Can You Have Both Ankylosing Spondylitis & Psoriatic Arthritis?

Ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are chronic inflammatory conditions that affect the joints, often presenting diagnostic challenges when symptoms of both diseases overlap. While they share genetic and immunologic features, they also have distinct characteristics that influence diagnosis and treatment.

Inflammatory Mechanisms

Both AS and PsA are driven by chronic inflammation but involve different immune pathways. AS is primarily associated with excessive activation of the interleukin-17 (IL-17) and interleukin-23 (IL-23) axis, leading to persistent inflammation in the axial skeleton. This process targets entheses—the connective tissue between tendons or ligaments and bone—resulting in new bone formation and spinal rigidity. PsA, in contrast, involves a broader inflammatory network, incorporating tumor necrosis factor-alpha (TNF-α), IL-17, and IL-22, which contribute to both joint and skin pathology.

Cellular involvement further distinguishes these conditions. AS is driven by innate immune cells such as γδ T cells and innate lymphoid cells (ILCs), which produce IL-17 and sustain inflammation in the sacroiliac joints and spine. PsA involves a complex interplay of innate and adaptive immune responses, with Th17 and Th1 cells playing a significant role. This broader immune activation may explain the more heterogeneous joint involvement seen in PsA.

Genetic predisposition also plays a role. The HLA-B27 gene is strongly linked to AS, promoting an exaggerated inflammatory response in the axial skeleton. While HLA-B27 can appear in PsA, its association is weaker, with HLA-Cw6 being more relevant, particularly in patients with psoriasis. These genetic differences influence disease expression and response to treatment.

Spine And Sacroiliac Involvement

Both AS and PsA affect the axial skeleton, but with different patterns. In AS, inflammation typically starts in the sacroiliac joints and progresses symmetrically up the spine, leading to syndesmophyte formation and the characteristic “bamboo spine” appearance in advanced disease. This process results in spinal rigidity and reduced mobility over time.

PsA, in contrast, affects the spine and sacroiliac joints in a more asymmetric and patchy manner. While sacroiliitis is nearly universal in AS, its presence in PsA varies, ranging from mild inflammation to severe joint erosion. Spinal changes in PsA also differ, with non-marginal syndesmophytes—irregular bony outgrowths that do not follow the linear progression seen in AS. These distinctions are evident in imaging studies, where PsA exhibits more erratic joint damage compared to AS’s uniform progression.

Pain patterns also differ. AS typically presents with deep-seated, bilateral inflammatory back pain that worsens with rest and improves with activity. PsA-related spinal pain is more variable, sometimes mimicking mechanical back pain due to its inconsistent distribution. Some PsA patients experience acute flares in different spinal segments, interspersed with symptom-free intervals, whereas AS follows a more persistent trajectory.

Peripheral Joint Patterns

PsA often presents with an unpredictable pattern of peripheral joint involvement, whereas AS primarily affects the spine and sacroiliac joints. PsA commonly manifests as asymmetric oligoarthritis, affecting fewer than five joints in an irregular distribution. In contrast, AS, when it involves peripheral joints, tends to do so in a more uniform, bilateral manner.

Dactylitis, or “sausage digit,” is a hallmark of PsA, involving diffuse swelling of an entire finger or toe due to inflammation of both joints and surrounding soft tissues. This feature is rare in AS and serves as an important diagnostic clue. Enthesitis, present in both diseases, also differs in its distribution. PsA frequently affects the Achilles tendon and plantar fascia, whereas AS more commonly involves the axial skeleton.

Joint deformities further highlight the differences between these conditions. PsA can lead to severe erosive arthritis, with “pencil-in-cup” deformities visible on radiographs. This destructive process is less common in AS, where peripheral joint damage is typically milder. PsA may also involve distal interphalangeal (DIP) joints, often alongside nail changes, which are rare in AS.

Dermatologic Manifestations

PsA is unique among inflammatory arthritides due to its association with psoriasis, a condition characterized by erythematous plaques covered with silvery-white scales. Psoriasis can precede joint symptoms by years, but some individuals develop musculoskeletal symptoms first, complicating early diagnosis. The severity of skin involvement does not always correlate with joint disease activity.

Nail involvement is another distinguishing feature of PsA, occurring in approximately 80% of patients. Nail pitting, onycholysis (separation of the nail from the nail bed), and subungual hyperkeratosis are common findings that provide a strong diagnostic clue. These changes are rarely seen in AS. Some PsA patients may also develop pustular or erythrodermic psoriasis, which can significantly impact quality of life.

Imaging And Laboratory Clues

Imaging and laboratory tests are essential for distinguishing AS from PsA. Radiographic findings reveal characteristic patterns of joint and bone involvement. AS typically presents with symmetric sacroiliitis, erosions, and sclerosis that progress to joint fusion. The spine develops marginal syndesmophytes—thin, vertically oriented bony growths contributing to spinal stiffness. PsA, in contrast, exhibits asymmetric sacroiliitis and non-marginal syndesmophytes that are bulkier and irregularly shaped.

MRI can detect early inflammatory changes before structural damage appears on X-rays. In AS, bone marrow edema at the sacroiliac joints and vertebral corners is common. PsA may also present with bone marrow edema but often involves more widespread enthesitis at peripheral sites.

Laboratory markers provide additional clues. Elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are common in both conditions, though more consistent in AS. The HLA-B27 genetic marker is strongly associated with AS, while PsA has a more heterogeneous genetic profile. Rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA) are typically negative in both diseases, helping differentiate them from rheumatoid arthritis.

Potential Disease Progression

The long-term progression of AS and PsA varies significantly. AS follows a more predictable course, often leading to progressive spinal fusion and functional impairment if untreated. Structural changes, including syndesmophyte formation and vertebral ankylosis, can severely restrict mobility and increase the risk of fractures, particularly in the cervical spine.

PsA presents a more unpredictable trajectory. Some patients experience mild, intermittent symptoms, while others develop aggressive joint destruction. Unlike AS, where new bone formation dominates, PsA often leads to erosive joint damage, particularly in peripheral joints, resulting in severe deformities and disability. PsA is also associated with an increased risk of cardiovascular disease, metabolic syndrome, and other systemic comorbidities, further complicating management. Early intervention is crucial in both conditions to prevent irreversible damage and improve long-term outcomes.