Periodontitis is an infectious disease caused from plaque or no plaque induced gingivitis with subsequent secondary parasitic infection by Entamoeba gingivatis and/or Trichomonas tenax.
Periodontal disease is a specific Oral Amebiasis and/or Oral Trichomoniasis infection secondary to a gingival inflammation with furnishes nutriments to aggressive acquired parasites from direct or indirect vector as most parasitic infections.
Everything clearly suggests local hygiene and systemic factors contributing to gingivitis are one of the major factors of the disease and secondary parasitic infection contribute exacerbation by disruption of inflammatory response toward connective tissue and bone loss.
Periodontitis is parasitic infection superposed on a gingivitis inflammation which conduct to destruction of the supporting tissues of the teeth, including connective tissue and bone.
Clinically, periodontitis is easy to prevent and treated when monitoring the biofilm with a hospital grade phase contrast microscope. Recurrence is low as long as gingivitis is discarded and entourage reassured.
Regeneration of hard tissue is predictable in vertical defects while health is maintained on a sufficient period.
Inflammation is easily controlled via biofilm monitoring and microscope.
Tissue regeneration occur when infection and inflammation is vanished.
In periodontal disease parasitic infection use inflammation response to feed on and release from disrupted PMN destructive uncontrolled enzymes who produce bone loss.
Disrupted PMN and particularly ghost cell release uncontrolled noxious enzymes leading to injury and loss of organ function. E.P.I.C. theory.
Tissue destruction result of parasitic sustained inflammatory cell disruption and chronic parasite proliferation and turnover.
Disrupted PMN loses their inherent capacity of resolving infection by absence of apoptosis and NETs normal activity and prevent wound healing
Steps in resolution of inflammation requires elimination of pathogen parasites, removal of active bacteria and correction of local defect including calculus as well as control of gingivitis whether plaque or not plaque induced.
Absence of gingivitis will prevent PMN inflammatory response and will render further parasitic infection impossible. Management of entourage and parasitic transmission (via human, pets, infected water, dishes) whether direct or indirect is clearly encouraged.
Periodontal Disease is Early Detectable, Easily Preventable and Completely Curable