Theories of Progression Flashcards
Who proposed the theories of progression and what are their names?
Socransky 1984: possible patterns and rate of progression of periodontitis
- continuous rate theory
- random burst theory
- asynchronous multiple burst theory
What is the continuous rate theory?
- sites are either active or inactive
- at active sites, progression continues at a constant rate over time unless treatment is carried out
- different active sites may be progressing at different rates
What is the random burst theory?
- sites can be active or inactive
- at active sites, random bursts of periodontal destruction followed by periods of no activity with possible periods of repair
What is the asynchronous multiple burst theory?
- similar to random burst except multiple active sites breakdown within a short defined period of time
- transient factor causes multiple sites to breakdown at the same time e.g. ill health, stress, other risk factors
- activity followed by long periods of no activity
What are the theories of RAL and GAL?
Rapid Attachment Loss: extensive LOA detected in a short period of time (manual periodontal probes)
Gradual Attachment Loss: small amounts of LOA over time either in lots of mini-bursts or slow continuous LOA (detected by sensitive electronic probes e.g. florida)
In the early changes from health to disease as plaque biofilm accumulates, evidence of gingival inflammation increases with evidence of what?
- increased GCF
- increase in inflammatory and immune cell infiltrate in the connective tissue underlying the JE
- fewer fibroblasts in the gingival connective tissue underlying JE
- reduction in the collagen content in the inflamed connective tissue under the JE
Which key publication classified the histopathological changes which take place during the progression from gingivitis to periodontitis?
Page and Schroeder 1976 divided progressing lesions into 4 phases:
- initial
- early
- established - clinically obvious gingivitis
- advanced - periodontitis
What is the initial lesion?
- occurs within 24-48 hours of plaque accumulation
- mainly gram positive aerobic bacteria
- vasodilation of blood vessels, increased number of neutrophils and increased GCF production
- tissue damage minimal
- inflammatory infiltrate confined to small area of connective tissue below JE
- bacterial factors/antigens initiate an inflammatory/immune response
What is the early lesion?
- occurs after approx 1 week
- immunoglobulin production and cytokines released
- increase in size of inflammatory infiltrate: mainly PMNs and lymphocytes (polymorphonuclear neutrophils)
- loss of fibroblasts and collagen in infiltrated area
- increased GCF
- PMNs accumulate in gingival crevice
- inflammatory swelling of the gingiva results in a deeper gingival crevice
- favours growth of GNAB with the associated release of endotoxins and enzymes which cause more damage
What is the established lesion?
- gingival connective tissue largely replaced by plasma cell inflammatory infiltrate (clinically gingivitis)
- JE replaced by ulcerated leaky pocket epithelium
- large numbers of PMNs in pocket epithelium and crevice/pocket
- increased complement and immunoglobulins
- bacterial products cause damage: directly by enzymes, indirectly by triggering host response (release of cytokines, complement, enzymes e.g. PMN release MMP8 and MMP9 resulting in connective tissue damage)
- continues loss of collagen in the gingival connective tissue
What is the advanced lesion?
- inflammatory infiltrate extends apically and laterally, >50% plasma cells
- continued loss of collagen
- ulceration and migration of JE apically onto the root surface
- corresponds to periodontitis
- advancing inflammatory front where the host attempts to prevent the spread of invading bacteria, breakdown of PDL fibres, bone loss seen with osteoclasts on periosteal and endosteal surfaces of crestal bone
- ideal environment for GNABs
What is the role of the host response?
Inflammatory and immune response have 2 purposes:
- protection of the host against local microbial attack
- prevention of spread of micro-organisms if manage to invade tissue
What damage is caused in the PDL?
- destruction of PDL fibres inserting into the bone and cementum
- loss of extracellular matrix (ECM)
- fibroblast damage
- loss of the surface cementoblast layer
How is bone resorption mediated in periodontitis?
- mediated by both host derived and bacterial factors
- release of factors produced by host response such as cytokines (IL-1) and prostaglandin E2 which lead to activation of osteoclasts
- these factors are secreted by many host cells (PMNs, macrophages, fibroblasts, endothelial cells and osteoblasts) during inflammatory and immune response
