Periodontitis Pathogen Reactions Flashcards
gingivitis
inflammation localised to gingival tissues, acute inflammation, normal physiological response to infection/injury
periodontitis
inflammation of gingival tissues and supporting periodontal structures, chronic inflammation, pathological inflammatory response associated with tissue destruction
what is the trigger for inflammation
oral biofilm, plaque
saliva role
contains vast array of antimicrobial peptides and proteins
cant remove accumulated biofilm
oral mucosa as barrier
physical - prevents microbes accessing underlying tissues
functional - expresses TLRs which detect microbial/pathogens associated molecular patterns [PAMPs DAMPs], in response epithelial cells release cytokines, chemokines and antimicrobial peptites
these signals recruit immune cells into gingival tissues
neutrophil as a defence
follow signals and traffic through gums, released in gingival margin. important defence against subgingival biofilm
periodontal pathogens
p.gingivalis
t.denticola
t.forsytha
polymicrobial dysbiosis
development of periodontal pocket, increases diversity and species richness
reinforces and exacerbates inflammation to initiate bone resorption
gingival inflammation alters competitiveness
p.gingivalis
immune evasion and subversion of immune responses, allowing it to thrive in inflammatory environment
aetiology of periodontitis
accumulated plaque bacteria, presence of periodontal pathogens, polymicrobial dysbiosis, in susceptible host, host-pathogen interactions determine susceptibility
hallmark clinical signs of periodontitis
attachment loss - manifests as increased pocket depth
alveolar bone destruction - persistent inflammation
gingivitis immune response
increased TLR stimulation, increased production of pro-inflammatory mediators
triggers acute inflammatory response - increased vasodilation, redness, swelling, bleeding, increased immune cell migration
neutrophuls remain prodominant cell type initial lesions, monocytes recrutited and diffrentiate to macrophages, lymphocytes recruited to fine-tune response
disruptive host-bacterial interactions are destructive in PD
immune system tries to control biofilm, dysbiotic biofilm persists and inflammation gets worse, this destroys tissues
increased immune and inflammatory cells in periodontium, effect goes from protective to destructive
surgical debridement is best, physically remove = return to homeostasis
role of neutrophils in PD destruction
aggressive perio - leukocyte adhesion defiency, cannot leave blood to enter tissues
without this gum protection, certain species will thrive and invade gum tissue, onset perio
too much is destructive - chronic inflammation, immune over reaction and destruction of tissues
microbial subversion, inflammatory cytokines, degradative enzymes degrade tissue + contribute to attachment loss and gives attachment to dysbiotic biofilm which colonises deeper in subgingiva margin, connective tissue destruction manifests as loss of attachment
adaptive immunity in PD destruction
control of dysbiotic biofilm, damaging tissues
T and B lymphocytes present, aggregates rich is CD4 T cells and B cells evident as lesion progresses, unable to regulate dybiotic biofilm, protective = limits systemic infection, destructive = inflammation induced alveolar bone loss
