OA is a joint disease that involves the degradation of joints, leading to cartilage destruction, bone erosions and regrowth, inflammation of the synovial tissue surrounding the affected joint, and other metabolic effects (Hinton, Moody, Davis, & Thomas, 2002). As cartilage begins to deteriorate, bone-on-bone contact restricts movement and triggers pain in the affected joint area. The effects of OA are limited to one or more impaired joints, with knees, hips, hands, and spine being the most frequently affected joints and wrists, shoulders, and elbows being the least frequently affected joints (Lawrence et al., 2008). Depression is a frequent comorbid condition, with approximately 19 % of OA patients in a primary care setting reporting moderately severe levels of depression (Rosemann et al., 2007), a rate that is substantially higher than the rate of approximately 9 % in unselected primary care patients of similar age (Backenstrass et al., 2006).

OA is the most prevalent arthritic condition, affecting an estimated 27 million adults in the United States (Lawrence et al., 2008). The risk of developing OA significantly increases with age, especially in those 65 years and older (Felson et al., 2000). Among those with OA, older adults report greater physical disability whereas younger individuals experience greater psychological disability and pain (Weinberger, Tierney, Booher, & Hiner, 1990). Before the age of 50, the incidence of OA in most joints is greater in men than women; however, after the age of 50, women show a greater incidence of OA in the knees, feet, and hands than men (as cited in Felson et al., 2000). Additional risk factors of OA include obesity, joint injury, muscle weakness, genetic predisposition, and the presence of additional arthritic conditions.

RA is a systemic autoimmune disease characterized by attacks on the synovial tissue lining the joints by the body’s own immune cells. As a result, the affected joint area becomes inflamed, causing tenderness, pain, stiffness, and fatigue (Harris, 1993). The most commonly affected joints are the proximal interphalangeal, metacarpophalangeal, and the wrists. More severe forms of RA involve widespread joint inflammation. RA is also associated with increased risk of psychopathology; more than 40 % of RA patients experience clinical levels of depression, anxiety, or both (Bruce, 2008; Covic et al., 2012).

The estimated prevalence of RA in the United States is 1.6 million individuals, which includes both juvenile and adult diagnoses (Helmick et al., 2008). Of note, juvenile forms of arthritis apply to individuals who are under the age of 16. Similar to OA, RA becomes more prevalent with increasing age. Individuals who develop RA at a younger age (e.g., 60 or younger) experience more severe disease activity (Harris, 1993) and greater psychological disability (e.g., depression; Wright et al., 1998), relative to those who have a later onset. Further, the risk of developing RA increases 2–4 times if first-degree relatives have been diagnosed (Silman & Pearson, 2002). In fact, studies demonstrate that two-thirds of RA risk may be heritable (Oliver & Silman, 2006). Current research evidence suggests that genetic predisposition alone is not sufficient for producing RA, however, and points to interactions between genes and environment as determining factors in the condition’s onset (e.g., Mahdi et al., 2009).

Like RA, SLE is an autoimmune disease. However, in SLE, the body’s immune system may target not only the joints but also the skin, blood vessels, and organs. Symptoms of pain and fatigue vary from person to person and over time, but a prominent feature of SLE is the development of nonerosive arthritis, with wrists, hands, fingers, and knees being the most frequently affected joints (Hochberg, 1997). The cause of SLE is unknown and its symptoms can range from mild to extreme, depending on the tissues that are attacked by the body’s immune system. For instance, affected individuals may develop skin rashes, cardiovascular conditions (e.g., stroke), gastrointestinal or renal diseases, or neuropsychiatric conditions (Smith & Gordon, 2010). Significant levels of psychological distress are also common among individuals with SLE, with up to 40 % qualifying for a psychological diagnosis (Segui et al., 2000). In fact, the rate of psychiatric disorders is higher in SLE than in other autoimmune conditions, including RA (Sundquist, Li, Hemminki, & Sundquist, 2008). Moreover, levels of distress have been associated with disease activity in SLE (Dobkin et al., 1998). Over time, however, both physical and psychological functioning among patients with SLE can improve (Dobkin et al., 2001).

The prevalence of SLE is lower than that of OA and RA, affecting an estimated 161,000–322,000 adults in the United States (Helmick et al., 2008). Although women are more often diagnosed with SLE than are men, men experience higher rates of morbidity than women. For example, men with SLE more frequently manifest hypertension and renal dysfunction than do women. The risk for developing SLE also varies by ethnicity; African-Americans and African-Caribbeans demonstrate an increased incidence of SLE compared to Caucasians (Hopkinson, Doherty, & Powell, 1994), a pattern that has been attributed to genetic as well as socioeconomic differences (e.g., Hopkinson, Jenkinson, Muir, Doherty, & Powell, 2000). Although the average age at onset for SLE is in the early 30s, it often develops earlier in African-Americans than in Caucasians (Petri, 2002).

A substantial body of work links the experience of minor life stresses with worsening of physical and psychological symptoms in arthritis patients. Among individuals with OA, for example, increases in daily life stressors are linked with greater pain, fatigue, and disability (Parrish, Zautra, & Davis, 2008; Weinberger et al., 1990). Psychological stress also contributes to disease activity and poorer outcomes in RA patients over time. In a comprehensive review of 27 independent studies involving over 3,000 patients, the stress of minor life events lasting hours to days was associated with increased disease activity among adult RA patients (Herrmann, Schölmerich, & Straub, 2000). For instance, minor daily stressors experienced by RA patients on one day were linked to their disease activity several days later (Zautra et al., 1997; Zautra et al., 1998). Moreover, elevations in daily stress have been related to increased next-day fatigue (Parrish et al., 2008) and to more bony erosions and a poorer outcome 5 years later in RA (Feigenbaum, Masi, & Kaplan, 1979). A similar pattern is evident among individuals with SLE (Adams, Dammers, Saia, Brantley, & Gaydos, 1994; Affleck, Tennen, Urrows, & Higgins, 1994; Pawlak et al., 2003). For example, among SLE patients who were followed daily over a 6-month period, experiencing worsened stress on one day was associated with worsened same-day and next-day clinical symptoms (Peralta-Ramírez, Jiménez-Alonso, Godoy-García, & Pérez-García, 2004). Although research comparing patient groups is fairly limited, some evidence suggests that SLE patients may be more vulnerable than are RA patients to the effects of everyday stress, with stronger links between daily stress and physical and psychological status in SLE versus RA patients (Wekking, Vingerhoets, van Dam, Nossent, & Swaak, 1991). RA patients, in turn, may be more vulnerable than OA patients; RA patients show more substantial increases in disease activity as well as depression and poor coping than do OA patients associated with elevations in daily stress (Zautra, Burleson, Matt, Roth, & Burrows, 1994).

Although the experience of minor life stress appears to heighten disease activity and disability, the evidence linking major life stress to health in arthritis patients is mixed. Some evidence suggests that exposure to major life stressors may dampen disease activity and symptoms. For example, a case study of a female RA patient followed weekly over 12 weeks revealed that her disease went into temporary remission during a week when she reported two unexpected family deaths (Potter & Zautra, 1997). In contrast, her minor stressors were related to symptom increases. These findings are consistent with data linking bereavement with immunosuppression in healthy individuals (Schleifer, Keller, Camerino, Thornton, & Stein, 1983). However, other data regarding major life stress and disease activity suggest that recent exposure to major events has no relation to current disease activity in RA or SLE (Chou & Hwang, 2002; Haller, Holzner, Mur, & Günther, 1997; Wallace & Metzger, 1994), and there is no evidence to suggest worsening in functional health over the long term (Da Costa et al., 1999).

The link between stress and health outcomes among arthritis patients may be due at least in part to stress-induced physiological responses. Experiencing stress sets in motion physiological changes, particularly in the nervous and endocrine systems that have evolved to promote survival and restore homeostasis. Two axes of the physiological stress response have been extensively studied: the sympathetic-adrenal medullary (SAM) axis, and the hypothalamic-pituitary-adrenocortical (HPA) axis.

The SAM axis is responsible for instigating the “fight or flight” response via activation of the sympathetic nerves that directly innervate not only the heart, blood vessels, immune organs, and other tissues, but also the adrenal medulla. When stress stimulates the SAM axis, the ensuing effects are immediate. Heart rate and blood pressure increase, and the adrenal medulla releases epinephrine and norepinephrine into the blood stream (Cannon, 1932), thereby propagating physiological arousal. Beyond producing cardiovascular arousal, acute activation of the SAM axis can influence the immune system via the anti-inflammatory effects of norepinephrine that is released not only into the bloodstream but also at sympathetic nerve terminals in the joints and other tissues (Elenkov, Wilder, Chrousos, & Vizi, 2000).

Whereas the SAM axis has both nervous system and endocrine components, the HPA axis is mainly an endocrine system, in which hormones released from glands travel through the bloodstream to target organs. Stimulation of the HPA axis begins when stress initiates the release of corticotropin-releasing hormone (CRH) from the hypothalamus, a gland within the central nervous system. CRH then travels to the anterior pituitary where it stimulates the release of adrenal corticotrophic hormone (ACTH) , which in turn, travels to the adrenal cortex where it triggers release of cortisol. Because it involves a cascade of hormones, the HPA axis is slower acting than the SAM axis; elevations in circulating levels of cortisol are evident approximately 20–30 min after the onset of stress. In healthy individuals, cortisol acts to dampen inflammation. Thus, by enhancing cortisol secretion, stress can serve an anti-inflammatory purpose and act to reestablish homeostasis. However, the impact of stress on cortisol varies depending on the nature of the stress experience. Short-term acute stressors that are characterized by uncontrollable social threat and long-term stressors that involve major life events are the types of stressors that most consistently elicit increases in cortisol (Dickerson & Kemeny, 2004).

The SAM and HPA axes respond in a coordinated fashion to influence immune functioning; thus, dysregulation in one or both systems can have profound implications for chronic inflammatory conditions like RA and SLE. Indeed, existing evidence points to dysregulation of these stress response axes in RA and perhaps SLE. Data gleaned from RA and SLE patients suggests that sympathetic tone is elevated in both conditions (Glück et al., 2000; Härle et al., 2006). Although increased SAM activity in healthy individuals is associated with anti-inflammatory effects, it may be ineffective in dampening inflammation or even fuel inflammation in patients with RA. For example, increased sympathetic activation fuels a pro-inflammatory immune profile in animal models of inflammatory arthritis, whereas blocking SAM activation attenuates inflammation and symptoms in RA patients (Bellinger et al., 2008). The absence of the usual anti-inflammatory effects of the SAM system in patients with autoimmune pain disorders may be at least in part because their immune cell receptors are relatively insensitive to SAM stimulation (Bellinger et al., 2008), and/or they experience a dramatic loss of sympathetic nerve fibers in inflamed tissue (Straub & Kalden, 2009).

Not only do RA and SLE patients show diminished benefits from SAM activation, but also they show decreased responsiveness of the HPA axis to provocation (Geenen, Van Middendorp, & Bijlsma, 2006; Härle et al., 2006; Straub, Dhabhar, Bijlsma, & Cutolo, 2005). In the face of short-term stressors, for example, individuals with RA fail to mount a significant HPA axis response, yielding an inadequate level of circulating cortisol in relation to the level of systemic inflammation (Capellino & Straub, 2008; Dekkers et al., 2001). Moreover, receptors on the surface of immune cells in RA patients show a diminished responsiveness to the anti-inflammatory effects of cortisol (Miller, Jüsten, Schölmerich, & Straub, 2000; Pawlak et al., 1999; Straub et al., 2005), particularly under conditions of minor daily stress (Davis et al., 2008). Taken together, the disturbances of the SAM and HPA axes in these pain conditions appear to create a pro-inflammatory physiological state that facilitates stress-induced aggravation of disease activity (Straub et al., 2005).

Physiological stress response systems are crucial components of the diathesis-stress model; individuals with a preexisting vulnerability at any point in the stress process may be unable to appropriately terminate a stress response and restore homeostasis. Although physiological and psychological responses to stress are determined to a significant extent by the magnitude and duration of stress, the extent of those responses hinges on the effectiveness of efforts to address the demands of the stressors. Thus, being able to manage emotional, cognitive, and behavioral responses to stress are key to sustaining psychological and functional health in patients with arthritis (e.g., Penninx et al., 1997).

The influence of stressors on somatic and physiological responses, and ultimately quality of life in arthritic conditions may depend on the ability to effectively manage emotional stress responses. The dynamic model of affect (DMA) offers a lens through which to view emotional responses to stress in chronic pain (Davis, Zautra, & Smith, 2004), positing that the complexity of emotional processing depends on the stressfulness of the context. According to the DMA, circumstances characterized by low stress allow complex processing of emotional and other information. During times of relative calm, negative and positive affect are experienced on separate dimensions and are relatively independent, and appropriate cognitive resources can be allocated to judge both positive and negative aspects of the environment and subsequently develop an adaptive response. In the face of stress, including the stress of pain, individuals experience more rudimentary emotional processing that is characterized by elevated negative affect and dampened positive affect (Zautra, Reich, Davis, Potter, & Nicolson, 2000). Thus, negative and positive affects are experienced as “black or white,” on a single dimension without complexity or subtlety. Likewise, attention narrows and information processing becomes quick, simple, and readily focused on the negative and demanding aspects of the environment. Such focused affective and cognitive processing is reflexive and is an appropriate response to situations that pose an imminent threat and require an immediate response. In that context, narrowed processing results in a limited ability to fully evaluate and employ the most adaptive response available (Hart, Wade, & Martelli, 2003).

The DMA framework is especially relevant for understanding emotional regulation among pain populations with arthritis. The chronic stress engendered by pain is capable of producing both simplified cognitive processing (Reich, Zautra, & Potter, 2001) and affective dysregulation that is characterized by a heightened level of negative affect and a diminished ability to sustain positive affect (e.g., depression; Romano & Turner, 1985). This affective disturbance is associated with poorer adaptation, reflected in greater pain and fatigue and reports of more frequent stressful experiences among patients (Sale, Gignac, & Hawker, 2008). Perhaps the most significant consequence of the emotion dysregulation experienced by many pain patients is the decline in positive affect, because it impairs the ability to recover from stress (Davis, Thummala, & Zautra, 2014). Numerous studies have documented the benefits of positive affect for limiting the negative impact of stressors and preserving functional health (Finan & Garland, 2015). For example, among women with OA or RA, those who were able to sustain their positive affect during weeks of high stress due to conflict and pain were protected from stress-related elevations in negative affect (Strand et al., 2006; Zautra, Johnson, & Davis, 2005). Boosts in positive affect may also help patients speed their recovery. For example, among depressed OA patients who discussed a stressful interpersonal event, those who subsequently viewed a video to boost positive mood showed decreases in pain relative to those who watched a neutral video (Davis et al., 2014).

It is worth noting that very little work examining affective regulation in response to pain and stress has been conducted in patients with SLE. As noted above, stress is an even more prominent component of daily life in individuals with SLE relative to those with RA (Wekking et al., 1991). In fact, SLE patients primarily perceive their physical health in terms of daily stressors (Dobkin et al., 1998). As a result, individuals with SLE experience higher levels of depressive symptoms and greater psychological distress overall than do individuals with RA (Kozora, Ellison, Waxmonsky, Wamboldt, & Patterson, 2005), which is especially prevalent among SLE patients with more active disease states who experience greater pain, helplessness, and physical disability (Seawell & Danoff-Burg, 2004). Thus, due to ongoing daily stressors, pain, and other disabling aspects of SLE, affective disturbances tend to become ingrained as part of the illness experience. The extent to which positive affect can offset the deleterious effects of stress among SLE remains to be determined, although there is no reason to expect that the pattern of findings evident for OA and RA patients will not hold for SLE patients as well.

One means for overcoming the emotional simplification associated with stress is maintaining or boosting positive mood, which acts as a source of resilience (i.e., Strand et al., 2006; Zautra et al., 2005). A second, less developed line of work points to another potential avenue to promote adaptive emotional regulation during stressful events: the development of mood clarity (Salovey & Mayer, 1989). Mood clarity refers to the ability to be able to distinguish between different emotions, an individual difference that should be relevant to sustaining affective differentiation during times of stress. In healthy subjects, higher levels of mood clarity are related to lower levels of depression, social anxiety, and cortisol secretion during stressful days (Salovey, Stroud, Woolery, & Epel, 2002), and among older adults to an attenuated relation between pain and subsequent depression (Kennedy et al., 2010). In pain patients, higher levels of mood clarity are linked with more distinct experiences of negative and positive affect, reflecting greater affective differentiation (Study 1; Zautra, Smith, Affleck, & Tennen, 2001). Thus, the accruing evidence points to the adaptive value of sustaining affective differentiation in general, and positive affect during times of stress in particular, for individuals managing chronic pain.

According to the Lazarus and Folkman (1984) model of stress and coping, cognitive-affective appraisals, or people’s evaluation of their pain, its meaning and significance, and the resources they have available to cope with it are all important determinants of adaptation to the stress of chronic pain. Pain-related beliefs and appraisals have often been found to be more important determinants of outcomes in arthritic conditions. One such cognitive appraisal, pain self-efficacy, characterized by positive expectancies about one’s ability to successfully cope with pain, has been proven to be one of the most potent predictors of improved outcomes and successful adaptation in arthritis patients (for a review, see Marks, Allegrante, & Lorig, 2005). On the other hand, excessive negative expectancies of future pain experiences, termed pain catastrophizing, have been proven to be an equally consistent and powerful predictor of poor adaptation among individuals with chronic pain (for a review, see Sullivan et al., 2001).

Self-efficacy has been established as an important construct that is predictive of positive emotional, physical, and functional outcomes for pain patients. Arthritis self-efficacy, in particular, is defined as an individual’s belief in his or her ability to successfully manage arthritic pain and other stressors generated by arthritis (Bandura, 1997). Studies in arthritis patients have shown that individuals vary in their self-efficacy for managing pain, with some feeling confident in their ability to cope with pain and its related stress, and others feeling less able to effectively manage the condition (Lorig, Chastain, Ung, Shoor, & Holman, 1989). Within OA patients, pain self-efficacy has been shown to account for a significant proportion of variance in physical health outcomes, with patients with higher self-efficacy reporting lower pain (Pells et al., 2008). Further, an inverse relationship between emotional distress and self-efficacy has often been demonstrated in RA patients; higher self-efficacy expectations consistently predict lower levels of stress, anxiety, and depression (Arnstein, Caudill, Mandle, Norris, & Beasley, 1999; Lowe et al., 2008; O’Leary, Shoor, Lorig, & Holman, 1988). Although the role of self-efficacy has not been extensively studied in SLE patients, many studies with chronic pain populations have demonstrated that individuals with greater self-efficacy experience less interference from pain in their daily physical functioning (Arnstein, 2000; da Cunha Menezes Costa, Maher, McAuley, Hancock, & Smeets, 2011).

Because pain self-efficacy is consistently linked to most of the markers of better adaptation to stress, several researchers have suggested inclusion of pain self-efficacy as a target in interventions for arthritis patients (American College of Rheumatology Subcommittee on Rheumatoid Arthritis, 2002; Marks et al., 2005; McKnight, Afram, Kashdan, Kasle, & Zautra, 2010). In fact, treatment-outcome studies in OA, RA, and SLE patients have shown that an increase in self-efficacy is not only related to improvements in psychological and functional variables such as reduced helplessness, anxiety, depression, and fatigue, and pain perception, but that it is also important to long-term maintenance of treatment gains (Chui, Lau, & Yau, 2004; Lorig, Mazonson, & Holman, 1993; Karlson et al., 2004; Keefe, Caldwell, et al., 1996; Keefe, Kashikar-Zuck, et al., 1996; for reviews, see Marks, 2001 and Seawell & Danoff-Burg, 2004).

While appraisals such as a self-efficacy are considered positive strengths, maladaptive cognitive responses such as catastrophizing are also powerful predictors of adaptation to stress and other outcomes for arthritis patients. Pain-related catastrophizing is the tendency to magnify the perception of pain or make exaggerated predictions about its damaging consequences (Rosenstiel & Keefe, 1983; Sullivan, Bishop, & Pivik, 1995). A propensity to catastrophize about pain has been associated with several negative outcomes, including higher levels of negative affect, increased risk of depression, and greater anxiety and overall emotional distress (Keefe et al., 1991; Moldovan, Onac, Vantu, Szentagotai, & Onac, 2009). In fact, within OA patients, pain catastrophizing has been shown to account for a significant proportion of variance in pain, both psychological and physical disability, and gait speed (Somers et al., 2009). Functional disability has also been consistently predicted by pain catastrophizing in RA patients (e.g., Keefe, Brown, Wallston, & Caldwell, 1989; Parker et al., 1989). This association between pain catastrophizing and increased disability may be due in part to high pain catastrophizers focusing more attention and coping efforts on potential or actual pain signals. A similar link between pain catastrophizing and functional outcomes likely exists in SLE patients, although this relation has not been examined to date.

Results of treatment studies demonstrate the importance of catastrophizing and self-efficacy appraisals in mediating and sustaining improvements in pain outcomes, but in the opposite directions. Pain catastrophizing is associated with increased disability and poor adaptation, whereas pain self-efficacy predicts a more resilient response. Thus, while both constructs are beliefs about one’s ability to cope with chronic pain, they tend to be inversely related (Asghari & Nicholas, 2001; Keefe et al., 1997; McKnight et al., 2010). Pain catastrophizing, in fact, may interfere with the development of self-efficacy because individuals dwell on their pain or the threat of pain, and interpret it as being out of their control. This sense of helplessness about one’s ability to deal with pain leads to further maladaptive cognitive processes, such as a hypervigilance to pain or the anticipation of pain onset. When attention is narrowed to this threat, opportunities for adaptive self-regulation become limited because switching to other adaptive behaviors or cognitions requires significant cognitive resources. However, some findings that suggest that well-timed, pain-relevant social support may provide a means of interrupting the cycle linking catastrophizing with poor functioning. In a daily diary study of individuals with RA, higher satisfaction with spousal pain-related support was protective against the detrimental effects of pain catastrophizing on subsequent increases in negative affect and pain (Holtzman & DeLongis, 2007).

More recently, the capacity to accept pain and other stressors has come to the fore as a potentially important cognitive coping response linked to better functional health among those in pain. Acceptance of pain is defined as the capacity to respond to pain without attempting to control or avoid it, and to remain willing to stay engaged in life despite pain (McCracken, 1998). The body of evidence, which to date is based primarily on general samples of chronic pain patients, points to the benefits of pain acceptance in promoting positive adaptation to pain and other stressors (McCracken & Zhao‐O’Brien, 2010). Pain acceptance shows cross-sectional associations with reports of lower pain intensity, pain-related distress and avoidance, depression, and disability (McCracken & Eccleston, 2006), and explains more variance in outcomes than more traditional coping strategies (McCracken & Eccleston, 2006). It is also linked with the capacity to limit increases in negative affect associated with acute pain flares in daily life (Kratz, Davis, & Zautra, 2007) and has been prospectively linked to decreased future pain and better functional health (McCracken & Eccleston, 2005). Some evidence suggests that the benefits of pain acceptance may be mediated via lessened attention to pain, greater engagement in daily activities, and higher efficacy to perform day-to-day activities (Viane, Crombez, Eccleston, Devulder, & De Corte, 2004).

Behavioral responses to pain and other stressors are influenced by two independent motivational systems: the avoidance system and the approach system (e.g., Davidson, 1992; Elliot & Thrash, 2002; Gray, 1994). Specifically, the avoidance system of motivation is activated by self-protective biases, aimed at escaping from an undesired state that is perceived to be threatening. In contrast, the approach system of motivation promotes behaviors and associated cognitions and emotions that are aimed at achieving a desired end state. Together, the motivational systems function to promote self-regulation and adaptation to positive and negative circumstances.

The fear-avoidance model of pain (Vlaeyen & Linton, 2000) posits that although avoidance may be adaptive in the acute pain stage by preventing further injury, for chronic pain sufferers, fear of pain and associated stressors may lead to consistent avoidance of important daily activities. Thus, the heightened attention to pain, difficulty disengaging from the threat of pain, and worry may fuel avoidance behaviors that have a deleterious effect on physical and emotional functioning over the long term. In addition to employing strategies to escape or avoid pain, pain patients may adopt another maladaptive pain management approach: withdrawal from engagement in valued activities. When preoccupied with the fear of pain, chronic pain sufferers refrain from initiating desirable activities or persisting in meeting meaningful goals. They may also withdraw socially from friends and family, thereby cutting off beneficial social support.