|Year : 2013 | Volume
| Issue : 1 | Page : 3-8
Hyperbaric oxygen therapy in periodontal diseases
Swapna A. Mahale, Pankaj K. Kalasva, Sunil Vinayak Shinde
Department of Periodontology and Implantology, MGV's K.B.H. Dental College and Hospital, Panchavati, Nashik, Maharashtra, India
|Date of Web Publication||9-Jun-2014|
Sunil Vinayak Shinde
'Shinde Niwas', Lane No. 6, Near Navbharat Chowk, Dhule - 424 001, Maharashtra
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Hyperbaric oxygen (HBO 2 ) has been successfully used in several medical fields. The therapeutic effect is related to elevated partial oxygen pressure in the tissues. The pressure itself enhances oxygen solubility in the tissue fluids. HBO 2 has shown to affect angiogenesis, bone metabolism and bone turnover. Studies have been conducted to analyze the effects of HBO 2 therapy on periodontal disease. HBO 2 increases local oxygen distribution, especially at the base of the periodontal pocket, which inhibits the growth of anaerobic bacteria and allows the ischemic tissues to receive an adequate intake of oxygen sufficient for a rapid recovery of cell metabolism. It is increasingly being accepted as a beneficial adjunct to diverse clinical conditions. Nonhealing ulcers, chronic wounds and refractory osteomyelitis are a few conditions for which HBO therapy (HBOT) has been extensively tried out. The dental surgeons have found a good ally in HBOT in managing dental condition.
Keywords: Anaerobic bacteria, angiogenesis, chambers, hyperbaric oxygen therapy, hyper-oxygenation
|How to cite this article:|
Mahale SA, Kalasva PK, Shinde SV. Hyperbaric oxygen therapy in periodontal diseases. J Int Clin Dent Res Organ 2013;5:3-8
|How to cite this URL:|
Mahale SA, Kalasva PK, Shinde SV. Hyperbaric oxygen therapy in periodontal diseases. J Int Clin Dent Res Organ [serial online] 2013 [cited 2019 Nov 11];5:3-8. Available from: http://www.jicdro.org/text.asp?2013/5/1/3/134129
| Introduction|| |
Although the application of compressed gas in medicine had its origins centuries ago, it is only in the last 40 years that good science has existed to support some of its current applications. A lack of soundly constructed scientific research, overenthusiastic reactions to isolated cases, public pressure and financial issues have all contributed to the skepticism, which has influenced the acceptance of HBOT into mainstream medicine.
| Historical background|| |
The concept of using respirable gases at raised ambient pressures in the treatment of illnesses dates back to 1662 when hyperbaric air was used by Henshaw for the treatment of "affections of the lung." In 1834 Junod, in France, built a chamber to treat pulmonary conditions at pressures between 2 and 4 atmospheres absolute (ATA). Hyperbaric air was used to treat a wide variety of ailments, including lung infections, cardiac disease, carcinomas, diabetes, and dementia.
Orville J Cunningham is regarded as being the last exponent of compressed air therapy. His observations that people with heart disease and other circulatory disorders did poorly at altitude and improved at sea level formed the basis for his use of hyperbaric air. In 1918, he successfully treated sufferers of the Spanish flu epidemic with hyperbaric air.
Oxygen, which was discovered in 1775 by Joseph Priestley was first used successfully by Behnke and Shaw in 1937 for the treatment of decompression illness. The application of hyperbaric oxygen (HBO 2 ) in clinical medicine really began with separate work done by Churchill-Davidson and Boerema in 1955 and 1956. Churchill-Davidson used it to enhance the radiosensitivity of tumors, while Boerema successfully used it in cardiac surgery to prolong the time allowed for cross-clamping of the major vessels. ,
| Hyperbaric oxygen|| |
Hyper "is simply an increase," while "baric" refers to the pressure. As a procedure or therapy, hyperbaric is simply the process of increasing the atmospheric pressure around the body. HBO therapy (HBOT) has been described as "a therapy in search of diseases." The pressure is usually about 2-4 absolute atmospheres or ATA; it is essentially the therapeutic use of oxygen as a drug. When oxygen is used as a drug, the dose is controlled by the technology of a HBO 2 chamber, which sets the dosage at 100% oxygen. Molecular oxygen is one of the crucial nutrients of the wound and has a central role in the reparative cases. Collagen synthesis, matrix formation, angiogenesis, epithelialization, and bacterial killing require molecular oxygen during the reparative process.
| Mechanism of action|| |
Hyperbaric oxygen therapy has two primary mechanisms of action: Hyper-oxygenation and a decrease in bubble size. Hyper-oxygenation results from an increase in dissolved oxygen in plasma as a result of increased partial pressure of arterial oxygen. A pressure of three ATA results in 6 ml of O 2 being dissolved per 100 ml of plasma, thus rendering as much O 2 delivery as by hemoglobin bound O 2 . It is useful in management of crush injury, compartment syndrome, flap salvage and acute blood loss anemia. High air pressure decreases the volume of gas bubbles in the blood 2-3 times that of normal air pressure. High oxygen (100%) intake saturates the blood plasma with oxygen. It is the primary mechanism at work in management of decompression sickness and arterial gas embolism. ,,,,,
Hyperbaric oxygen therapy exerts both direct and indirect effects against bacteria. Direct bactericidal and bacteriostatic effects occur through the generation of oxygen free radicals. This free radical oxidizes proteins and membrane lipids, damages DNA, and inhibits metabolic functions essential for the growth of organisms.
Indirect effect of HBO 2 in bacterial killing is through improving leukocytes function and is regarded as being more significant than the direct bactericidal and bacteriostatic effects. Neutrophils require oxygen as a substrate for microbial killing, after phagocytosis occurs. Hypoxia reduces this function. Significant reductions in the killing capacity of leukocytes occur when tissue pO 2 falls below 30 mmHg. Infected and traumatized tissues often have a partial pressure of oxygen below this, making them much more susceptible to infection due to decrease in neutrophil activity.
Hyperoxia and HBO 2 influence the activity of some antibiotics, enhancing the effectiveness of some and inhibiting others.
Physiologic and biochemical effects of hyperoxia:
- Suppression of alpha-toxin production by Clostridium perfringenes.
- Bacteriostatic for some species of Escherichia More Details and Pseudomonas and also for a range of enteric bacteria ( Salmonella More Details, Shigella and Proteus).
- Improved leukocyte killing activity.
- Promotion of fibroblast proliferation, collagen formation, and angiogenesis in problem wounds, flaps, and irradiated tissues.
- Reduced falls in adenosine triphosphate and phosphocreatinine levels in burns and postischemic tissue.
- Decreased white cell adherence to capillary walls.
- Vasoconstriction in normal blood vessels.
- Decreased posttraumatic tissue edema.
- Reduced half-life of carboxyhemoglobin, improved dissociation of carbon monoxide from cytochrome-C oxidase and prevention of neuronal injury in carbon monoxide poisoning.
| Types of chambers|| |
These units can accommodate between 2 and 18 or more patients and commonly incorporate a minimum pressure capability of 6.0 ATA.
- Constant patient attendance and evaluation (particularly useful in treating evolving neurological diseases such as decompression sickness and cerebral arterial gas embolism).
- Multiple patients treated per session.
- Greater working pressure.
- Higher capitalization requirements.
- Major space requirements; basement and/or ground floor level limitations.
- Higher operating costs.
They were designed for single occupancy and usually constructed of acrylic, having a pressure capability of 3.0 ATA, and compressed with 100% oxygen. The high flow oxygen requirement is ideally supplied via a hospital's existing liquid oxygen system.
- Cost efficient delivery of HBO 2 .
- No risk of decompression sickness.
- Portable, less space, less equipments, no hood or mask.
- No risk of iatrogenic decompression sickness in patient or staff.
- Relative patient isolation.
- Associated fire hazard.
- Inability to use certain diagnostic and/or therapeutic equipment.
| Topical hyperbaric oxygenation|| |
The rationale for the topical approach is that when topical oxygen dissolves in sufficient quantity, it exert bactericidal and angiogenic effects.
The devices employed in the topical application of oxygen typically consist of a compartment to encase the affected portion of the body. The compartments that enclose the wound may be box-like or function as disposable plastic bags.
| Indications|| |
- Air or gas embolism.
- Carbon monoxide poisoning or carbon monoxide poisoning complicated by cyanide poisoning.
- Clostridal myositis and myonecrosis (gas gangrene).
- Crush injury, compartment syndrome, and other acute traumatic ischemia.
- Decompression sickness.
- Enhancement of healing in selected problem wounds;
- Diabetically derived illness, such as diabetic foot, diabetic retinopathy, diabetic nephropathy.
- Exceptional blood loss (anemia).
- Intracranial abscess.
- Necrotizing soft tissue infections (necrotizing fasciitis).
- Osteomyelitis (refractory).
- Delayed radiation injury (soft tissue and bony necrosis).
- Skin grafts and flaps (compromised).
- Thermal burns. 
| Contraindications|| |
- Untreated tension pneumothorax. 
- Concurrent administration of certain medications like.
- Bleomycin - Causes interstitial pneumonia.
- Cisplatin - Causes impaired wound healing.
- Doxorubicin - Causes cardiotoxicity. ,
- Disulfiram - Blocks superoxide dismutase, which is protective against oxygen toxicity.
- Sulfamylon - Causes impaired wound healing.
- Upper respiratory tract infection.
- Chronic pulmonary obstructive disease.
- Congenital spherocytosis.
- Eustachian tube More Details dysfunction.
- Seizure disorder.
| Preparations before hyperbaric oxygen therapy|| |
The HBO 2 technician will obtain a complete drug history before treatment since some medications are not compatible with HBOT. These include: High doses of prednisolone (or similar cortisone type drugs), and morphine, or alcohol, insulin within 8 h of treatment. Such drugs should be substituted for another drug. Patients will be instructed to take a regimen of high potency nutritional supplements containing vitamin E and other antioxidants during a course of HBOT.
Cold and other symptoms
Patients with the symptoms of a cold or the flu, fever, cough, sore throat, runny nose, cold sore, nausea, vomiting or diarrhea are not helped by oxygen. HBO 2 treatments may need to be postponed until symptoms have subsided.
Hyperbaric oxygen therapy will not be effective in patients who use tobacco in any form like cigarettes, pipe tobacco, and cigars, as well as chewing tobacco and snuff.
Cosmetics, hair spray, nail polish, perfume, or shaving lotion containing petroleum, alcohol or oil base are not allowed while in the HBO 2 chamber. It is important to discuss all skin care products with the HBO 2 technician, so they may assure safety.
Patients are provided with 100% cotton gowns to wear during treatment. No articles containing nylon or polyester can be worn in the chamber. ,
| Are There Any Negative Effects After Therapy?|| |
- A "cracking" sensation in their ears between treatments as a pressure difference develops between their middle ear and the chamber atmosphere. 
- Feeling of light headedness for a few minutes immediately following a treatment.
| Potential complications of hyperbaric oxygen therapy|| |
- Oxygen toxicity - Seizures, dry cough, chest pain or burning.
- Visual refraction changes - Cataract, progressive myopia with prolonged number of treatments.
- Barotrauma - In ears, sinus, lungs, tooth caries/fillings. 
| Hyperbaric oxygen and periodontitis|| |
Hyperbaric oxygen therapy showed to increase oxygen distribution at the base of the pocket which is deleterious to periodontal pathogens, particularly to the anaerobic microorganisms.  Cultivation of plaque microorganisms from sites of chronic periodontitis reveals high percentages of anaerobic (90%) bacterial species.  HBO 2 increases generation of oxygen free radicals, which oxidize proteins and membrane lipids, damage deoxyribonucleic acid and inhibit bacterial metabolic functions. It also facilitates the oxygen-dependent peroxidase system by which leukocytes kill bacteria. HBO 2 also improves the oxygen-dependent transport of certain antibiotics across bacterial cell walls.  In this way HBOT results in inhibition of bacterial growth.
While on the other hand, HBOT would also allow the ischemic tissues to receive an adequate intake of oxygen sufficient for a rapid recovery of cell metabolism.  Oxygen tension in periodontal pockets is very low (pO 2 5-27 mmHg) when compared with atmospheric pO 2 (155 mmHg), the arterial blood pO 2 (95 mmHg), and the venous blood pO 2 (20-40 mmHg).  Fibroblast and leukocyte function are severely compromised when pO 2 is ≤30 mmHg. HBO 2 increases collagen formation for capillary growth. HBO 2 also promotes fibroblast replication and collagen formation, while the patient is in the hyperbaric chamber.  It also increases bactericidal function of leukocytes. HBOT also improve gingival microcirculation and increase gingival blood flow. 
Thus in periodontal tissues, HBOT showed to have a deleterious effect on periodontal microorganisms as well as beneficial effects on periodontal healing by raising oxygen tension in pocket.
Manhold et al.  showed through an experiment that some commercially available oxygenating agents demonstrated shorter healing times when applied on inflamed gingiva.
Hirsch et al.  studied the effect of locally released oxygen on the development of plaque and gingivitis in man and concluded that there was no significant effect of oxygen on plaque formation, crevicular fluid flow, or the number of gingival bleeding sites.
Schlagenhauf et al.  used repeated subgingival oxygen irrigations in previously untreated periodontal patients. They concluded that repeated oxygen insufflations resulted in a significant clinical improvement of the periodontal baseline conditions superior to the one found in the control.
Gaggl et al.  applied localized oxygenation in contrast to systemic oxygen therapy, to help treat acute necrotizing periodontal diseases. In both groups of patients, colonization with Prevotella intermedia, Tannerella forsythia, and Treponema denticola was initially positive. None of these microorganisms were completely eradicated in any of the patients in the group without oxygen therapy within the first 10 days.
Signoretto et al.  evaluated the effects of HBO 2 on patients suffering from adult chronic periodontitis in comparison with surgical intervention (scaling and root planning [SRP]), as well as the effects of a combination of both therapies on the evolution over time of the microflora of the periodontal pockets and found that the combination of HBO 2 and SRP substantially reduced (by up to 99.9%) the Gram-negative anaerobe loads of the subgingival microflora. The low values of pathogens persisted for at least 2 months after the therapy. HBO 2 or SRP alone produced a temporarily more limited effect on periodontal anaerobes. In addition, molecular detection of the main periodontopathogenic bacteria significantly reduced in the number of dental sites, which harbored them.
Nogueira-Filho et al.  evaluated the effect of HBOT as an adjunct to SRP on the treatment of severe cases of periodontitis. They concluded that HBOT had a short-term beneficial effect on pocket reduction and bacterial elimination, and may be considered potential adjunct therapeutic option to improve the clinical outcomes of scaling in severe cases of chronic periodontitis.
Chen et al.  investigated the effects of HBO 2 on aggressive periodontitis (AgP), and subgingival obligate anaerobes in Chinese patients and concluded that HBO 2 inhibits the growth of subgingival obligate anaerobes and facultative anaerobes and Bacteroides melaninogenicus thus promoting healing of peridontium, which will be of help in the treatment of AgP. HBO 2 therapy combined with SRP appears to be even better for synergistic treatment of AgP. The effects can last >2 years.
| Hyperbaric oxygen and implant|| |
Dental implants offer a way to replace missing teeth. Patients who have undergone radiotherapy or surgery may benefit from reconstruction with implants.
Hyperbaric oxygen has been shown to affect angiogenesis, bone metabolism bone turnover. In relation to radiotherapy, HBO 2 can thus counteract some of the negative effects from irradiation and actually act as a stimulator of osseointegration.
The exact mechanisms at the cellular level where HBO 2 act remain obscure. It has been recently shown that HBO 2 and basic fibroblast growth factor (bFGF) acts synergistically in irradiated bone. Factors that could be involved in bone protection by bFGF and HBO 2 are bone marrow radioprotection, induction of oxygen radical scavengers and production of different cytokines.
Hyperbaric oxygen and bFGF can also enhance the level of insulin-growth factor, which is known to promote proliferation and differentiation of bone. They could also affect bone progenitor cells by promoting DNA synthesis, stimulating enzymes involved in bone formation or affect membrane receptors. HBO 2 has furthermore been shown to affect the interface between the titanium implant and bone, which could be different from cellular effect. 
Oxygen under hyperbaric conditions could thus play a role in osseointegration by affecting bone cell metabolism, implant interface and capillary network in the implant bed.
Taylor and Worthington  reported that when implants were placed in conjunction with HBOT healing was more reliable, although still slow. They recommended HBO 2 for patients treated with >50 Gy.
Marx and Morales  reported a 5-year survival in 622 out of 748 osseointegrated implants after HBO 2 treatment.
Granstrφm et al.  in a case-controlled study found that about 53.7% implants failed in the irradiated group compared to 13.5% in nonirradiated group and 8.1% for irradiated HBO 2 -treated group.
Esposito et al.  in a systematic review found only one randomized controlled trials (RCTs) comparing HBO 2 with no HBO 2 for implant treatment in irradiated patients and they concluded that HBOT in irradiated patients requiring dental implants may not offer any appreciable clinical benefits. There is a definite need for more RCTs to ascertain the effectiveness of HBO 2 in irradiated patients requiring dental implants.
| Conclusion|| |
Hyperbaric oxygen therapy can be used as an adjunct to SRP to treat moderate-to-severe periodontitis. It has been shown to decrease load of anaerobic microbes and thus significantly improve periodontal health. However, further advancement should be made to use this therapy routinely in clinical practice.
Consideration must be given to both the benefits and the risks of a therapy when contemplating its application in any clinical situation.
Although HBOT is not without side-effects, most specialists in the field consider the risk profile for patients acceptable when treating the conditions for which HBO 2 is clearly indicated.
| Acknowledgments|| |
Dr. Nitin Dani (HOD, Department of Periodontology, MGV'S K.B.H. Dental College and Hospital, Panchavati, Nashik, Maharashtra, India).
| References|| |
|1.||Neubauer RA, Maxfield WS. The polemics of hyperbaric medicine. J Am Physicians Surg 2005;10:15-7. |
|2.||Sharkey S. Current indications for hyperbaric oxygen therapy. J Aust Def Health Serv (ADF Health) 2000;1:64-72. |
|3.||Jørgensen TB, Sørensen AM, Jansen EC. Iatrogenic systemic air embolism treated with hyperbaric oxygen therapy. Acta Anaesthesiol Scand 2008;52:566-8. |
|4.||Latham E, Hare MA, Neumeister M. Hyperbaric oxygen therapy. Available from: http://www.emedicine.medscape.com/article/1464149-overview. [Last accessed on 2008 Nov 07]. |
|5.||Michael N. Hyperbaric oxygen therapy. eMedicine. In: Cram AE, Talavera F, Newsome RE, Slenkovich NG, Torre JT, editors. Medscape. Available from: http://www.emedicine.com/plastic/topic526.htm. [Last accessed on 2005 May 20]. |
|6.||Leach RM, Rees PJ, Wilmshurst P. Hyperbaric oxygen therapy. BMJ 1998;317:1140-3. |
|7.||Bhutani S, Verma R. Hyperbaric oxygen therapy in non-healing wounds. J Mar Med Soc 2010;12:89-92. |
|8.||Undersea & Hyperbaric Medical Society. Indications for hyperbaric oxygen therapy, 2011. Available from: http://www.uhms.org/?page=Indications. [Last retrieved on 2011 Aug 21]. |
|9.||Broome JR, Smith DJ. Pneumothorax as a complication of recompression therapy for cerebral arterial gas embolism. Undersea Biomed Res 1992;19:447-55. |
|10.||Moon RE, Camporesi EM. Problems in Respiratory Care, Clinical Applications of Hyperbaric Oxygen. Philadelphia: JB Lippincott Co.; 1991. p. 4. |
|11.||Grande CM, Myers RA. Trauma Anesthesia, Hyperbaric medicine: A trauma Perspective; Chapter 14: 368-406. |
|12.||Lehm JP, Bennett MH. Predictors of middle ear barotrauma associated with hyperbaric oxygen therapy. SPUMS J 2003;33:127-33. |
|13.||Chen T, Zhou Y, Liu J, Xu B, Wu Z, Li D. Biological effects of hyperbaric oxygen on human severe periodontitis. Undersea Hyperb Med 2002;29:159-66. |
|14.||Teughels W, Quirynen M, Jakubowics N. Periodontal microbiology. In: Newman MG, Takei HH, Klokkevold PR, Carranza FA, editors. Carranza's Clinical Periodontology. 11 th ed. St. Louis, Missouri: Saunders Publication; 2012. |
|15.||Gill AL, Bell CN. Hyperbaric oxygen: Its uses, mechanisms of action and outcomes. QJM 2004;97:385-95. |
|16.||Mettraux GR, Gusberti FA, Graf H. Oxygen tension (pO 2 ) in untreated human periodontal pockets. J Periodontol 1984;55:516-21. |
|17.||Marx RE. Osteoradionecrosis: A new concept of its pathophysiology. J Oral Maxillofac Surg 1983;41:283-8. |
|18.||Chen TL, Lin SL, Liu JC. Effects of hyperbaric oxygen on experimental periodontitis and gingival flow in animal. J Stomatol 2002;22:60-1. |
|19.||Manhold JH, Weisinger E, Rustogi K. Gingival tissue oxygenation: The effect of daily application of four commercial preparations. J Periodontol 1974;45:312-3. |
|20.||Hirsch RS, Clarke NG, Townsend GC. The effect of locally released oxygen on the development of plaque and gingivitis in man. J Clin Periodontol 1981;8:21-8. |
|21.||Schlagenhauf U, Horlacher V, Netuschil L, Brecx M. Repeated subgingival oxygen irrigations in untreated periodontal patients. J Clin Periodontol 1994;21:48-50. |
|22.||Gaggl AJ, Rainer H, Grund E, Chiari FM. Local oxygen therapy for treating acute necrotizing periodontal disease in smokers. J Periodontol 2006;77:31-8. |
|23.||Signoretto C, Bianchi F, Burlacchini G, Canepari P. Microbiological evaluation of the effects of hyperbaric oxygen on periodontal disease. New Microbiol 2007;30:431-7. |
|24.||Nogueira-Filho GR, Rosa BT, David-Neto JR. Effects of hyperbaric oxygen therapy on the treatment of severe cases of periodontitis. Undersea Hyperb Med 2010;37:107-14. |
|25.||Chen TL, Xu B, Liu JC, Li SG, Li DY, Gong GC, et al. Effects of hyperbaric oxygen on aggressive periodontitis and subgingival anaerobes in Chinese patients. J Indian Soc Periodontol 2012;16:492-7. |
|26.||Johnsson K, Hansson A, Granström G, Jacobsson M, Turesson I. The effects of hyperbaric oxygenation on bone-titanium implant interface strength with and without preceding irradiation. Int J Oral Maxillofac Implants 1993;8:415-9. |
|27.||Taylor TD, Worthington P. Osseointegrated implant rehabilitation of the previously irradiated mandible: Results of a limited trial at 3 to 7 years. J Prosthet Dent 1993;69:60-9. |
|28.||Marx RE, Morales MJ. The use of implants in the reconstruction of oral cancer patients. Dent Clin North Am 1998;42:177-202. |
|29.||Granström G, Tjellström A, Brånemark PI. Osseointegrated implants in irradiated bone: A case-controlled study using adjunctive hyperbaric oxygen therapy. J Oral Maxillofac Surg 1999;57:493-9. |
|30.||Esposito M, Grusovin MG, Patel S, Worthington HV, Coulthard P. Interventions for replacing missing teeth: Hyperbaric oxygen therapy for irradiated patients who require dental implants. Cochrane Database Syst Rev 2008;1:CD003603. |