Periodontitis affects approximately 80% of adults but patients never present with “pain” as their chief complain. The most common chief complaints reported by chronic periodontitis patients are “I was told I have gum disease” or “I would like to save my mobile teeth.” Periodontitis is a chronic inflammatory disease and yet it is pain free. It was Bayliss in 1901 who first proposed the involvement of sensory nervous system in generating some of the manifestations of inflammation. The periodontal as well as pulpal tissues contain many nociceptors, a primary sensory neuron, which when activated are capable of tissue damage. These sensory systems are not dedicated and hard wired but are held in a steady state by elaborate dynamic control mechanisms. Following tissue damage due to pathogen, a number of changes take place within pain‑conducting systems resulting in abnormal signal transmission patterns between immune and nervous systems. The factors that play a major role in making periodontits painfree are:
- Painless gene or the “pain sensors” are responsible for the initiation of signaling pathway and this gene is responsible for producing an ion channel of TRPV (transient receptor potential family V member 1 cation channel). TRPV is a gateway for pain transduction. It responds the noxious stimuli and modulates the nerve excitability meaning it causes pain on detecting the noxious stimuli. Certain periodontal bacterias s.a Lactobacillus reuteri attacks these TRPV and leads to decrease in pain. Also prolonged exposure to lipopolysaccharide found on the cell membrane of periodontal bacteria can desensitize TRPV and stop the pain signals to bacterial challenge.
- Calcitonin Gene Related Peptide: This again is involved in transmission and modulation of pain information in peripheral and central nervous system. Constituents of GCF in deep pockets process and degrade it explaining the absence of pain as a major symptom in periodontitis.
- Certain inflammatory mediators such as B-endorphins, dynorphin A, met enkephalins inhibit pain by activating opioid receptors and these factors increases with the progression of inflammation which explains the absence of pain even with increase in chronicity of periodontitis.
- Butyric acid is an extracellular metobilte produced by periodontal bacterias. In low conc it leads to neurite non proliferation and in high conc it favours neurodegeration leading to absence of pain
- Difference in the phenotype of nerves found in pulp and periodontium also plays an important role in difference in pain perception. The neuron in pulp are larger Isolectin B4 positive whereas the periodontal neurons are smaller and Isolectin (IB4) negative. IB4-positive neurons have longer-duration action potentials. So, this means that there is electrophysiological difference in that way these neurons detect, process and responds to the noxious stimuli. This explains the lack of pain in periodontitis.
Lack of pain is an obvious advantage to the patients but this also makes patients unaware of the disease which becomes a major hurdle in convincing periodontal patients for any kind of surgical treatment.
To read this article in more detail: http://www.jorr.org/text.asp?2019/11/2/84/262763