Abstract
Introduction Understanding how annular failure might occur following increased nuclear pressurisation requires an experimental approach that avoids artefactual injury to the annulus but reveals structural disruption resulting directly from the pressurisation event. The aim of this study was to investigate the fundamental mechanisms by which both intra and inter-lamellar relationships are disrupted by nuclear pressurisation, with the development of a model that might accurately reproduce mechanisms of intervertebral disc injury secondary to events causing raised intradiscal pressure.
Methods Bovine motion segments were subjected to internal pressurisation using a novel “through vertebra” method. Intra and inter-lamellar sections were deliberately chosen so as to expose systematic patterns of structural disruption resulting from the pressurisation event. This micro-disruption was investigated using a novel method which combined microtensile manipulation and simultaneous differential contrast imaging of the fully hydrated unstained sections.
Results The inner annulus was most severely disrupted. The middle regions developed a series of regular clefts along axes of weakness within the in-plane arrays of fibres in each lamella with a slight oblique passage radially away from the centre. These annular clefts separated the pre-existing transverse or side-to-side interconnections within the longitudinal fibre arrays. Progression to the peripheral lamellae occurred when the clefts crossed lamellae with associated inter-lamellar junction separation, with progressively lesser degrees of disruption further from the central area of pressurisation.
Discussion This study demonstrates that raised intradiscal pressure creates a consistent pattern of annular failure, which may preceed clinically relevant disc lesions, and specifically annular lesions. These findings offer a possible explanation for (a) annular weakening that alters the ability of the nucleus to maintain hydration after load, (b) the initiation of paths for annular tear development, (c) pathways that may expand to allow disc prolapse and (d) pathways for ingrowth of inflammatory and neural tissue mediating disc pain.
The abstracts were prepared by Assoc Prof Bruce McPhee. Correspondence should be addressed to him at the Division of Orthopaedics, The University of Queensland, Clinical Sciences Building, Royal Brisbane Hospital, Herston, Brisbane, 4029, Australia.
