**5. Discussion**

Laminitis influences the occurrence of other claw lesions and disorders such as sole ulcer, white line separation, double (underrun) soles, sole bruising (erosion) and heel erosion [6–8, 15, 26]. The occurrence of laminitis in dairy cows is predisposed by an interactive array of multiple risk factors [2, 6]. The high prevalence of laminitis and laminitis-related lesions/disorders in the dairy cow claws from Kiserian abattoir and Wangige slaughter slab can probably be attributed to the types of modern farming systems adopted in the dairy business enterprises in which the dairy cows are confined for long hours on hard unyielding concrete floors with much concentrate feeding. Such housing and feeding factors have been incriminated as risk factors for the development of laminitis [6, 7, 23, 27, 28]. The smallholder zero-grazing dairy units expose the cows to additional suboptimal management conditions such as prolonged presence of slurry, lack of claw trimming, and defective concrete floors apart from concentrate feeding [2, 8].

The high prevalence of prominently dilated vascular channels in the distal phalanges of the claws with laminitis particularly chronic laminitis corroborates previous documented observations that dilated vascular channels are consistent observations in subclinical and chronic laminitis. These previous reports indicated that in laminitis, both dilated and non-dilated vascular channels could be found [29]. The more prominent and excessively dilated vascular channels seen in chronic laminitis compared to subclinical laminitis could probably be associated with the greater damage internally in the claws during chronic laminitis [8].

The observed exostoses in the distal phalanges of claws with chronic laminitis are similar to an old report, which found exostosis in the pyramidal process of the pedal bone [30]. Occurrence of these exostoses could be associated with periostitis of the distal phalanges owing to prolonged inflammatory stimuli in chronic laminitis [8]. Although the factors associated with exostosis were not determined in this study, non-infective claw-horn disruption lesions (CHDL) have previously been incriminated as being associated with extra bone development particularly on the caudal aspect of the distal phalanx. The cows that had suffered chronic lameness from CHDL were found to have greater extra bone growth on the caudal aspect of distal phalanx, which was verified both by morphological gross observations and and histologically. This extra bone growth was more in quantity on the lateral claws of the hind limbs and medial claws of the forelimbs [31]. Extra bone development on the distal phalanges was reported to be positively correlated with the age of the cow [32]. Since, the claws in the current study were from culled aged dairy cows

**51**

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

associated with extra bone growth in the distal phalanges [31].

claws of the hind limbs of cattle than the medial claws [35, 36].

and had signs of non-infective claw-horn disorders, the findings corroborate these previous reports. It has also been suggested that infectious claw lesions are not

Narrowing (tapering) of the pedal bone towards the apex is a feature not previously described. Closely resembling this, is the atrophy of pedal bone reported in cattle with chronic laminitis [33]. This narrowing of the pedal bone could probably be attributed to osseous tissue necrosis (osteosis), which is linked to the deprivation of the nutrients and oxygen especially when local blood supply is compromised similar to what occurs in the claws with chronic laminitis [34]. Thromboembolic blockage of blood vessels with chronic local anaemia may also lead to osteosis unless supplemented by the presence of effective collateral circulation. However, bones have poor and inefficient collateral circulation owing to small anastomosing vasculature incapable of adequate compensatory dilatation. This makes them prone to osseous ischaemia that leads to necrosis with subsequent resorption of the necrotic bone by the osteoclasts [34]. If this process takes place during chronic laminitis with extreme twisting of the toe, then there would be likelihood of pedal bone narrowing. This could also explain the observation in some of the pedal bones that had absence of the apex from claws with chronic laminitis. Moreover, atrophy of the pedal bone reported previously in chronic laminitis could also be incriminated in

Pedal bone osteolysis could be associated with reduced overall density of the bone in chronic laminitis as reported previously with crooked toe [30]. Productive periostitis of the pedal bone could be a response to irritation of the periosteum in claws with excessive inflammation of the corium in chronic laminitis. This could also lead to the irregular margins observed towards the distal margins of the pedal bone. The pedal bones in the lateral claws of the hind limbs had more severe and extensive radiographic changes than those of the medial claws. This corroborates earlier reports of higher prevalence and severity of lesions occurring on the lateral

The observation of arteriovenous shunts (AVs) in this study was similar to previ-

The vascular damage in this study, which affected mainly dermal arteries, has been reported previously [38]. The pressure build-up from intermittent vasodilation and vasoconstriction of the corium microvasculature during laminitis may be the cause of this vascular damage [6]. The build-up of local blood pressure due to the initial increase in blood flow and pooling of blood within the corium capillarybed, may lead to blood vessel rupture followed by haemorrhages and seepage of serum [6]. This eventually leads to the observation of haemorrhages seen macro-

Thickening of vascular wall particularly of the arteries was similar to proliferated tunica intima, hypertrophied tunica media and fibrotic tunica adventitia reported earlier in laminitis [41]. The thickened arterial wall would obviously interfere with the function of the blood vessel. Vascular thrombosis is an almost invariable occurrence in the corium of claws with laminitis whether subclinical or chronic [6, 42]. The formation of thrombi might result from vascular damage particularly the endothelium, or from influence of the vasoactive substances within vascular circulation [6, 43]. Numerous capillary network is normal in the corium of the claws [40]. However, the vascular proliferation observed in this study, which

ous reports in which the same was found [6, 37]. These shunts are normally not seen in healthy claws [38]. The arteriovenous shunts mainly involved the arterioles and venules. Arteriovenous shunts could be attributed to the fact that narrowed vessels have a likelihood of being affected by changes in blood pressure involved in the microcirculation of the corium [39], in which the arteriovenous shunts form as

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

the pedal apical absence [33].

structural change adjustment [40].

scopically on the sole in cases of laminitis.

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

and had signs of non-infective claw-horn disorders, the findings corroborate these previous reports. It has also been suggested that infectious claw lesions are not associated with extra bone growth in the distal phalanges [31].

Narrowing (tapering) of the pedal bone towards the apex is a feature not previously described. Closely resembling this, is the atrophy of pedal bone reported in cattle with chronic laminitis [33]. This narrowing of the pedal bone could probably be attributed to osseous tissue necrosis (osteosis), which is linked to the deprivation of the nutrients and oxygen especially when local blood supply is compromised similar to what occurs in the claws with chronic laminitis [34]. Thromboembolic blockage of blood vessels with chronic local anaemia may also lead to osteosis unless supplemented by the presence of effective collateral circulation. However, bones have poor and inefficient collateral circulation owing to small anastomosing vasculature incapable of adequate compensatory dilatation. This makes them prone to osseous ischaemia that leads to necrosis with subsequent resorption of the necrotic bone by the osteoclasts [34]. If this process takes place during chronic laminitis with extreme twisting of the toe, then there would be likelihood of pedal bone narrowing. This could also explain the observation in some of the pedal bones that had absence of the apex from claws with chronic laminitis. Moreover, atrophy of the pedal bone reported previously in chronic laminitis could also be incriminated in the pedal apical absence [33].

Pedal bone osteolysis could be associated with reduced overall density of the bone in chronic laminitis as reported previously with crooked toe [30]. Productive periostitis of the pedal bone could be a response to irritation of the periosteum in claws with excessive inflammation of the corium in chronic laminitis. This could also lead to the irregular margins observed towards the distal margins of the pedal bone. The pedal bones in the lateral claws of the hind limbs had more severe and extensive radiographic changes than those of the medial claws. This corroborates earlier reports of higher prevalence and severity of lesions occurring on the lateral claws of the hind limbs of cattle than the medial claws [35, 36].

The observation of arteriovenous shunts (AVs) in this study was similar to previous reports in which the same was found [6, 37]. These shunts are normally not seen in healthy claws [38]. The arteriovenous shunts mainly involved the arterioles and venules. Arteriovenous shunts could be attributed to the fact that narrowed vessels have a likelihood of being affected by changes in blood pressure involved in the microcirculation of the corium [39], in which the arteriovenous shunts form as structural change adjustment [40].

The vascular damage in this study, which affected mainly dermal arteries, has been reported previously [38]. The pressure build-up from intermittent vasodilation and vasoconstriction of the corium microvasculature during laminitis may be the cause of this vascular damage [6]. The build-up of local blood pressure due to the initial increase in blood flow and pooling of blood within the corium capillarybed, may lead to blood vessel rupture followed by haemorrhages and seepage of serum [6]. This eventually leads to the observation of haemorrhages seen macroscopically on the sole in cases of laminitis.

Thickening of vascular wall particularly of the arteries was similar to proliferated tunica intima, hypertrophied tunica media and fibrotic tunica adventitia reported earlier in laminitis [41]. The thickened arterial wall would obviously interfere with the function of the blood vessel. Vascular thrombosis is an almost invariable occurrence in the corium of claws with laminitis whether subclinical or chronic [6, 42]. The formation of thrombi might result from vascular damage particularly the endothelium, or from influence of the vasoactive substances within vascular circulation [6, 43]. Numerous capillary network is normal in the corium of the claws [40]. However, the vascular proliferation observed in this study, which

*Veterinary Anatomy and Physiology*

**5. Discussion**

*blue stain, ×200).*

**Figure 15.**

Laminitis influences the occurrence of other claw lesions and disorders such as sole ulcer, white line separation, double (underrun) soles, sole bruising (erosion) and heel erosion [6–8, 15, 26]. The occurrence of laminitis in dairy cows is predisposed by an interactive array of multiple risk factors [2, 6]. The high prevalence of laminitis and laminitis-related lesions/disorders in the dairy cow claws from Kiserian abattoir and Wangige slaughter slab can probably be attributed to the types of modern farming systems adopted in the dairy business enterprises in which the dairy cows are confined for long hours on hard unyielding concrete floors with much concentrate feeding. Such housing and feeding factors have been incriminated as risk factors for the development of laminitis [6, 7, 23, 27, 28]. The smallholder zero-grazing dairy units expose the cows to additional suboptimal management conditions such as prolonged presence of slurry, lack of claw trimming, and defective concrete floors apart from concentrate feeding [2, 8].

*Connective tissue degeneration manifested by deeply stained degenerated fibroblasts (bold arrows) and fibres (dotted arrows) in the histological sections of the corium of dairy cow claws with chronic laminitis (Toluidine* 

The high prevalence of prominently dilated vascular channels in the distal phalanges of the claws with laminitis particularly chronic laminitis corroborates previous documented observations that dilated vascular channels are consistent observations in subclinical and chronic laminitis. These previous reports indicated that in laminitis, both dilated and non-dilated vascular channels could be found [29]. The more prominent and excessively dilated vascular channels seen in chronic laminitis compared to subclinical laminitis could probably be associated with the

The observed exostoses in the distal phalanges of claws with chronic laminitis are similar to an old report, which found exostosis in the pyramidal process of the pedal bone [30]. Occurrence of these exostoses could be associated with periostitis of the distal phalanges owing to prolonged inflammatory stimuli in chronic laminitis [8]. Although the factors associated with exostosis were not determined in this study, non-infective claw-horn disruption lesions (CHDL) have previously been incriminated as being associated with extra bone development particularly on the caudal aspect of the distal phalanx. The cows that had suffered chronic lameness from CHDL were found to have greater extra bone growth on the caudal aspect of distal phalanx, which was verified both by morphological gross observations and and histologically. This extra bone growth was more in quantity on the lateral claws of the hind limbs and medial claws of the forelimbs [31]. Extra bone development on the distal phalanges was reported to be positively correlated with the age of the cow [32]. Since, the claws in the current study were from culled aged dairy cows

greater damage internally in the claws during chronic laminitis [8].

**50**

led to an increased capillary network, could be a response to inflammatory reaction occurring in laminitis [14]. Enlarged veins seen only in chronic laminitis, which remained widely open appeared like venous dilatation rather than thickening of the wall. This feature has not been described previously in laminitis.

Oedema that was seen in the corium and in the connective tissue of the sole has been reported previously [6]. It occurs as a result of rising capillary pressure together with post-capillary resistance, which enhances transvascular fluid seepage followed by increased pressure within the tissues. Digital venous constrictions are thought to be the initial step in these processes [39]. Subsequently, oedema expands the corium, which causes pain that leads to lameness seen in laminitis [6, 44].

Although chronic degenerative change in the bovine corium of the claw has been reported in chronic laminitis previously [45], the disruptive connective tissue damage particularly involving fibroblasts has not been reported previously. This disruptive damage is probably a degenerative change associated with enzymatic action of matrix metalloproteinases (MMPs) and gelatinolytic protease known as hoofase [46]. It may also be a biochemical alteration in the connective tissue [20]. The degenerative disruption of the connective tissue was observed only in specimens from claws with chronic laminitis.

Disruption of the dermal-epidermal junction is an invariable finding in subclinical and chronic laminitis owing to compromised microvasculature of the corium, which causes nutrients and oxygen to be diminished to the extent of not reaching the epidermal cells. This causes breakdown of the stratum germinativum in the epidermis, the corium becomes degenerated and eventually a breakdown in dermalepidermal junction that results in separation between the stratum germinativum and the corium [44]. Spongiosis and hyperplasia of the epidermis have not been reported previously. Both of these histological changes occurred in subclinical as well as in chronic laminitis. Probably, they are due to inflammation triggered by pressure irritation on the soft tissues located between the pedal bone and the horn of the sole after the claw comes into contact with the hard treading surface when the cow is in standing posture or in locomotion.

Previous studies have shown that laminitis and laminitis-related claw disorders have various cow-level and farm management-level risk factors [2, 6–8]. Although the cows whose claws were used in this study had been pregnant several times, the number of pregnancies and the stage of lactation were not ascertained from the zero-grazing units in which they were kept. It would therefore be recommended that further study be conducted relating macroscopic, radiographic and histopathologic findings on the claws with number of parities, state of pregnancy and stage of lactation of the cows. This will reveal the nature of correlation between these factors, thus indicating the factors exacerbating morphological changes on the dairy cow claws. This should also include correlation with the seasons of the year.

### **6. Conclusions**

The study concluded that claw disorders are prevalent in dairy cows kept under zero-grazing system. The most commonly occurring macroscopic disorders are sole bruising (erosion), claw deformities, heel erosion, double soles, both subclinical and chronic laminitis and white line separation. The radiographic changes found in the claws were mainly associated with chronic laminitis. These occurred on the pedal bone and included dilated vascular channels, irregular bone margins, narrowing of the bone towards the apex and osteolysis. The histopathologic changes were common in the corium of both subclinical and chronic laminitis claws, which included mainly changes in the vasculature such as venular wall damage, arterial

**53**

**Author details**

Nairobi, Kenya

James Nguhiu-Mwangi1

provided the original work is properly cited.

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\* and Peter M.F. Mbithi1,2

2 Office of Vice-Chancellor, University of Nairobi, Kenya

\*Address all correspondence to: jamesnguhiumwangi@gmail.com

1 Department of Clinical Studies, Faculty of Veterinary Medicine, University of

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

wall thickening, vascular thrombosis, connective tissue changes including oedema and degeneration. Most of these changes are evidently irreversible, hence making dairy cows suffering chronic laminitis coupled with extreme claw deformities to

We are grateful to the University of Nairobi Deans Committee for provision of funds to carry out this research. We thank the Chairman of the Department of Clinical Studies for allowing us the use of Departmental laboratory and imaging

There is no conflict of interest for this project and publication whatsoever.

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

facilitation to carry out this research.

have poor prognoses.

**Acknowledgements**

**Conflict of interest**

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

wall thickening, vascular thrombosis, connective tissue changes including oedema and degeneration. Most of these changes are evidently irreversible, hence making dairy cows suffering chronic laminitis coupled with extreme claw deformities to have poor prognoses.
