The Effect of NSAID on Serum Periostin

The Effect of Non-steroidal Antiinflammatory Drug on the Serum Periostin Level in Patients of Degenerative Disc Disease

Low back pain (LBP) is one of the most prevalent musculoskeletal disorders worldwide and constitutes a major source of disability and socioeconomic burden. Intervertebral disc degeneration (IVDD) is recognized as one of the primary etiological contributors to LBP, and its prevalence increases substantially with age. The intervertebral disc (IVD) is a complex fibrocartilaginous structure composed of a central gelatinous nucleus pulposus (NP), a surrounding annulus fibrosus (AF), and superior and inferior cartilaginous endplates. The NP and AF cells synthesize a water-rich extracellular matrix (ECM) that confers the disc with its biomechanical properties, enabling load distribution and flexibility of the spinal column.

Under physiological conditions, ECM homeostasis within the IVD is tightly regulated; however, various intrinsic and extrinsic stimuli can disrupt this balance and initiate the degenerative cascade. IVDD has been attributed to a multitude of factors, including aging, obesity, genetic predisposition, mechanical overload, degeneration of the multifidus and psoas muscles, osteoporosis, oxidative stress, and chronic low-grade inflammation. Dysfunction of NP and AF cells, compounded by excessive endplate metabolic activity, leads to progressive endplate calcification, loss of disc hydration, structural failure of the AF, and ultimately irreversible IVDD. Among these contributing factors, elevated oxidative stress and increased secretion of pro-inflammatory cytokines-such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6)-have been shown to markedly accelerate the progression of IVDD by promoting ECM catabolism and suppressing anabolic repair processes.

Periostin (gene symbol: POSTN) is a matricellular ECM protein originally identified in the periosteum and periodontal ligament. It belongs to the fasciclin superfamily and plays a critical role in ECM assembly, tissue remodeling, and cell-matrix interactions. Periostin has been identified as a key mediator of mechanical stress responses, inflammatory signaling, and aging-related tissue changes, and is increasingly recognized as an important contributor to musculoskeletal pathology. Within the IVD, periostin binds to structural ECM molecules-including fibronectin, tenascin-C, and collagens-and participates in disc maintenance and repair. Conversely, dysregulated periostin expression promotes excessive ECM turnover and accelerates IVD degeneration through both mechanosensory and pro-inflammatory pathways. Importantly, serum periostin levels have been reported to be significantly elevated in patients with severe IVDD, and a recent clinical study demonstrated a strong positive correlation between serum periostin concentration and the Pfirrmann grading system, the most widely used MRI-based classification of disc degeneration severity.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly prescribed pharmacological treatments for LBP, recommended in current clinical guidelines as first-line analgesic therapy. NSAIDs exert their primary effects through inhibition of cyclooxygenase (COX) enzymes, thereby suppressing prostaglandin synthesis and attenuating the inflammatory cascade. Beyond analgesia, NSAIDs may modulate the systemic inflammatory milieu in patients with IVDD by reducing circulating pro-inflammatory cytokine levels. Periostin expression is known to be upregulated by inflammatory mediators, including IL-4, IL-13, and TNF-α, and is closely linked to the overall inflammatory burden. It is therefore plausible that NSAID use may indirectly attenuate serum periostin elevation in patients with IVDD-related LBP; however, direct evidence for this hypothesis is currently lacking.

To date, no study has systematically compared serum periostin and inflammatory cytokine concentrations among patients with IVDD-related LBP who are using NSAIDs, those who are not using NSAIDs, and healthy controls without LBP. Elucidating these differences would not only advance our understanding of the role of systemic inflammation and ECM remodeling in IVDD pathophysiology, but would also help clarify whether NSAID use influences the biomarker profile of affected patients-with important implications for patient stratification and biomarker-guided management.

Study Overview

• Status: Recruiting
• Conditions: Intervertebral Disc Disease

• Study Type: Observational
• Enrollment (Estimated): 121

Contacts and Locations

• Study Contact: Name: JIHEE Hong; Phone Number: 01046794343; Email: swon13@daum.net
• Study Contact Backup: Name: Sungwon Jung; Email: swon12@daum.net

Study Locations

• South Korea
  • Daegu, South Korea
    • Recruiting
    • Hong Ji Hee
    • Contact: Sungwon Jung; Email: swon12@daum.net
    • Contact: JIHEE Hong, Professor; Phone Number: 01046794343; Email: swon13@daum.net

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: Adult; Older Adult
• Accepts Healthy Volunteers: Yes

• Sampling Method: Probability Sample

Study Population

low back pain population with disc degeneration confirmed in MRI

Description

Inclusion Criteria:

• lumbar disc herniation
• lumbar spinal canal stenosis
• patients who have MRI

Exclusion Criteria:

• allergic disease
• allergic rhinitis
• asthma
• atopic dermatitis
• chronic sinusitis
• history of cancer
• fracture within 6 months
• severe osteoporosis
• knee osteoarthritis
• hip osteoarthritis
• spinal surgery within 6 months
• myocardiac infarction
• heart failure
• liver cirrhosis
• chronic kidney disease
• rheumatoid disease
• systemic lupus erythematosus
• ankylosing spondylitis
• Crohn's disease
• Ulcerative colitis
• systemic steroid user
• acute or chronic infection
• BMI > 30
• uncontrolled hypertension
• uncontrolled diabetes
• recent hisory vaccination

Study Plan

How is the study designed?

Number of groups / cohorts

3

Cohorts and Interventions

Group / Cohort
NSAID taking group; NSAID taking group with low back pain
non-NSAID taking group; non-NSAID taking group with low back pain
Control group; non-NSAID taking group without low back pain

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Time Frame
the level of serum periostin	Day1

Secondary Outcome Measures

Outcome Measure	Time Frame
The level of serum inflammatory cytokine	Day1

Collaborators and Investigators

• Sponsor: Keimyung University Dongsan Medical Center

Study record dates

Study Major Dates

• Study Start (Actual): June 22, 2026
• Primary Completion (Estimated): May 30, 2028
• Study Completion (Estimated): May 30, 2028

Study Registration Dates

• First Submitted: June 17, 2026
• First Submitted That Met QC Criteria: June 17, 2026
• First Posted (Actual): June 23, 2026

Study Record Updates

• Last Update Posted (Actual): June 29, 2026
• Last Update Submitted That Met QC Criteria: June 24, 2026
• Last Verified: June 1, 2026

More Information

Terms related to this study

• Keywords: intervertebral disc disease
• Additional Relevant MeSH Terms: Intervertebral disc disease
• Other Study ID Numbers: 2026-04-072

Plan for Individual participant data (IPD)

• Plan to Share Individual Participant Data (IPD)?: NO

Drug and device information, study documents

• Studies a U.S. FDA-regulated drug product: No
• Studies a U.S. FDA-regulated device product: No