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Immediately after the body is injured, it starts the processes of stopping blood loss, restoring function, and preventing infection from pathogens on the skin or objects that may have caused the damage. The microenvironment of the injured area is in constant flux with the host cells continuously responding to the fluids, bacteria, and the dead and dying cells at the wound site.

One of the first phases of the healing process is for circulating platelets to attach to a fibrous scaffold, a matrix, to stop blood flow. Platelets, recently defined as immune cells, release cytokines, immune messengers, which permit cells to communicate with one another.

 Once the flow of blood ceases, specialized immune cells enter the area setting up an inflammatory response that “cleans” the wound site and removes bacteria, damaged tissues, and foreign matter. In order to achieve the appropriate levels of inflammation, many complex cell-to-cell interactions occur in specific order.

Accumulation of fluids, exudates, results from inflammation, along with swelling at the wound site. Exudates are essential for the healing process and contain debris, inflammatory cells, bacteria, and a large variety of immune proteins. Depending on their concentrations, factors may enhance healing or interfere with the process. Proteins found in exudates have a variety of functions including regulation of inflammatory responses, triggering growth of new blood vessels, and stimulating growth of new cells.

A delicate balance of inflammatory and anti-inflammatory messengers is crucial and it determines the pace, and outcome of healing. Homeostatic, balanced, inflammatory responses are essential. Too little, too great, or too lengthy of an inflammatory response damages healthy tissue and delays healing.

The remodeling phase is one where tissues regenerate and close the wound. Closure occurs as cells cross-link and organize themselves attaching to a scaffold, a matrix that will draw edges of the skin closed and cover the area.

Poorly Healing Wounds

The presence of bacteria, foreign bodies, a lack of oxygen in the tissues, and/or fragments of necrotic, dead, tissue can stimulate inflammatory cells continuously, resulting in uncontrolled inflammation and wounds that heal poorly.

Infection of a wound site also interferes with proper healing. Communities of bacteria tend to organize themselves into a biofilm, a thin sheet of bacteria. Biofilms increase survival of bacteria colonies, reducing chances that inflammatory immune responses, or antibiotics, can control them.

Exudates in poor healing wounds contain an over abundance of inflammatory cells and immune mediators that increase inflammation. Sufficient anti-inflammatory factors to control the damaging effects of excessive inflammation may not be available.

Proteolysis is another one of the steps required for healthy healing. This is an event during which the body degrades necrotic tissue, and dead and dying pathogens. [Think of proteolysis as an acid/enzyme reaction that breaks down tissues.] When immune cells release too many proteolytic proteins over a longer period, they become destructive of healthy tissue, and the body’s ability to heal the wound is overwhelmed.

Individuals with non-healing skin ulcers, such as those found in diabetics, not only struggle with excessive inflammatory responses, but their proteolytic enzyme levels are significantly elevated giving rise to further imbalances in inflammatory responses and interference with the body’s repair mechanisms.

Summary

The sensitive balance between stimulating and inhibitory mediators during diverse repair of wound is crucial to achieving tissue homeostasis following injury. Once unbalanced and excessive inflammation is controlled, will healing begin.

 
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The mouth is a unique bio-environment for bacteria and other microorganisms. The oral cavity must always be in microbial and immune homeostasis (balance).. Hundreds of types of bacteria need to be properly balanced to protect the mouth from infection or severe gum disease can result from microbial imbalances or “dysbiosis”.

Oral Disease
Many microorganisms in the mouth attach to the teeth. The accumulation of microbes on the surface of teeth is called a “biofilm”, which may eventually calcify into a matrix of hard material called “plaque”.

If not removed, biofilms can lead to inflammation of the gums; a first step in the development of dental caries and “gingivitis”. This mild form of gum disease results in swollen and red gums that may exude pus and bleed easily upon brushing. If left untreated, gingivitis may escalate to periodontitis. In periodontitis, pockets of microbes form and the infection spreads and grows below the gum line, damaging bone, and loosening teeth.

Oral Inflammation
Periodontal-causing pathogens in the mouth trigger defense mechanisms resulting in defensive inflammation. However, when inflammation is not controlled, bone and connective tissues are damaged; the gums pull away from the teeth and leave them in danger of falling out.

When dysbiosis occurs, pathogenic periodontal bacterial communities may overpopulate the mouth. The bacteria are able to circumvent immune cell attacks. As the number of bacteria increase, they stimulate more inflammatory responses leading to bone loss and worsening periodontitis.
As might be expected, treating periodontitis decreases the biomarkers of inflammation throughout the body.

Atherosclerosis and cardiovascular disease
Inappropriate levels of inflammation in the mouth can lead to inflammation throughout the body. It is therefore not surprising that periodontal disease increases the risk of having other inflammatory conditions such as atherosclerosis and cardiovascular disease. Indeed, individuals with atherosclerosis and periodontitis share genes that appear to stimulate similar inflammatory pathways.

Alzheimer’s Disease (AD).
Amyloid plaque accumulation in the brain is a major feature of Alzheimer’s disease (AD); heightened levels of amyloid have been associated with greater risk of periodontal disease. Even in seemingly healthy elderly individuals, those with periodontal disease have more amyloid in their brains than those without oral disease.

Individuals with strong immune responses to periodontal pathogens are at greater risk of developing Alzheimer’s than people who have more limited responses. This has led investigators to suggest that inflammation-associated periodontal disease may be a contributor to Alzheimer’s.

Homeostasis
A major function of the immune system is to keep the numerous bacterial communities on and throughout the body in check. To accomplish this, the body maintains immune homeostasis, exquisitely balanced inflammatory responses.

One might predict that maintaining good oral health would decrease one’s risk of inflammatory diseases including diseases such as cardiovascular and Alzheimer’s Disease.

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