INFLAMMATION: WHAT IS IT?

Inflammation or phlogosis is the response of vascularized tissues to an endogenous or exogenous insult and aims to convey defensive materials (cells and fluids from the vascular compartment) to the site of tissue damage. The inflammatory response is characterized by three main functions: temporarily occupying the affected area of tissue damage with a material called “inflammatory exudate” consisting of protein-rich fluid and cells from the blood vessels; eliminating any harmful agents (e.g., bacteria) that have caused inflammation; removing the damaged tissue and proceeding with tissue repair.

The causes that lead to an inflammatory response are multiple:
1) Microbial infections;
2) Viruses;
3) Parasites;
4) Some physical agents: trauma, ultraviolet rays, ionizing radiation, and extreme temperatures;
5) Irritating chemical substances (acidic, alkaline, and oxidizing agents);
6) A powerful inflammatory stimulus is represented by tissue necrosis secondary to reduced blood flow
with oxygen deficiency as occurs, for example, in myocardial infarction.

CARDINAL SIGN
The four cardinal signs of an acute inflammatory reaction were described by CELSO in the 1st century AD.
They are:

• Redness (rubor)
• Heat (colour)
• Swelling (tumor)
• Pain (dolor)
  These aspects are present regardless of the cause of inflammation. Many of these symptoms can be
  attributed to vasodilation and increased capillary permeability.

CELLS INVOLVED IN INFLAMMATION
Each cell of the immune system is in some way specialized and can perform a specific function in the different phases of inflammation. Granulocytes (polymorphonuclear leukocytes) represent 60% of the leukocytes normally present in the circulatory system. Neutrophils migrate in response to chemical stimuli produced by microorganisms called chemotactic factors. Activated neutrophils cross the vascular endothelium and penetrate the site of inflammation.
CHEMICAL MEDIATORS
There are lipid molecules characterized by arachidonic acid metabolism. These molecules derive from a 20-carbon fatty acid. Arachidonic acid can be metabolized through two pathways:
Cyclooxygenase, which generates prostaglandins and thromboxanes
Lipoxygenase, which produces leukotrienes
Cytokines are polypeptide messengers synthesized by multiple activated immune cells (monocytes, macrophages, dendritic cells, T and B lymphocytes, mast cells, and basophils) and secreted during cellular activation. For example, interleukin 1 (IL1,) activates T lymphocytes and is implicated together with tumour necrosis factor (TNF-) in raising body temperature during inflammation. Chemokines and nitric oxide are other mediators of inflammation. In conclusion, the inflammatory process can be interpreted as a sophisticated mechanism capable of limiting damage and promoting “restitutio ad integrim”. If the agent responsible for inflammation is not removed, progression to chronic inflammation can occur, which can persist for months, years, or even a lifetime.

USAGE INSTRUCTIONS:
Standard: O3ZONE SIZE 00 CAPSULES

• 4 CAPSULES PER DAY
  MINIMUM DURATION 60 DAYS
  (2 in the morning and 2 in the evening)
  Frail Patient: O3ZONE SIZE O CAPSULES
• 6 CAPSULES PER DAY
  MINIMUM DURATION 60 DAYS
  (3 in the morning and 3 in the evening)
  Severe: O3ZONE SIZE 00 CAPSULES
• 6 CAPSULES PER DAY
  MINIMUM DURATION 60 DAYS
  (3 in the morning and 3 in the evening)
  Frail Patient: O3ZONE SIZE O CAPSULES
• 6 CAPSULES PER DAY
  MINIMUM DURATION 60 DAYS
  (3 in the morning and 3 in the evening)

ADMINISTRATION METHOD:
ENTERIC-COATED CAPSULES FOR SYSTEMIC USE ORALLY

TREATMENT DURATION:
2-3 MONTHS

EXCLUSION CRITERIA:
Pregnant women;
Internal and external bleeding;
Surgical procedures (discontinue treatment 3 days before and resume 7-10 days after);
Hyperthyroidism;
G6PD deficiency.

TREATMENT OBJECTIVE:
The goal of integrated treatment is to upstream inhibit the cascade of arachidonic acid
metabolism.
RECOMMENDED AS INTEGRATED THERAPY IN:
Inflammatory pathologies.

Therapeutic activity of ozone in inflammation:
The main characteristic of ozone is to upstream inhibit the cascade of arachidonic acid metabolism, inhibiting the synthesis of chemical mediators of inflammation, leading to modulation of immune mediators exerting an anti-inflammatory, anti-edematous, and antioxidative effect, counteracting the action of free radicals by reactivating the
microcirculation, increasing red blood cell deformability with a relative increase in oxygenated haemoglobin concentration.
Ozone also allows the activation of cytokine phagocytosis and enzymes that block peroxides and free radicals in red blood cells, leading to increased deformability and reduced blood viscosity. In conclusion, ozone’s inhibition of pro-inflammatory cytokines promotes the reduction of inflammation, lowers elevated temperature, and alleviates pain.