Depression in Osteoarthritis: Current Understanding

Abstract

Depression, one of the most common comorbidities with osteoarthritis (OA), affects patient prognosis and quality of life. It also increases the overall burden of disease. This subgroup of patients has not been effectively managed in clinical settings. The study aimed to direct physicians’ attention to the co-occurrence of depression and OA. Therefore, this review summarizes the relevant literature published over the past 10 years. The focus is on the prevalence of and risk factors for depression in OA, the effects of depression on OA development and treatment response, comorbidity mechanisms, screening, and non-pharmacological treatment. The research on the etiology of depression has been driven largely by epidemiological studies. Recent studies have shown that high levels of pain, poor levels of function, high numbers of OA sites, and slow gait might be associated with depression. However, the pathophysiology of OA and depression comorbidities remains unclear. In addition to immune inflammation and structural changes in the brain, which have been documented in brain imaging studies, psychosocial factors may also play a role. The evidence indicates that depression can be treated with early intervention; however, adjustments may need to be made for individuals with comorbid depression in OA. It is recommended that health care providers pay more attention to depressive symptoms in patients with OA. Clinicians should develop and implement an individualized and comprehensive treatment plan for patients based on a mental health assessment and in teams with other professionals to optimize treatment outcomes.

Potential value of serum brain-derived neurotrophic factor, vascular endothelial growth factor, and S100B for identifying major depressive disorder in knee osteoarthritis patients

“…(1) in comparison with OA participants without depressive behaviors, a significant decrease in serum BDNF and significant increase in serum VEGF and S100B and VAS scores in OA participants with MDD were observed; (2) in OA participants, there were significant correlations between serum levels of BDNF, VEGF, and S100B and depression and pain assessment scores in MDD patients; (3) particularly, a mediation of the association was found between the VAS scores and the HAMD-17 scores through the BDNF as mediator in OA participants with MDD; (4) significantly lower baseline BDNF levels and higher baseline S100B levels were detected in OA participants who transforming to MDD after a 3-year follow-up when compared with those who showed normal behaviors; (5) at the end of follow-up, significant associations of serum BDNF and S100B with the performance of depression and pain were found in the trans-MDD group; (6) in OA participants, the composite indicator of BDNF, VEGF, and S100B had optimal power to differentiate MDD patients from controls, and the combination of BDNF and S100B could effectively predict the transformation of MDD after the 3-year follow-up. Taken together, serum BDNF, VEGF, and S100B may be a potential diagnostic biomarker of MDD in knee OA, with serum BDNF and S100B in particular being able to predict the occurrence of MDD in the development of OA.…”

“…Pain is the dominant symptom of OA, and in particular, the pain in knee OA is considered as typically transitioning from intermittent weight-bearing pain to a chronic pain ( 3 ). Due to the current clinical therapies are difficult to cure OA completely, the chronic pain and functional limitations can increase risk of negative psychological outcomes, such as major depression disorder (MDD), which will further diminishes quality of life for OA patients ( 4 – 6 ). Furthermore, individuals with MDD exhibit more significant anhedonia and greater daily negative affect compared to non-depressed ones ( 7 ), which may aggravate the feelings of pain in OA.…”

Awareness of Drug–Drug Interaction in Elderly Patients with Osteoarthritis and Depression [Letter]

“…We read with great interest the study by Wang et al, 1 which direct health care providers’ attention to the co-occurrence of depression and osteoarthritis (OA). We especially appreciate the viewpoint that clinicians should implement an individualized and comprehensive treatment plan for osteoarthritic patients with depression.…”

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“…In addition, a failure to contain the pain associated with the disease along with preventable forms of injury may increase this noxious sensation markedly and more extensively thus inducing a need for high levels of dangerous narcotics, as well as reactive depression, and associated self-management challenges, including fears of movement, [22][23][24][25][26][27][28] and the inability to move without pain and immense distress. 29,30 There may also be varying degrees of muscle pathology, a high rate of muscle protein degradation and muscle volume losses, related problems that stem from damage or dysfunction of the joint sensory and motor nerves, muscle inhibition and/or weakness, plus evidence of increasing postural instability in weight bearing joints.…”