Unravelling the relationship between age, nociception and joint destruction in naturally occurring osteoarthritis of Dunkin Hartley guinea pigsMcDougall, Jason J.*; Andruski, Benjamin; Schuelert, Niklas; Hallgrímsson, Benedikt; Matyas, John R.PAIN: February 2009 - Volume 141 - Issue 3 - p 222–232 doi: 10.1016/j.pain.2008.10.013 Articles Buy Abstract Author InformationAuthors Article MetricsMetrics ABSTRACT Osteoarthritis (OA) is a debilitating and painful disease, the incidence of which increases with advancing age. One of the confounding aspects of OA is that there is a disconnect between the severity of joint degeneration and the intensity of pain reported. This study examined the relationship between age, joint nociception, and joint pathology in an animal model of naturally occurring OA. Dunkin Hartley guinea pigs were grouped according to age: young (2–5 months) and senescent (17–37 months). Joint nociception was objectively measured in these animals by recording electrophysiologically from knee joint primary afferents in response to non-noxious and noxious movements of the knee. Joint pathology in the same knees was then determined by histomorphology and micro-computerized tomography (micro-CT). A principal components analysis was carried out on the data to determine if any correlation exists between each of the measured variables. In aged guinea pigs, 33% of joint mechanosensory nerves were spontaneously active, whereas young animals showed no such neural activity at rest. The frequency of afferent firing evoked by noxious movements was greater in old guinea pigs. Micro-CT and histopathological determination of OA positively correlated with age; however, there was no significant correlation between the severity of joint degeneration and nociception. In the Dunkin Hartley model of inveterate OA, the level of joint pathology correlates well with increasing age. This study also provides the first objective evidence that there is no correlation between joint nociception and articular damage, thereby corroborating the clinical observation that pain is a poor predictor of OA severity. Department of Physiology & Biophysics, University of Calgary, 3330, Hospital Drive NW, Calgary, AB, Canada T2N 4N1 *Corresponding author. Tel.: +1 403 220 4507; fax: +1 403 210 3949. E-mail address:firstname.lastname@example.org ARTICLE INFO Article history: Received July 8, 2008 Received in revised form August 28, 2008 Accepted October 20, 2008. © 2009 Lippincott Williams & Wilkins, Inc.