Periodontitis
defined as the loss of clinical connective tissue attachement
Gingivitis
inflammation confined to the gingiva without clinical attachment loss and bone loss
Describe gingivitis
no clinical attachment loss, no apical migration of JE, direct response to dental biofilm at gingival margin, pseudo pockets
Describe periodontitis
clinical attachment loss, true pockets, destruction of tissue, apical migration of JE- B cell, alveolar bone and supporting bone loss, immune and inflammatory response
Perio pocket
apical migration of the JE
Active perio
2-3 mm change of JE and BOP
What does the immune response result in?
elimination or retardation of the invader bacteria, limiting of further tissue destruction, beginning of healing
What are the key elements in the inflammatory response?
PMN's- phagocytes- release cytokines
Macrophages- phagocyte in CT
Mast cells- release heparin and histamine
Serum complement- stimulate inflammation
GCF- cleansing from crevice; antimicrobial properties
What is the process of inflammation?
first inflammation response is vascular changes->histamine and PGE2 -> vasodilation -> outflow of blood, fluid, proteins, and PMN's into CT -> edema/erythema -> increased permeability -> margination, pavmenting, emigrating -> increased GCF
What is the peak days for PMN's to go through JE and GCF?
6-12 days
BOP Flow chart
Plaque and Host -> initial response: vasodilation in lamina propria -> increased permeability(allows exchange between blood and CT) -> increased migration of PMN's(lamina propria to JE) -> changes in lamina propria(edema, redness) -> ulceration in epithel
Story of the B-cell
B cells are born in bone marrow; live in lymph tissue;
B cell -> plasma cells -> antibodies -> kill antigen; *involved in perio
Story of the T-cell
born in bone; mature in thymus, live in blood(circulate); active in HIV; helper T cells secrete cytokines activate phagocytic cells, make interleukin-1 and activate B cells.
Macrophages
antigen presenting in the immune system(link inflammatory and immune response); phagocytic in inflammatory; produce interleukin-1 and PGE2(both cytokines)