The host immune response is important in maintaining the health of periodontal tissues. The presence of pathogens in periodontal pockets will activate innate and adaptive immune responses in an attempt to clear the pathogenic threat as well as promote tissue homeostasis. However, the persistent presence of pathogens can cause the continuous activation of innate and adaptive immune responses; which in turn causes inappropriate inflammatory mediator (cytokine, chemokine, antimicrobial proteins and enzymes) synthesis and secretion that directly or indirectly lead to periodontal tissue destruction.
These inflammatory mediators, which can be produced by periodontal host cells in response to pathogen, are known to cause degradation of extracellular …show more content…
Without mechanical disruption, the biofilm will grow into a thick mature biofilm extending into the subgingival area (subgingival biofilm). The subgingival biofilms are comprised of mostly Gram-negative, anaerobic bacteria which lead to the deposition of virulence factors into the gingival crevicular fluid (GCF). These substances can cause injury to host cells directly. However, the host is equipped with an innate defence system which is designed to recognise these substances and protect the tissue from microbial …show more content…
In health the presence of commensal bacteria in a dental biofilm activate a low level innate immune response. This low level response is important in priming host tissue cells and promoting tissue homeostasis. A shift in the composition of the dental biofilm and the presence of pathogenic organisms however cause an amplification of this immune response by localized cells.
Many of the pathogenic organisms found in dental biofilm possess alot of virulence factors. Many of these virulence factors are termed MAMPs. MAMPs are highly conserved structures of microorganisms such as lipopolysaccharide (LPS), peptidoglycan, lipoprotein, bacterial DNA and double stranded RNA.
The greater presence of pathogenic organisms leads to an increase in the number of microbe associated molecular patterns (MAMPs) derived from pathogens which drive tissue inflammation. Numerous resident and recruited host cells of periodontal tissues express surface TLRs. These include neutrophils, Langerhans cells, monocytes/macrophages, osteoblasts, periodontal ligament fibroblasts, gingival fibroblasts and gingival epithelial
These inflammatory mediators, which can be produced by periodontal host cells in response to pathogen, are known to cause degradation of extracellular …show more content…
Without mechanical disruption, the biofilm will grow into a thick mature biofilm extending into the subgingival area (subgingival biofilm). The subgingival biofilms are comprised of mostly Gram-negative, anaerobic bacteria which lead to the deposition of virulence factors into the gingival crevicular fluid (GCF). These substances can cause injury to host cells directly. However, the host is equipped with an innate defence system which is designed to recognise these substances and protect the tissue from microbial …show more content…
In health the presence of commensal bacteria in a dental biofilm activate a low level innate immune response. This low level response is important in priming host tissue cells and promoting tissue homeostasis. A shift in the composition of the dental biofilm and the presence of pathogenic organisms however cause an amplification of this immune response by localized cells.
Many of the pathogenic organisms found in dental biofilm possess alot of virulence factors. Many of these virulence factors are termed MAMPs. MAMPs are highly conserved structures of microorganisms such as lipopolysaccharide (LPS), peptidoglycan, lipoprotein, bacterial DNA and double stranded RNA.
The greater presence of pathogenic organisms leads to an increase in the number of microbe associated molecular patterns (MAMPs) derived from pathogens which drive tissue inflammation. Numerous resident and recruited host cells of periodontal tissues express surface TLRs. These include neutrophils, Langerhans cells, monocytes/macrophages, osteoblasts, periodontal ligament fibroblasts, gingival fibroblasts and gingival epithelial