Introduction

Lameness is a common affliction of dairy cows that causes pain, decreases production and increases likelihood of culling. Many diseases cause lameness, and can be grouped as either infectious (e.g. digital dermatitis) or the noninfectious: the claw horn lesions (most commonly, sole ulcer, sole haemorrhage and white line disease). However, the mechanisms by which the claw horn lesions occur are incompletely understood. Recent and ongoing work at the University of Nottingham, School of Veterinary Medicine and Science, explores the disease process, to help understand why the claw horn lesions occur and what can be done to prevent them. Described here are two studies that summarise our understanding of the claw horn lesions. 

The claw horn lesions almost certainly occur through a similar mechanism. This mechanism appears to be through compression of and contusion within the germinal epithelium in the sole of the foot that produces the claw horn. Contusions occur to differing extents and at different locations, which appears to cause the differences between lesion location (e.g. sole versus white line) and severity (e.g. haemorrhage vs ulceration). Two factors are pivotal in the formation of these lesions: greater downward forces exerted by the pedal bone and poorer cushioning of these forces; both result in greater forces exerted on the germinal epithelium and increased likelihood of damage. Many factors such as claw overgrowth, lying times and social competition, underfoot conditions and physiological changes around parturition can increase or prolong the downwards forces exerted through the pedal bone (Newsome et al., 2016, open access). In addition to these, the capacity of the digital cushion in dissipating the forces during foot strike is instrumental to protecting the germinal epithelium of the sole from compression and disruption of growth.

Study 1: The digital cushion

The digital cushion is a connective tissue structure that sits beneath the pedal bone of the foot, and contains large depots of adipose tissue. The fat is high in mono-unsaturated fatty acids and is bound by a connective tissue capsule. It acts as a noncompressible fluid structure that dissipates forces during foot strike, transferring the forces to the structures that are designed to absorb shock and bear weight: the wall. This reduces the peak load on the germinal epithelium at any point and protects against claw horn lesion formation.

Epidemiological work has demonstrated that body condition loss preceded lameness events, whether lameness was defined by poor mobility (Randall et al., 2015, Lim et al., 2015) or by the treatment of lesions (Green et al., 2014). Cross-sectional work has also shown that body condition score was associated with digital cushion thickness (Bicalho et al., 2009).

The hypothesised reason for body condition loss predisposing lameness is that thinning of the digital cushion leads to poorer cushioning capacity and greater forces on the germinal epithelium of the sole. A thin digital cushion has been shown to increase risk of lesions and lameness (Machado et al., 2011, Toholj et al., 2013), but no work has yet repeatedly measured the digital cushion to assess whether change in thickness occurs with body condition loss, or whether thinning of the digital cushion, rather than absolute thinness, leads to lameness.

The first aim of this study was to determine how the digital cushion changes throughout lactation and with changes in body fat measures. The second aim was to discern whether absolute or changes in digital cushion thickness influence future lameness and lesions.

Study 1: Materials and methods

A longitudinal study monitored 180 cows on 2 high yielding robotic dairy herds (>11,500 litres per 305 day lactation) throughout 1st, 2nd, 3rd and 4th lactations at 5 assessment points: approximately 8 weeks prior to calving and during the 1st, 9th, 17th and 29th week of lactation. The digital cushion and corium were measured using ultrasonography at each assessment point. Additionally, body condition score and back fat thickness (measured ultrasonographically) were recorded. Lesions present on claws were recorded at assessment points, and cows were mobility scored fortnightly throughout the study.

Three statistical models were built to assess:
1. The association between digital cushion thickness and body fat.
2. The effect of a thin digital cushion and low body condition on future lesion formation.
3. The effect of a thin digital cushion and low body condition on future lameness.

Study 1: Results

Firstly, digital cushion thickness was associated with body fat measures. However, this association was obscured at some assessment points by lesion occurrence: the digital cushion was abnormally thickened when a sole ulcer was present, pointing to inflammation in and thickening of the digital cushion. Secondly, the digital cushion was thinnest immediately after calving, before cows had lost condition. Thirdly, the thin digital cushion thickness at any point during the study increased the risk of subsequent lesions and lameness. Only sometimes was the thin digital cushion related to body condition. 

Study 1: Discussion

The results present a novel insight into the role of the digital cushion in lameness. They add to the evidence that body condition loss is a key component of claw horn lesions, and additionally highlight that body condition is only one of many factors that must be addressed in lameness control: many factors could cause a thin digital cushion, such as periparturient hormones causing laxity in the suspensory apparatus of the foot (as seen immediately after calving, and all of these have potential implications on lameness.

The work also demonstrates the inflammation present during lesion formation. This strengthens the message that lameness is a manageable disease, that early detection and effective treatment are instrumental in controlling it and that non-steroidal anti-inflammatories are an essential component of treatment (Thomas et al., 2015).

Study 2: Bone development on the pedal bone with repeated lameness (published open access: Newsome et al., 2016, in press)

Study 2: Introduction

A second study looked at chronicity of the claw horn lesions. It has been shown that delayed treatment increases recovery time, occurrence of lesions increases risk of further lesions in subsequent lactations (Hirst et al., 2002) and that the lesions can become chronic, whilst early detection and effective treatment reduces recurrence of lameness (Groenevelt et al., 2014). Untreated lesions could incur damage to the internal anatomy of the foot, including to the flexor tuberosity of the pedal bone, upon which bone development occurs with age (Tsuka et al., 2012). Similar bone development occurs in humans where high load passes around ligament insertions, often as incidental findings with no clinical significance (Benjamin et al., 2000). Our aim was to assess whether bone development at slaughter was associated with poor locomotion and CHL incidence during a cow’s life.

Study 2: Materials and methods

A retrospective cohort study imaged 142 hind feet from 72 HolsteinFriesian dairy cows culled from a research herd (SRUC Dairy Research Centre, Dumfries, UK) using computed tomography. Bone development on the pedal bone was measured and tested as the outcome in a linear regression model. Explanatory variables described mobility score, which had been assessed weekly throughout life from first calving, age and occurrence of lesions throughout life.

Study 2: Results

Bone development increased with age, was greater in cows that had experienced a claw horn lesion during life, and was greater with poorer mobility (the mobility score variable tested was ‘the proportion of weekly mobility scores at which a cow was lame, during the 12 months preceding slaughter’). The bone development on the most severely affected foot was best predicted by lameness history.

Study 2: Discussion

Age explained much variation in bone development. The association between bone development and a previous history of lameness was a novel finding, and bone development appeared to be specific to claw horn lesions.

Several mechanisms for the formation of bone development are plausible. Inflammation occurring at the sole ulcer site during sole ulcers (as seen in Study 1) could elicit bone development on the flexor tuberosity, which then exerts greater forces on and cause further contusions within the germinal epithelium of the sole during foot-strike. Inflammation could also utilise fat depots within the digital cushion for the production of inflammatory mediators and decrease its future cushioning capacity. Both of these mechanisms could precipitate further lameness and could become self-perpetuating. In order to stop irreparable anatomical damage within the foot, early identification of claw horn lesions and effective treatment could be critical, particularly for first lifetime cases of lameness.This further emphasizes the importance of non-steroidal anti-inflammatories in lesion treatment, to resolve inflammation at the sole ulcer site and prevent permanent damage to the surrounding structures.

Conclusions

The claw horn lesions are principally a result of two factors: downward forces on the germinal epithelium of the sole through the pedal bone, and cushioning of forces during foot strike. Many factors, including body condition, can influence the function of the digital cushion. If the digital cushion becomes too thin, lesions and lameness occur. Further, inflammation at the sole ulcer site likely initiates bone development on the pedal bone, which then places greater forces on the germinal epithelium and causes lameness to perpetuate. These studies suggest that managing the risk factors for lameness, in addition to early detection and effective treatment of lameness, which includes nonsteroidal anti-inflammatory therapy, are pivotal to lameness control on farm.

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