The prevalence of enthesitis in patients with PsA runs between 25% and 53% when defined by physical exam findings alone.6 When identified by imaging, the prevalence is much higher, likely because the nearness of entheses to joints may result in clinical misdiagnosis of enthesitis as synovitis or fibromyalgia tender points.
Enthesitis may also be asymptomatic or subclinical. Young age, increased disease duration, HLA-B27 alleles, active peripheral joint disease and elevated body mass index are risk factors for developing enthesitis.6-9
Pathophysiology
Dactylitis is digital inflammation affecting multiple superimposed, anatomical layers. There is uncertainty about the initial lesion in dactylitis. In a systematic literature review of ultrasound and MRI findings in dactylitis, the most commonly seen pathologies were flexor tenosynovitis and joint synovitis (90%).9 In a high-resolution MRI study of dactylitic fingers, additional findings included collateral ligament enthesitis (75%), flexor tendon pulley/flexor sheath microenthesopathy (50%), bone marrow edema and diffuse extracapsular soft tissue edema.11
We can conclude dactylitis is a quantitatively and qualitatively heterogeneous process distinguished by inflammation crossing anatomical structures, and there is significant overlap with enthesitis and synovitis (see Figures 3 and 5). Clinical diagnosis of dactylitis may identify an already advanced inflammatory process. This may explain the association of clinical dactylitis with joint erosions and damage in the affected digits, and as an overall prognostic indicator for aggressive disease.
Enthesitis is a hallmark of PsA, but the exact reason why this manifestation occurs remains unclear. Enthesitis may occur in healthy individuals due to mechanical stress (e.g., Achilles tendinitis, tennis elbow, etc.), but it occurs more frequently and diffusely in patients with PsA. In PsA, inflammatory changes of the entheses mostly involve the fibrocartilaginous, rather than membranous, attachments.12 Some researchers postulate the trigger for entheseal inflammation is a mechanical insult, followed by an excessive inflammatory reaction driven by the innate immune response.
Prostaglandin E2 (PGE2), the main enzymatic product of cyclo-oxygenases, is a vital early mediator of inflammation. PGE2 induces vasodilation, which could facilitate neutrophil migration from the bone marrow to the neighboring entheseal compartment. Thereafter, interleukin (IL) 17, IL-23 and TNF-α are instrumental in augmenting inflammation.6
The end result of enthesitis? New bone formation, tendon integrity disruption and neovascularization, features that can be quantified using ultrasonography.
Enthesophytes are caused by excessive local apposition of periosteal bone to entheseal sites. To correlate it clinically, entheseal inflammation of the anterior longitudinal spinal ligament results in syndesmophytes with spinal ankylosis, and entheseal inflammation of the plantar fascia results in calcaneal spurs.6
