Numerous protective mechanisms interact to maintain the healthy environment of the oral cavity. Both soft and hard tissues have to be protected against microbial challenge. The first line of defence, the so called ―defence line 0‖ is the saliva.
THE ROLE OF SALIVA IN HOST RESPONSE
The role of saliva is ambivalent: although it has numerous protective antimicrobial properties, pellicle formation results in the attachment of microorganisms with the help of saliva, and it may play a role in the development of calculus through the precipitation of soluble minerals, and saliva also serves as nutrient for some microbes.
Saliva plays an important role in the protection against microorganisms, maintains healthy oral environment, digestion and bolus formation. The role of saliva is summarised in the next figure (Figure 1.40.)
ANATOMY, PHYSIOLOGY, MICROBIOLOGY
The role of saliva
Numerous protective mechanisms of the saliva are part of the antimicrobial defence system: it binds the components of microbe metabolism, some salivary proteins destroy bacterial cell walls with the help of enzymes, secretory IgA inhibits microbial adhesion by binding (agglutination) microorganisms. Saliva also controls the adhesion or colonisation of bacteria via its buffering capacity, serves as a catalyst for redox reactions leading to the formation of antibacterial products, proline-rich proteins inhibit the spontaneous precipitation of calcium-phosphate salts and the growth of hydroxyapatite crystals on tooth surfaces and prevent the formation of salivary and dental calculus.
Saliva protects against environmental challenges by maintaining the integrity of the oral mucosa via physicochemical mechanisms, antibacterial effects and the absorption of water.
THE ROLE OF GINGIVAL SULCUS IN HOST RESPONSE
Numerous mechanisms serve to maintain clinically healthy conditions in the gingiva; however, continuous host-microbial interactions can be seen in the periodontal environment. The protective processes in the gingival sulcus prevent damage to gingival epithelial layers.
The regular shedding of epithelial cells and the positive flow of gingival crevicular fluid may remove unattached and epithelially attached plaques, as well as toxic products of bacterial metabolism and host response.
Cells of the junctional epithelium continually dissolve and re-establish their hemidesmosomal attachments leading to the migration of defence cells and constituents of the complement system into the sulcus from adjacent venules of the dentogingival plexus. The initial reaction for the microbial challenge is the activation of the complement system in the gingival sulcus by both classical and alternative pathways. The intermediary factors of the complement cascade may play a role in the phagocytosis by opsonisation, activation of mast cells and acting as important chemotactic proteins. The leukocytes (PMN) and the end products of the complement cascade cause osmotic lysis of the targeted microbes, leading to the release of cytotoxic products for epithelial cells. The migrated monocytes remove these metabolites from the sulcus, so a small number of microbes can be eliminated without causing damage to the epithelium. The IgG and IgA of the sulcular fluid may play a role in the opsonisation and removal of toxic bacterial products.
THE ROLE OF THE GINGIVAL EPITHELIUM IN THE HOST RESPONSE
ANATOMY, PHYSIOLOGY, MICROBIOLOGY
The gingival epithelium serves as a physicochemical barrier with its tight intercellular connection, fast regeneration and salivary cover. The fast regeneration of the epithelium and the continuous desquamation of keratinised cells helps to remove microorganisms.
The gingival epithelium is not only a physical barrier characterised by effective innate functions, but it is also strongly associated with host defence processes of the underlying connective tissue and the adaptive defence system. The cells of the epithelium play an important role in the recognition of the commensal flora, differentiate it from pathogen microbes by Toll-like receptors, CD-1 receptors and soluble LPS-binding proteins. Damage to the epithelial surfaces causes the release of chemokines, cytokines and end products of arachidonic acid cascade. The secretion of IL-8 initiates innate immune system- and later on adaptive immune responses. As a result of cytokine expression, vascular changes occur: dilatation of the capillaries facilitate the migration of PMNs, monocytes and the accumulation of immunomodulatory cells in the epithelium. The Langerhans cells have a key role in the epithelial responses: they play a role in antigen presentation, stimulate the release of intercellular adhesion molecules, secretion of cytokines and chemokines and modulation of T-cell responses.
Antimicrobial peptides play an important role in maintaining the balance between health and disease in the oral environment. Human beta-defensins (hBDs) are constitutively expressed in gingival epithelial cells; however the human beta-defensin 2 is an inducible protein; normal uninflamed oral epithelial tissue is activated to express hBD-2. This exposure represents a useful interaction between the commensal bacteria and the tissue, resulting in an enhanced expression of hBD-2, thereby providing an advantage response to other potentially pathogenic organisms. The amount of alpha-defensins released from neutrophil granulocytes in saliva and crevicular fluids proportional with severity of infection. Alpha-defensins have an effect on a wide spectrum of pathogens, both Gram-positive and Gram-negative microbes, similar to Cathelicidin (LL-37) released by PMNs. In addition, they also have an antifungal effect. The antifungal action of histatin has been known: it binds surface proteins of Candida albicans, then penetrates the cytoplasm and destroys of microorganisms.
HOST RESPONSE OF THE CONNECTIVE TISSUE OF THE GINGIVA
The inflammatory response leads to the accumulation of immune cells: however, the PMNs migrate through the junctional epithelium to bind to the Fc receptor of opsonising antibodies and destroy harmful agents.
Lymphocytes accumulate in the connective tissue of the gingiva, fixed by CD-44 molecules.
The dendritic (Langerhans) cells migrate to the lymph nodes to present antigens to CD4 T-cells, which will result in the migration of the lymphocytes to the places of the injuries: the B-cells transform into plasma cells, while the T-cells play a role in immune reactions; both cellular and humoral responses.
Specific antibodies released in the gingiva and regional lymph nodes migrate to the damage of the periodontal tissues and act in phagocytosis and lysis of microorganisms and microbe aggregation. Host response leads to the release of harmful, destructive, cytopathic, proteolytic enzymes inhibited by 1-microglobulins and alpha-2-antitripsins.
SYSTEMIC IMMUNE RESPONSE
Exposure to several microbes is considered to be pathogenic and it initiates the production of specific antibodies detectable in the serum. IgG and IgM mediated processes result in the protective action of PMNs and the complement system, while IgA-mediated processes do not support the inflammatory reactions.