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[Morphological investigations of deep sole ulcers in cattle. Part 1: The complicated Rusterholz ulcer].

作者信息

Gehringer Susanne, Müller Matthias, Maierl Johann

机构信息

Dr. Susanne Gehringer, Bayerisches Landesamt für Gesundheit und Lebensmittelsicherheit, Eggenreuther Weg 43, 91058 Erlangen, E-Mail:

出版信息

Tierarztl Prax Ausg G Grosstiere Nutztiere. 2017 Feb 9;45(1):5-17. doi: 10.15653/TPG-141138. Epub 2017 Jan 10.

Abstract

OBJECTIVE

In the context of a larger study on morphological changes of deep sole ulcers, claws with Rusterholz ulcer (RU) were investigated to describe the varied pathological changes of the RU.

MATERIAL AND METHODS

Hind limbs of 55 cows displaying external signs of complicated sole ulcers were examined externally and internally. To examine the samples internally, a sagittal section was performed. Furthermore, the material was examined histologically and after bone maceration. A total of 59 claws of 112 digits with 120 deep sole ulcers displayed a complicated RU.

RESULTS

The most frequent findings were: fibrosis of the heel cushion, partly in conjunction with cartilaginous/osseous areas; osteomyelitis of the tuberculum flexorium, resulting in osteolysis of the macerated bones, often together with peripheral periosteal exostoses; avulsion fracture of the tuberculum flexorium in severely deformed claws; arthritis in the distal joint, frequently in conjunction with subchondral osteomyelitis, with the macerated bone showing osteolyses near the fossae synoviales and in the periphery of the joint surface as well as periosteal exostoses on the insertion point of the joint capsule. Changes in the bursa podotrochlearis, the common digital flexor tendon sheath and the pastern joint occurred less frequently.

CONCLUSIONS AND CLINICAL RELEVANCE

Fibrosis and ossification of the heel cushion were classified as metaplasia, because these processes were considered an adaption to non-physiological strain of the heel. As the infection of the RU spreads, the tuberculum flexorium may play a central role. In advanced cases, an inflammation-related weakening of the bone tissue can lead to a pathological fracture with avulsion of the deep digital flexor tendon. Secondary infection of the distal joint may occur subsequent to any avulsion of the tendon in combination with opening of the joint cavity. More frequently, the infection is likely to have expanded from the insertion point of the joint capsule to the subchondral bone to ultimately infest the joint cavity. Changes in the bursa podotrochlearis, the common digital flexor tendon sheath and the pastern joint are assumed to develop as a consequence of arthritis in the distal joint.

摘要

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