**1. Introduction**

This chapter is about a descriptive presentation of the anatomic and physiological changes of the claws, which are the most vital part of the locomotor system of a dairy cow. The health of the claws allows free movement of the cow, which enhances adequate feeding time that leads to optimal reproduction and production, thus fulfilling the farmers' main purpose for keeping dairy cows. Over 80% of the dairy cattle herd in Kenya is under smallholder production [1], in most of which

the dairy cows are kept in zero-grazing units with the animals confined for a long time [2]. Many of these smallholder zero-grazing units have improperly designed cattle-rearing structures, defective and unsuitable treading floors, inadequate and inconsistent nutritional diets, as well as generally poor husbandry and management practices [2]. All these factors interact synergistically and predispose dairy cows to laminitis and related non-infectious claw disorders [2–3]. It has been observed that housing of dairy cows in confinement leads to an increased prevalence of claw disorders. This is particularly true when the cows are confined on hard unyielding floors such as concrete, which exert immense pressure against the claws after loading them heavily under the opposing animal weight to ground forces [4–5]. Some of the non-infectious claw disorders such as white line separation, sole ulcer, double (underrun) soles, sole bruising/sole erosion and heel erosion can be the result or the cause of laminitis [6].

Laminitis tends to affect all the claws simultaneously in a single cow and when it advances to the chronic phase, there are obvious macroscopic claw deformities that make it difficult to reshape them to their normal anatomical appearance. These macroscopic deformities are often accompanied by irreversible damage to the internal structure of the claws [6–9]. Initially, laminitis occurs in a subtle clinically unrecognised state referred to as subclinical laminitis, which can only be discerned through claw trimming as sole and white line haemorrhages [6, 10, 11]. The haemorrhages are associated with pododermal microvasculature changes that lead to extravasation of serum and blood elements with subsequent staining of the internal layers of the horn next to the corium of the claw and later following horn-growth towards the surface of the sole, becomes visible externally as sole haemorrhages [6, 11, 12]. If claw trimming or keen observation is not done routinely in individual dairy cows, subclinical laminitis advances to chronic phase of laminitis and predisposes to laminitis-related non-infectious claw disorders with likelihood of occurrence of irreversible internal damage in the claws [6, 13].

The structural changes in the claws that result from laminitis and laminitisrelated disorders are initially evident histologically, later they can be seen macroscopically and radiographically. Publications on comprehensive description of macroscopic, radiographic and histopathologic changes occurring in the claws during laminitis and laminitis-related disorders in dairy cows are scarce. The available publications describe scantly and separately the changes discernible through these three observational methods. The aim of this chapter is to comprehensively describe in a single publication the macroscopic, radiographic and histopathologic changes in the claws of dairy cows following subclinical and chronic laminitis, as well as laminitis-predisposed claw disorders. The study observed claws collected from abattoirs, which originated from slaughtered culled dairy cows. The publication also presents a comprehensive literature review on the structural changes affecting the claws from the various non-infectious disorders, especially laminitis.

## **2. Literature review**

Laminitis is an aseptic diffuse inflammation of the pododerm (corium), which is the dermis of the claw. There is a progressive damage of the microvasculature of the corium, which compromises oxygen and nutrient supply to the corium cells, thus resulting in the production of low quality weak claw-horn [6, 14]. The low quality horn predisposes the claws of dairy cows to occurrence of various claw disorders associated with disruption of the claw-horn. These include sole ulcer,

**39**

lactations [21].

*Macroscopic, Radiographic and Histopathologic Changes of Claws with Laminitis…*

white line separation, double (underrun) soles, sole bruising (erosion) and heel erosion [6–8]. Claw-horn disruption is mainly thought to emanate from laminitis; hence, conclusion of association between laminitis and the claw disorders mentioned above [15]. Another factor that has the likelihood of causing claw-horn disruption in dairy cows is exertion of excessive forces on the germinal epithelium responsible for production of new claw horn. These excessive forces penetrate into the claw after depletion of adipose tissue in the digital cushion and the sole soft tissue thickness. The overall digital cushion and the sole soft tissue thickness become thinner to the extent that they cannot dissipate the concussion forces [16]. These authors have stated that the likelihood of having claw lesions has been associated with thin digital cushion. Impaired claw function has also been traced to weakened claw structures including subcutaneous tissue (digital cushion), dermis (corium) and suspensory apparatus. These lead to the damage of the vascular system of the dermis, disruption of dermal-epidermal junction as well as the horn

The prevailing factors during the peri-parturient period predispose dairy cows to likelihood of more claw-horn wear and negative horn-growth. This effect leads to thinned soles that subsequently allow pressure penetration into the corium exacerbating its fragility and injury, consequently producing poor quality horn. Other structural changes in the claws occurring during the peri-parturient period in dairy cows include the slight shifting of the distal phalanx within the claw horn capsule. The distal phalanx rotates and sinks lower into the claw capsule. This movement of the distal phalanx is incriminated on the rising levels of the enzyme "hoofase" that occurs in the peri-parturient period, which causes more flexibility of the connective tissue suspending this bone within the claw horn capsule [18]. Studies have shown that sole haemorrhages were absent in heifers that had not calved, while these haemorrhages occurred after the heifers calved [19]. This confirms the role played by peri-parturient factors in predisposing to the occurrence claw-horn lesions. During the peri-parturient period, digital cushion and sole soft tissue become thinner, hence the germinal epithelium of the corium becomes predisposed to pressure. This results in production of poor quality horn as well as reduced horn production, especially the horn of the sole [16]. The alterations of thickness of sole soft tissue during the peri-parturient period are thought to be influenced by reproductive hormones relaxin and oestrogens. These hormones cause activation of the enzymes metalloproteinases, which degrade collagen [20]. The scores of lesions in the sole are higher during the postpartum period. These lesions decrease in the late lactation. Wider outward angle of the hind limbs caused by the size and weight of the udder in early lactation, predisposes the claws especially the lateral claws to occurrence of lesions [21]. Apart from hormonal factors during early postpartum period and in early lactation, metabolic changes associated with parturition and lactation similarly contributes to increased locomotion as well as lesion scores in dairy cows [20]. Lesions causing structural changes in the claws are more common and with higher locomotion scores in dairy cows that have had greater number of parities/lactations, especially five or more

Dairy cow housing-related factors are major contributors to the occurrence of claw lesions and structural changes. This is particularly common in the more confined dairy cows such as the smallholder zero-grazing units [2]. The type of floor on which the cows live and walk is the main housing factor predisposing them to develop claw lesions. This is determined by either rough or slippery floor texture [22], as well as defective concrete floors with small or large pot-holes [2]. The distribution of the weight of the cow on the claws is influenced by the hardness of the floor. Hard floors cause most of the animal weight to be loaded on the abaxial wall of

*DOI: http://dx.doi.org/10.5772/intechopen.81255*

producing cells [17].

#### *Macroscopic, Radiographic and Histopathologic Changes of Claws with Laminitis… DOI: http://dx.doi.org/10.5772/intechopen.81255*

white line separation, double (underrun) soles, sole bruising (erosion) and heel erosion [6–8]. Claw-horn disruption is mainly thought to emanate from laminitis; hence, conclusion of association between laminitis and the claw disorders mentioned above [15]. Another factor that has the likelihood of causing claw-horn disruption in dairy cows is exertion of excessive forces on the germinal epithelium responsible for production of new claw horn. These excessive forces penetrate into the claw after depletion of adipose tissue in the digital cushion and the sole soft tissue thickness. The overall digital cushion and the sole soft tissue thickness become thinner to the extent that they cannot dissipate the concussion forces [16]. These authors have stated that the likelihood of having claw lesions has been associated with thin digital cushion. Impaired claw function has also been traced to weakened claw structures including subcutaneous tissue (digital cushion), dermis (corium) and suspensory apparatus. These lead to the damage of the vascular system of the dermis, disruption of dermal-epidermal junction as well as the horn producing cells [17].

The prevailing factors during the peri-parturient period predispose dairy cows to likelihood of more claw-horn wear and negative horn-growth. This effect leads to thinned soles that subsequently allow pressure penetration into the corium exacerbating its fragility and injury, consequently producing poor quality horn. Other structural changes in the claws occurring during the peri-parturient period in dairy cows include the slight shifting of the distal phalanx within the claw horn capsule. The distal phalanx rotates and sinks lower into the claw capsule. This movement of the distal phalanx is incriminated on the rising levels of the enzyme "hoofase" that occurs in the peri-parturient period, which causes more flexibility of the connective tissue suspending this bone within the claw horn capsule [18]. Studies have shown that sole haemorrhages were absent in heifers that had not calved, while these haemorrhages occurred after the heifers calved [19]. This confirms the role played by peri-parturient factors in predisposing to the occurrence claw-horn lesions. During the peri-parturient period, digital cushion and sole soft tissue become thinner, hence the germinal epithelium of the corium becomes predisposed to pressure. This results in production of poor quality horn as well as reduced horn production, especially the horn of the sole [16]. The alterations of thickness of sole soft tissue during the peri-parturient period are thought to be influenced by reproductive hormones relaxin and oestrogens. These hormones cause activation of the enzymes metalloproteinases, which degrade collagen [20]. The scores of lesions in the sole are higher during the postpartum period. These lesions decrease in the late lactation. Wider outward angle of the hind limbs caused by the size and weight of the udder in early lactation, predisposes the claws especially the lateral claws to occurrence of lesions [21]. Apart from hormonal factors during early postpartum period and in early lactation, metabolic changes associated with parturition and lactation similarly contributes to increased locomotion as well as lesion scores in dairy cows [20]. Lesions causing structural changes in the claws are more common and with higher locomotion scores in dairy cows that have had greater number of parities/lactations, especially five or more lactations [21].

Dairy cow housing-related factors are major contributors to the occurrence of claw lesions and structural changes. This is particularly common in the more confined dairy cows such as the smallholder zero-grazing units [2]. The type of floor on which the cows live and walk is the main housing factor predisposing them to develop claw lesions. This is determined by either rough or slippery floor texture [22], as well as defective concrete floors with small or large pot-holes [2]. The distribution of the weight of the cow on the claws is influenced by the hardness of the floor. Hard floors cause most of the animal weight to be loaded on the abaxial wall of

*Veterinary Anatomy and Physiology*

cause of laminitis [6].

the claws [6, 13].

especially laminitis.

**2. Literature review**

the dairy cows are kept in zero-grazing units with the animals confined for a long time [2]. Many of these smallholder zero-grazing units have improperly designed cattle-rearing structures, defective and unsuitable treading floors, inadequate and inconsistent nutritional diets, as well as generally poor husbandry and management practices [2]. All these factors interact synergistically and predispose dairy cows to laminitis and related non-infectious claw disorders [2–3]. It has been observed that housing of dairy cows in confinement leads to an increased prevalence of claw disorders. This is particularly true when the cows are confined on hard unyielding floors such as concrete, which exert immense pressure against the claws after loading them heavily under the opposing animal weight to ground forces [4–5]. Some of the non-infectious claw disorders such as white line separation, sole ulcer, double (underrun) soles, sole bruising/sole erosion and heel erosion can be the result or the

Laminitis tends to affect all the claws simultaneously in a single cow and when it advances to the chronic phase, there are obvious macroscopic claw deformities that make it difficult to reshape them to their normal anatomical appearance. These macroscopic deformities are often accompanied by irreversible damage to the internal structure of the claws [6–9]. Initially, laminitis occurs in a subtle clinically unrecognised state referred to as subclinical laminitis, which can only be discerned through claw trimming as sole and white line haemorrhages [6, 10, 11]. The haemorrhages are associated with pododermal microvasculature changes that lead to extravasation of serum and blood elements with subsequent staining of the internal layers of the horn next to the corium of the claw and later following horn-growth towards the surface of the sole, becomes visible externally as sole haemorrhages [6, 11, 12]. If claw trimming or keen observation is not done routinely in individual dairy cows, subclinical laminitis advances to chronic phase of laminitis and predisposes to laminitis-related non-infectious claw disorders with likelihood of occurrence of irreversible internal damage in

The structural changes in the claws that result from laminitis and laminitis-

Laminitis is an aseptic diffuse inflammation of the pododerm (corium), which is the dermis of the claw. There is a progressive damage of the microvasculature of the corium, which compromises oxygen and nutrient supply to the corium cells, thus resulting in the production of low quality weak claw-horn [6, 14]. The low quality horn predisposes the claws of dairy cows to occurrence of various claw disorders associated with disruption of the claw-horn. These include sole ulcer,

related disorders are initially evident histologically, later they can be seen macroscopically and radiographically. Publications on comprehensive description of macroscopic, radiographic and histopathologic changes occurring in the claws during laminitis and laminitis-related disorders in dairy cows are scarce. The available publications describe scantly and separately the changes discernible through these three observational methods. The aim of this chapter is to comprehensively describe in a single publication the macroscopic, radiographic and histopathologic changes in the claws of dairy cows following subclinical and chronic laminitis, as well as laminitis-predisposed claw disorders. The study observed claws collected from abattoirs, which originated from slaughtered culled dairy cows. The publication also presents a comprehensive literature review on the structural changes affecting the claws from the various non-infectious disorders,

**38**

the claws, while soft yielding floors lead to significant distribution of weight to the sole. The overall effect of the weight force against the mechanical pressure from the floor depends on the architectural arrangement of the claw wall determined by the interrelationship arrangement of tubular, intertubular and laminar horn cells. The numerical density of the horn tubules determines the differences in the stiffness and elasticity of the various parts of the claw horn capsule. The degree of the effect of the mechanical forces from the animal weight and floor pressure is associated with the degree of horn capsule elasticity and stiffness [22]. The longer the dairy cow stands on hard unyielding floor such as concrete, the more the likelihood of developing claw lesions [23]. Besides the pressure transmitted to the inside of the claws from the hard floors, the floor abrasiveness has a significant contribution to the occurrence of claw lesions, mainly due to excessive wearing of the claw-horn [24]. The claws are particularly prone to this abrasiveness of the floor when the horn produced is weak following bouts of laminitis [8]. Conversely, the claw-horn does not wear off when the cow lives and walks on soft yielding floors such as earthen floors or straw yards. This leads to inevitable overgrowth of the claws with subsequent overloading of the region towards the heel bulb, which is soft, hence the ease of transmission of pressure to the inner claw tissues, thus damaging them. The result of this is the production of poor quality horn [23]. All these factors have an overall effect of causing changes in the claw shape as well as structural changes internally.
