zinc, and copper cause, as their major clinical signs of deficiency, skeletal abnormalities. A number of nutrient interactions in metabolism and digestive absorption have shown that proper nutrient balance is critical to prevent skeletal deformities. Hence, the role of nutrients in skeletal deformities represents a significant part of this symposium and is addressed by H. Edwards.
Genetic selection and single gene mutations have been shown to greatly influence the development of the skeletal system. Leach (Penn State) and McDaniel (Auburn) have selected lines of broiler chickens that have a high or low incidence of tibial dyschondroplasia. Nestor (Ohio) has developed lines of turkeys selected for shank width that have greatly influenced the incidence of long bone distortion. Smith (Massachusetts) maintains an ametapodia line (single gene mutation) with compete absence of the tarsometatarsus. Bitgood (Wisconsin) has maintained single gene mutations resulting in wingless and limbless mutants, mutants with additional digits on the legs and wings (Talpid), and a shankless mutation in which the tarsometatarsus is shortened. Mycotoxins and a number of other chemicals have been shown to induce a variety of skeletal abnormalities. The Fusarium mycotoxin, fusachromanone, has been shown to be a potent inducer of TD (Wu et al., 1993). Other chemicals known to induce TD include thiram (a fungicide), antabuse (drug), homocysteine, cysteine, and histidine (Cook et al., 1994). Hester (1994) reviewed management factors involved in skeletal disorders. This symposium provides an update on systems to reduce the spontaneous occurrence of skeletal problems. Lighting programs, litter or floor conditions, rate of growth, air quality, and biosecurity are wellknown management methods to reduce leg problems in poultry. However, with all of the above causes of skeletal problems managed properly, skeletal defects in poultry remain a research problem worthy of pursuit. A more thorough understanding of the basic biology of bone development and remodeling should continue to expand the list of corrective actions to minimize poultry skeletal defects.
MODEL FOR HUMAN DISEASE Although there are dissimilarities between human and avian bone development, the avian model is valuable in studying select human skeletal defects. For example, chickens were a primary model used to define nutrients necessary for normal long-bone growth. We proposed the use of the chicken model to study the cause of a human bone disease, Kashin-Beck disease (Chu et al., 1995), and showed similarities in glycosaminoglycan metabolism (Chu et al., 1996). The chicken may serve as a useful model in understanding bone defects that occur in people with homocystinuria (Orth et al., 1992; Bai et al., 1994). The reviews that follow illustrate the importance of the chicken in understanding fundamentals in bone development disease and repair.
REFERENCES Bai, Y., M. L. Sunde, and M. E. Cook, 1994. Molybdenum but not copper counteracts cysteine-induced tibial dyschondroplasia in broiler chicks. J. Nutr. 124:588–593. Cook, M. E., Y. Bai, and M. Orth, 1994. Factors influencing growth plate cartilage turnover. Poultry Sci. 73:889–896. Chu, Q., W. Wu, M. E. Cook, and E. B. Smalley, 1995. Induction of tibial dyschondroplasia and suppression of cell-mediated
Downloaded from http://ps.oxfordjournals.org/ at Washington University, Law School Library on July 2, 2014
cesses of bone elongation to better define other potential causes of this skeletal defect. Rickets is probably one of the best-characterized skeletal diseases in poultry. This disorder occurs when bone mineralization is decreased. It is largely caused by calcium, phosphorus, or cholecalciferol deficiency or an imbalance of these nutrients. Although well defined, field cases of rickets that do not appear to be nutritionally linked still occasionally occur in poultry. Another disease syndrome involving poor bone mineralization is femoral head necrosis. From personal experience, this syndrome, largely of unknown causes, can afflict an entire flock of young growing broilers. The most obvious clinical sign is the inability of birds to stand. Often, the onset appears rapidly. When birds are necropsied, the proximal end of the femur is poorly calcified or completely eroded. Although the birds may respond to vitamin D3 supplementation in the water, such treatment does not always result in remission of the clinical signs. Chondrodystrophy is another well-characterized bone abnormality. Poultry deficient in any of a number of water-soluble vitamins or manganese or zinc will develop shortened bones with valgus or varus leg deformities. If the deficiency is severe enough, the gastrocnemius tendon will slip off the supporting articulating cartilage. The bestcharacterized molecular explanation for one of these nutrients (manganese) was provided by Leach (1968). Infectious diseases were also classified by the NC-187 as inducers of skeletal problems. These infectious agents include reovirus, Mycoplasma synoviae, retroviruses, and Staphylococcus aureus. However, note that infectious agents generally affect the soft tissue (tendons and synoviae) and joint space (fluid accumulation) and do not directly influence the skeletal system. Staphylococcus infects the epiphyseal growth plate (osteomyelitis) creating a food safety issue, but it has only limited effects on skeletal developments. Avian retrovirus (Leukosis complex) is perhaps the only infectious agent that can severely affect bone development. The occurrence of leukosis-related bone disorders (characterized by the overgrowth of bone tissue known as osteopetrosis) are rare among commercial strains.
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immunity in chickens by Fusarium oxysporum grown on sterile corn. Avian Dis. 39:100–107. Chu, Q., W. Wu, M. E. Cook, and E. B. Smalley, 1996. Elevated plasma glycosaminoglycans in chickens with tibial dyschondroplasia induced by a Fusarium oxysporum isolate. Avian Dis. 40:715–719. Hester, P. Y., 1994. The role of environment and management on leg abnormalities in meat-type fowl. Poultry Sci. 73:904–915. Leach, R. M., Jr., 1968. Effect of manganese upon the epiphyseal growth plate in the young chick. Poultry Sci. 47:828–830. Morris, M. P., 1993. National survey of leg problems. Broiler Ind. May:20–24. Orth, M. W., Y. Bai, I. H. Zeytun, and M. E. Cook, 1992. Excess levels of cysteine and homocysteine induce tibial dyschondroplasia (TD) in broiler chicks. J. Nutr. 122:482–487.
Orth, M. W., and M. E. Cook, 1994. Avian tibial dyschondroplasia: A description of the growth plate disease as well as the conditions that induce it. Vet. Pathol. 31:403–414. Randall, C. J., and C.P.J. Mills, 1981. Observations on leg deformity in broilers with particular reference to the intertarsal joint. Avian Pathol. 10:407–431. Schoeff, R. A., and P. Lobo, 1998. USA Feed Market: Most feed potential is up, except—surprise—for broilers. Feed Manage. Oct.:7–16. Sullivan, T. W., 1994. Skeletal problems in poultry: Estimated annual cost and description. Poultry Sci. 73:879–882. Wu, W., M. E. Cook, Q. Chu, and E. B. Smalley, 1993. Tibial dyschondroplasia of chickens induced by fusachromanone, a mycotoxin. Avian Dis. 37:302–309.
Downloaded from http://ps.oxfordjournals.org/ at Washington University, Law School Library on July 2, 2014
ABSTRACT Much has been done to characterize skeletal deformities in poultry and to identify the causes of these deformities. However, skeletal problems in poultry continue to cost poultry producers over $100 million per year. A basic understanding of bone growth and develop-
2000 Poultry Science 79:982–984
INTRODUCTION
SKELETAL PROBLEMS IN POULTRY
In 1997, approximately 200 million pullets, 7.5 billion broilers, and 300 million turkeys were raised in the US. In addition, 300 million layers were maintained in production (Schoeff and Lobo, 1998). Although skeletal problems typically are not a major problem in light breeds of chickens (pullets and layers), with the exception of cage layer fatigue, losses due to skeletal problems in broilers and turkeys are significant. Morris, in a survey conducted in 1993, estimates that losses caused by skeletal defects in broilers due to mortality, culling, and condemnation represented about 3.2% (Sullivan, 1994). These estimated losses have cost the broiler industry an estimated $120 million per year, or $.016 per broiler raised in the US.
The committee classified 12 types of skeletal abnormalities in poultry. These skeletal problems have both unique and overlapping pathologies and causes. Many of the pathological skeletal deformities are still commonplace and do not appear to be linked to defined causes. Long bone distortions (valgus or varus) are still commonplace, although the causes of these deformities in nutrient adequate diets are generally unknown. Valgus deformities result in a “knock-kneed” appearance (Randall and Miles, 1981). The tarsometatarsus deviates out laterally when placed in line with the tibiotarsus. Valgus deviations are the most common form of long bone distortion; however, they are rarely severe. Varus deviations result in a bow-legged appearance (Randall and Mills, 1981) in which the tarsometatarsus deviates inward when placed in line with the tibiotarsus. Although varus deviations are less common, they can result in more severe walking difficulty in poultry than valgus deviations. One observation that we and others have made, after observing thousands of chickens, is that the severity of the deviation is greatest in the right leg. This observation merits additional study. Tibial dyschondroplasia (TD) is another skeletal disease with many underlying causes that have yet to be defined (Orth and Cook, 1994). Tibial dyschondroplasia appears to be the result of an uncoupling of growth plate chondrocyte proliferation during bone elongation and endochondrial ossification. The resulting lesion is a mass of uncalcified cartilage in the proximal end of long bones (primarily the tibiotarsus, but not exclusively). Basic research is still needed to define the cellular and molecular pro-
NORTH CENTRAL-187 In the mid 1980s, a North Central Regional Committee (NC-187) was formed to address the issue of skeletal problems in poultry. Although this committee has now terminated, it summarized its findings in a symposium in 1994 (introductory paper, Sullivan, 1994). This committee provided the framework upon which many scientists have dedicated their studies to skeletal problems in poultry. A number of the speakers at this symposium, as well as the organizers (N. C. Rath and R. M. Leach), were longterm members of this committee. One of the missions of the committee was to develop and characterize a list of skeletal problems, their common names, clinical signs, and causes (Sullivan, 1994). In addition, the committee developed proposed research to answer many questions regarding skeletal problems in poultry.
Received for publication December 15, 1999. Accepted for publication February 29, 2000. 1 To whom correspondence should be addressed: mcook@facstaff. wisc.edu.
Abbreviation Key: NC-187 = North Central Regional Committee; TD = tibial dyschondroplasia.
982
Downloaded from http://ps.oxfordjournals.org/ at Washington University, Law School Library on July 2, 2014
(Key words: skeletal disease, chicken, turkey, health, economics)
SYMPOSIUM: SKELETAL BIOLOGY AND RELATED PROBLEMS IN POULTRY
CAUSES OF SKELETAL DEFORMITIES Since the 1930s, numerous causes of skeletal deformities in poultry have been identified. Nutrients (toxicities, deficiencies, and imbalances), genetics, pathogens, mycotoxins, and management practices have all been shown to directly affect normal skeletal growth and development. Deficiencies of vitamins A and D, biotin, niacin, pantothenic acid, pyridoxine, choline, folic acid, calcium, phosphorus, manganese, zinc, and copper cause, as their major clinical signs of deficiency, skeletal abnormalities. A number of nutrient interactions in metabolism and digestive absorption have shown that proper nutrient balance is critical to prevent skeletal deformities. Hence, the role of nutrients in skeletal deformities represents a significant part of this symposium and is addressed by H. Edwards.
Genetic selection and single gene mutations have been shown to greatly influence the development of the skeletal system. Leach (Penn State) and McDaniel (Auburn) have selected lines of broiler chickens that have a high or low incidence of tibial dyschondroplasia. Nestor (Ohio) has developed lines of turkeys selected for shank width that have greatly influenced the incidence of long bone distortion. Smith (Massachusetts) maintains an ametapodia line (single gene mutation) with compete absence of the tarsometatarsus. Bitgood (Wisconsin) has maintained single gene mutations resulting in wingless and limbless mutants, mutants with additional digits on the legs and wings (Talpid), and a shankless mutation in which the tarsometatarsus is shortened. Mycotoxins and a number of other chemicals have been shown to induce a variety of skeletal abnormalities. The Fusarium mycotoxin, fusachromanone, has been shown to be a potent inducer of TD (Wu et al., 1993). Other chemicals known to induce TD include thiram (a fungicide), antabuse (drug), homocysteine, cysteine, and histidine (Cook et al., 1994). Hester (1994) reviewed management factors involved in skeletal disorders. This symposium provides an update on systems to reduce the spontaneous occurrence of skeletal problems. Lighting programs, litter or floor conditions, rate of growth, air quality, and biosecurity are wellknown management methods to reduce leg problems in poultry. However, with all of the above causes of skeletal problems managed properly, skeletal defects in poultry remain a research problem worthy of pursuit. A more thorough understanding of the basic biology of bone development and remodeling should continue to expand the list of corrective actions to minimize poultry skeletal defects.
MODEL FOR HUMAN DISEASE Although there are dissimilarities between human and avian bone development, the avian model is valuable in studying select human skeletal defects. For example, chickens were a primary model used to define nutrients necessary for normal long-bone growth. We proposed the use of the chicken model to study the cause of a human bone disease, Kashin-Beck disease (Chu et al., 1995), and showed similarities in glycosaminoglycan metabolism (Chu et al., 1996). The chicken may serve as a useful model in understanding bone defects that occur in people with homocystinuria (Orth et al., 1992; Bai et al., 1994). The reviews that follow illustrate the importance of the chicken in understanding fundamentals in bone development disease and repair.
REFERENCES Bai, Y., M. L. Sunde, and M. E. Cook, 1994. Molybdenum but not copper counteracts cysteine-induced tibial dyschondroplasia in broiler chicks. J. Nutr. 124:588–593. Cook, M. E., Y. Bai, and M. Orth, 1994. Factors influencing growth plate cartilage turnover. Poultry Sci. 73:889–896. Chu, Q., W. Wu, M. E. Cook, and E. B. Smalley, 1995. Induction of tibial dyschondroplasia and suppression of cell-mediated
Downloaded from http://ps.oxfordjournals.org/ at Washington University, Law School Library on July 2, 2014
cesses of bone elongation to better define other potential causes of this skeletal defect. Rickets is probably one of the best-characterized skeletal diseases in poultry. This disorder occurs when bone mineralization is decreased. It is largely caused by calcium, phosphorus, or cholecalciferol deficiency or an imbalance of these nutrients. Although well defined, field cases of rickets that do not appear to be nutritionally linked still occasionally occur in poultry. Another disease syndrome involving poor bone mineralization is femoral head necrosis. From personal experience, this syndrome, largely of unknown causes, can afflict an entire flock of young growing broilers. The most obvious clinical sign is the inability of birds to stand. Often, the onset appears rapidly. When birds are necropsied, the proximal end of the femur is poorly calcified or completely eroded. Although the birds may respond to vitamin D3 supplementation in the water, such treatment does not always result in remission of the clinical signs. Chondrodystrophy is another well-characterized bone abnormality. Poultry deficient in any of a number of water-soluble vitamins or manganese or zinc will develop shortened bones with valgus or varus leg deformities. If the deficiency is severe enough, the gastrocnemius tendon will slip off the supporting articulating cartilage. The bestcharacterized molecular explanation for one of these nutrients (manganese) was provided by Leach (1968). Infectious diseases were also classified by the NC-187 as inducers of skeletal problems. These infectious agents include reovirus, Mycoplasma synoviae, retroviruses, and Staphylococcus aureus. However, note that infectious agents generally affect the soft tissue (tendons and synoviae) and joint space (fluid accumulation) and do not directly influence the skeletal system. Staphylococcus infects the epiphyseal growth plate (osteomyelitis) creating a food safety issue, but it has only limited effects on skeletal developments. Avian retrovirus (Leukosis complex) is perhaps the only infectious agent that can severely affect bone development. The occurrence of leukosis-related bone disorders (characterized by the overgrowth of bone tissue known as osteopetrosis) are rare among commercial strains.
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immunity in chickens by Fusarium oxysporum grown on sterile corn. Avian Dis. 39:100–107. Chu, Q., W. Wu, M. E. Cook, and E. B. Smalley, 1996. Elevated plasma glycosaminoglycans in chickens with tibial dyschondroplasia induced by a Fusarium oxysporum isolate. Avian Dis. 40:715–719. Hester, P. Y., 1994. The role of environment and management on leg abnormalities in meat-type fowl. Poultry Sci. 73:904–915. Leach, R. M., Jr., 1968. Effect of manganese upon the epiphyseal growth plate in the young chick. Poultry Sci. 47:828–830. Morris, M. P., 1993. National survey of leg problems. Broiler Ind. May:20–24. Orth, M. W., Y. Bai, I. H. Zeytun, and M. E. Cook, 1992. Excess levels of cysteine and homocysteine induce tibial dyschondroplasia (TD) in broiler chicks. J. Nutr. 122:482–487.
Orth, M. W., and M. E. Cook, 1994. Avian tibial dyschondroplasia: A description of the growth plate disease as well as the conditions that induce it. Vet. Pathol. 31:403–414. Randall, C. J., and C.P.J. Mills, 1981. Observations on leg deformity in broilers with particular reference to the intertarsal joint. Avian Pathol. 10:407–431. Schoeff, R. A., and P. Lobo, 1998. USA Feed Market: Most feed potential is up, except—surprise—for broilers. Feed Manage. Oct.:7–16. Sullivan, T. W., 1994. Skeletal problems in poultry: Estimated annual cost and description. Poultry Sci. 73:879–882. Wu, W., M. E. Cook, Q. Chu, and E. B. Smalley, 1993. Tibial dyschondroplasia of chickens induced by fusachromanone, a mycotoxin. Avian Dis. 37:302–309.
Downloaded from http://ps.oxfordjournals.org/ at Washington University, Law School Library on July 2, 2014