Understanding Stiffness: The Role of Inflammation in Your Body
- Matt Kurz PT, DPT

- Nov 29
- 5 min read
Inflammation often gets blamed for stiffness and pain—and that is justified. This response of the body, characterized by redness, swelling, heat, and pain, is often viewed negatively, especially when it leads to discomfort and limitations in mobility. However, it is important to recognize that inflammation serves a crucial purpose in our body’s defense mechanisms. When tissues are injured or infected, the immune system triggers an inflammatory response to initiate healing. This process is not merely a byproduct of injury; it is a vital part of the body’s complex healing system. Here’s what is really happening during inflammation and why it isn’t all bad.
Why does inflammation create stiffness:

Swelling and pressure:
When inflammation occurs, the body reacts by increasing blood flow to the affected area, which leads to the accumulation of extra fluid in the tissues. This excess fluid, often referred to as edema, can significantly elevate tissue pressure within the inflamed region. As a result, the increased pressure can physically compress surrounding tissues, including muscles, nerves, and blood vessels. This compression can lead to discomfort, pain, and a noticeable restriction in the range of motion.
Chemical mediators:
Inflammation is the body's complex response to harmful stimuli like pathogens or irritants. Key to this process is the release of cytokines and prostaglandins. Cytokines are proteins that help immune cells communicate, coordinating defense mechanisms, while prostaglandins are lipids that modulate inflammation and pain. During inflammation, cytokines sensitize nerve endings, increasing pain perception and potentially leading to chronic pain. Prostaglandins amplify inflammation by promoting blood flow and enhancing pain receptor sensitivity, resulting in discomfort and protective muscle guarding. This response limits movement to prevent further injury.
Joint changes:
Inflammation in the joints is a complex biological response that can significantly affect joint function and mobility. When inflammation occurs, it leads to a thickening of the synovium, which is the delicate, thin membrane lining the joints. This thickening is often accompanied by an increase in the production of synovial fluid, which, although intended to lubricate the joint, can become more viscous in nature due to the inflammatory processes at play. As a result, the normal, smooth gliding motion of the joint is impaired, leading to discomfort and stiffness.
Pain-avoidance:
From the pain that inflammation causes, you find yourself moving less because each movement is accompanied by discomfort and agony. This reduction in physical activity can quickly lead to significant changes in the muscle structure and function, including muscle shortening and atrophy.
Tissue changes:
Heat and acidity significantly influence the behavior of collagen, a vital protein that plays a crucial role in maintaining the structural integrity of various tissues in the body. When exposed to elevated temperatures, collagen undergoes denaturation, a process that alters its molecular structure and can affect its mechanical properties. This change may result in decreased tensile strength and elasticity, making tissues more susceptible to injury. Similarly, the pH level, particularly in acidic environments, can disrupt collagen's normal function. Acidity can lead to the breakdown of collagen fibers, impairing the tissue's ability to heal and regenerate effectively. Chronic inflammation, often resulting from persistent injuries, infections, or autoimmune conditions, can exacerbate these effects. The inflammatory response triggers the release of various cytokines and growth factors that can alter the normal balance of collagen synthesis and degradation. Over time, this imbalance can lead to excessive production of fibrous tissue, a condition known as fibrosis.
Why does Inflammation create pain:
Chemical sensitization:
Mediators (prostaglandins, bradykinin, histamine, cytokines like IL‑1/TNF‑α, NGF) lower nociceptor thresholds, making nerves fire more easily, creating hyperalgesia and allodynia. Nociceptors are sensory neurons that detect potentially damaging stimuli.
Ion channel changes:
Upregulation of TRPV1, ASICs, and Nav channels increases nerve excitability. Increased nerve excitability causes pain because it leads to the continuous and amplified transmission of pain signals to the brain.
Tissue swelling/pressure:
Swelling can raise interstitial pressure. Increased interstitial pressure causes pain because the excess fluid stretches and applies pressure to tissues, activating pain receptors (nociceptors) and leading to a feeling of tightness or soreness. This buildup can also trap inflammatory substances, which further stimulate pain signals and can lead to chronic pain syndromes.
How Inflammation benefits us:
Rapid defense:
Inflammation recruits immune cells to kill pathogens and contain their spread. This crucial process begins when the body detects the presence of harmful microorganisms, such as bacteria, viruses, or fungi. The immune system responds by sending signals that attract various types of immune cells to the site of infection. Among these cells are neutrophils, macrophages, and natural killer cells, each playing a distinct role in the immune response.
Debris cleanup
Macrophages and neutrophils clear debris and microbes and orchestrate the immune response. Through cytokines and chemokines, they regulate inflammation and tissue repair, ensuring efficient infection response and promoting healing. Their combined efforts are crucial for maintaining homeostasis and protecting the body from pathogens and debris.
Triggers repair:
Releases growth factors that initiate angiogenesis, the formation of new blood vessels from existing ones, crucial for wound healing, tissue repair, and regeneration. Angiogenesis is stimulated by growth factors like VEGF, FGF, and PDGF, which promote endothelial cell proliferation and migration essential for new vessel formation. These growth factors also activate fibroblasts, cells that synthesize the extracellular matrix and collagen, key for tissue repair. Fibroblast activation and collagen deposition provide structural support to new tissue, maintaining integrity and strength. The interaction between growth factors, fibroblasts, and collagen synthesis is vital for restoring tissue architecture and function after injury or disease.
Protective signals:
By inducing pain, the body instinctively prompts the individual to limit movement and avoid further damage to the affected tissue, allowing time for recovery and repair to take place. Furthermore, the swelling that accompanies inflammation can create a physical barrier that protects the injured site from external irritants and potential reinjury, thus facilitating the healing process.
Training effect:
Controlled exposures, such as those experienced during regular exercise, induce a temporary state of inflammation that plays a crucial role in the body's adaptive response. This brief period of inflammation is not merely a byproduct of physical activity; rather, it serves as a powerful mechanism that strengthens various tissues throughout the body, including muscles, tendons, and ligaments. When we engage in exercise, the micro-tears that occur in muscle fibers trigger an inflammatory response. This response is characterized by the release of pro-inflammatory cytokines and growth factors, which facilitate the repair and rebuilding of these tissues, ultimately leading to enhanced strength and resilience over time.
Inflammation is a necessary evil for the protection and healing of our bodies. It can, however, make day-to-day life pretty uncomfortable. Managing inflammation can help accelerate healing, tissue adaptation, and decrease pain. Our next blog post will go over managing inflammation, the best practices to decrease stiffness and pain, and promote the best healing environment for an injury.




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