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Gum Disease (Periodontal Disease) Advice
I went to a biological dentist today. I have gum disease although no cavities. The biological dentist recommended a very expensive set of treatments involving lasers, platelet rich fibrin, and so forth. Also, I will need to go in for a cleaning every three months for the rest of my life. I don't have any concerns that the dentist is working in bad faith just to make money.
I can see two approaches. What do people here think? Has anyone received from gum disease with a low vitamin A diet?
- Do not get the treatments and hope a low vitamin A diet cures my gum disease in a timely manner.
- Get the treatments and nuke my oral microbiome (and wallet).
Does anyone have any ideas?
Hi @jeremy Both I and my husband completely recovered from advanced gum disease that lasted for more than ten years as a result of :
- red laser treatment done twice
- taking oral probiotics for about 6 months (only Probiora3 really worked
- After that we were on the low vA diet and it was the road to real recovery. We had a few times bad episodes of detox with very swollen gums with sharp pains when masticating, but every time this was less.
Maybe the two first points were not necessary. Maybe just the probiotics would cut down the price. Also there is a yoga trick to divert the lymph away from the gums that helps. It takes about two months for effects to stick : when peeing or passing stools, you should lock your teeth and bite as hard as you can.
We had tried oil pulling, it helps a bit but is no cure.
After 18 months on the low vA diet, we are completely free from periodontal disease. Maybe the gums will grow back!
Thanks a lot! This is very helpful!
I don't see a production called Probiora3. They might have changed the names up. Can you figure out which of the current lineup is the closest to the probiotic that you took?
I would floss and brush your teeth after every meal. Also, the attached website suggests some natural remedies.
Streptococcus oralis KJ3® (S. oralis KJ3), Streptococcus uberis KJ2® (S. uberis KJ2), and Streptococcus rattus JH145® (S. rattusJH145
Ingredients of ProBiora Plus
Difficult to get, often out of stock, Google in Europe does not allow the search. I managed to buy on ebay. Good luck!
We do not need it anymore, haven’t used it for more than a year now, but it was very helpful a the beginning of the diet.
Weak immunity. That's why I am avoiding fiber(SCFA). Are you still consuming "healthy" vegetables and fruits?
Butyric Acid in Saliva of Chronic Periodontitis Patients Induces Transcription of the EBV Lytic Switch Activator BZLF1: A Pilot Study
http://iv.iiarjournals.org/content/34/2/587.full
Background/Aim: Epstein-Barr virus (EBV) associates with human chronic periodontitis (CP) progression. We previously demonstrated that butyric acid (BA), produced by periodontopathic bacteria, induced EBV lytic switch activator BZLF1 expression. We investigated whether short chain fatty acids (SCFAs) in CP patients' saliva enabled EBV reactivation. Materials and Methods: Saliva was collected from seven CP patients and five periodontally healthy individuals. SCFAs were quantified using HPLC. BZLF1 mRNA and its pertinent protein ZEBRA were determined with Real-time PCR and western blotting. Histone H3 acetylation (AcH3) was further examined. Results: BZLF1 mRNA expression and transcriptional activity in EBV-infected Daudi cells were induced only when treated with the CP saliva. Among SCFAs, BA alone correlated significantly with the BZLF1 transcription (r=0.88; p<0.02). As expected, CP patients' saliva induced AcH3. Conclusion: BA in saliva may play a role in EBV reactivation and hence contribute to EBV-related disease progression in CP patients.
Results
Saliva of CP[chronic periodontitis] patients contains relatively high levels of SCFAs. Previous studies have reported that the periodontal pockets and dental plaques of CP[chronic periodontitis] patients contain high concentrations (mM levels) of SCFAs (24-26). However, the amounts of SCFAs have not been investigated in the saliva of Japanese CP patients. Therefore, we measured the concentrations of SCFAs in the saliva of seven CP patients and five healthy controls by HPLC. As presented in Figure 1, the saliva of CP patients contained significantly higher levels (p<0.01) of BA[butyric acid], PA[propionic acid], and AA[acetic acid]. On the other hand, the amounts of isoBA and isovaleric acid in the saliva were very low.
...
The saliva of patients with periodontitis contains EBV-infected B cells, and bleeding of the gums is often observed in these patients (7, 15-17). In addition, it was recently reported that EBV infects the oral epithelial cells of patients with periodontitis in addition to the epithelial cells of the upper aerodigestive tract (30). The extent of gingival epithelial EBV infection is correlated with the severity of CP (30). Moreover, previous reports, as well as the present study, indicated that EBV also contributes to the progression of periapical periodontitis (20, 31). These findings and previous observations suggest the potential risks of BA[butyric acid] in saliva for the progression of periodontitis and periapical periodontitis. We assume that microbial synergy by the interaction between periodontopathic bacteria and EBV leads to the following negative chain of pathological events in the oral cavity: 1) periodontopathic anaerobic bacteria, such as P. gingivalis and F. nucleatum, produce BA; 2) BA induces EBV reactivation; 3) EBV impairs local host defences, 4) which leads to increased proliferation of periodontopathic bacteria; 5) increased BA and inflammatory cytokine production by the synergistic effects of EBV and periodontopathic bacteria; and 6) periodontitis escalation.
...
Periodontitis and EBV are spreading worldwide. Although our findings suggest a relationship between the saliva of patients with periodontitis and EBV reactivation, additional basic and clinical studies with greater numbers of cases are needed. Furthermore, prevention and early treatment of periodontitis involving elimination of BA[butyric acid]-producing bacteria could effectively block further clinical progression of EBV infection.
Short chain fatty acid butyrate promotes virus infection by repressing interferon stimulated genes
https://www.biorxiv.org/content/10.1101/2020.02.04.934919v1.full
Butyrate is an abundant metabolite produced by the gut microbiota and is known to modulate multiple immune system pathways and inflammatory diseases. However, studies of its effects on virus infection of cells are limited and enigmatic. We found that butyrate increases cellular infection and virus replication in influenza virus, reovirus, and human immunodeficiency virus infections.
No fruits and vegetables for me.
Interesting but it doesn't follow to avoid a food group that is a normal part of the human diet. SCFAs are the main energy source for the colon. Even if you avoid fruit and vegetables, if you have dysbiosis of the oral microbiome, SCFAs will still be produced from any carbohydrate that is consumed and to a lesser degree, from protein:
Intestinal Short Chain Fatty Acids and their Link with Diet and Human Health
Short chain fatty acids (SCFA) are volatile fatty acids produced by the gut microbiota in the large bowel as fermentation products from food components that are unabsorbed/undigested in the small intestine; they are characterized by containing fewer than six carbons, existing in straight, and branched-chain conformation. Acetic acid (C2), propionic acid (C3), and butyric acid (C4) are the most abundant, representing 90–95% of the SCFA present in the colon. The main sources of SCFA are carbohydrates (CHO) but amino acids valine, leucine, and isoleucine obtained from protein breakdown can be converted into isobutyrate, isovalerate, and 2-methyl butyrate, known as branched-chain SCFA (BSCFA), which contribute very little (5%) to total SCFA production.
It's more helpful to look at causes for why dysbiosis is occuring. It's likely that elevated levels of retinoic acid are a major cause. Insulin resistance is another. Just like every other health problem it's important to look at gum disease holistically. It's also important to treat the dysbiosis locally with mouthwash.
ABSTRACT
Objective: The oral microbiota is associated with the risk of type 2 diabetes (T2D), but the relationship between the oral microbiota and disease progression in the elderly population remains to be determined.
Design: In our study, we recruited 150 elderly Chinese residents and divided them into three groups according to their fasting glucose (FG) level: normal (N), high (H), and very high (VH). Their biochemical indexes were analyzed using blood samples. Saliva samples were collected and the oral microbiome was profiled by high-throughput sequencing of the V3-V4 area of the 16S rRNA gene.
Result: Our results revealed that the VH group showed deterioration of the metabolic phenotype and dysbiosis of the oral microbiota simultaneously when compared to the other two groups. Furthermore, potential disease-associated bacterial genera including Leptotrichia, Staphylococcus, Catonella, and Bulleidia were significantly enriched in the VH group.
Conclusions: These results suggest that dysbiosis of the oral microbiota may be a typical feature of hyperglycemia and might also contribute to disease aggravation in the progression of hyperglycemias.
Most of the times fiber comes in a conditionally bad package consisting of polyphenols, phytosterols, lectins, some toxins, oxalates, salicylates....
All of the above could contribute to hypo via different pathways.
Even fiber, indirectly, could lead to increased toxemia through bugs refeed with corresponding killing by polyphenols(phenolic class antibiotics), and toxemia raises cortisol(so insulin resistance, fat gain, immune system shutdown like from glucocorticoids).
Maybe as a decoration its ok though. And it all depends on the overall level of health. The more person is sick the more diet should be restricted IMO, especially avoiding things contributing to metabolism slow down.