HYPERBARIC OXYGEN THERAPY AND ITS RELATION TO PERIODONTITIS

1. HYPERBARIC OXYGEN
THERAPY(HBOT)
Presented by
Dr Manu Bhaskaran Nair

2. CONTENTS
• Definitions
• History
• Principles of HBOT
• Physiology
• Mechanism of action
• Dosage and delivery
• Monoplace and multiplace chambers
• Indications
• Contraindications
• Preparations before HBOT
• Negative effects
• Complications
• Applications in dentistry
• Conclusion
• References

3. DEFINITIONs
• HYPER (increase) + BARIC(pressure)
• Hyperbaric oxygen therapy (HBOT) involves the
“intermittent, usually daily, inhalation of 100 percent
humidified oxygen under pressure,greater than 1
atmospheric absolute pressure(ATA).”- Neelima
Malik,3 rd edition.
• The Committee on Hyperbaric Medicine defines HBO
therapy as “A mode of medical treatment in which the
patient is entirely enclosed in a pressure chamber and
breathes 100% oxygen at a pressure >1 atmosphere
absolute (ATA).”

4. •ATA is the unit of pressure
•1 ATA is equal to 760 mm of mercury or pressure at sea level.
• Hyperbaric Oxygen Therapy (HBOT) is the use of high
pressure oxygen as a drug to treat basic pathophysiologic
processes and their diseases -
Textbook of Hyperbaric Medicine,3 rd edition

5. HISTORY
• 1662-hyperbaric air was used by Henshaw for
the treatment of “affections of the lung”.
• He built a structure called the domicilium that
was used to treat a multitude of diseases. The
chamber was pressurized with air or
unpressurized using bellows.

6. HENSHAW’S DOMICILIUM
Henshaw IN, Simpson A. Compressed Air as a Therapeutic Agent in the
Treatment of Consumption, Asthma, Chronic Bronchitis and Other Diseases.
1857.

7. • 1775- English scientist named
Joseph Priestly
first discovered oxygen ,
which ultimately would have
had a profound effect on
hyperbaric medicine.
• 1777-Name oxygen was coined by Antoine Lavoisier
• 1789-Unfortunately, Lavoisier and Seguin reported ill-
defined toxic effects of concentrated oxygen, thereby
increasing the hesitation to use hyperbaric oxygen
therapy (HBOT).

8. • 1878 - Paul Bert documented more clearly the
toxic effects of oxygen on the central nervous
system that were manifested as seizures.(Jain KK.
The History of Hyperbaric Medicine).
• 1879-The idea of treating patients under
increased pressure was continued by the French
surgeon
Fontaine, who built a
pressurized, mobile
operating room.
(Kindwall E, Whelan H. Hyperbaric Medicine
Practice. 2nd ed.)

9. • 1928-Dr. Orville Cunningham, a professor of
anesthesia, ran what was known as the "Steel
Ball Hospital.“

10. • The structure, was 6 stories high and 64 feet in
diameter.
• The hospital could reach 3 atmospheres of
pressure.
• The hospital was closed in 1930 because of the
lack of scientific evidence indicating that such
treatment alleviated disease.
• It was deconstructed during World War II for
scrap.
( Reference-Jain KK. The History of Hyperbaric
Medicine.)

11. • 1937- Behnke and Shaw first used hyperbaric
oxygen successfully for the treatment of
decompression sickness sufferred by deep sea
divers.
• In 1950’s: The modern clinical application of
HBO began, in parallel with an increased
understanding of blood gas analysis and gas
exchange physiology.

12. • In 1960’s – 2 institutions preeminently
pursued the clinical aspects of high pressure
oxygenation.
• Dr. Bakers from the University of Amsterdam
developed the use of intermittent HBO, for
the treatment of gas-gangrene.
• Second major focus of interest in this area was
Royal Infirmary of Glassgow, where various
anesthetic and surgical aspects of HBO were
applied and discussed.

13. • 1965: It was first used to assist wound healing when it was
noted that burns of
the victims of
coalmine explosions
treated with HBO2
healed faster.
• Since 1970: Most of the instructional courses, research work and
guidance have been provided by Under seas and Hyperbaric Medical
Society (Headquarters in Kensington, Maryland).
• This medical organization publishes guidelines for hyperbaric
oxygenation every 2-3 years.

14. PRINCIPLES OF HBOT
• based on how gases of different solubilities,
most importantly oxygen, behave under
changing pressures and volumes, within
tissues and fluid -
• Henry’s Law of gas behavior
• Fick’s Law of gas behavior
• Boyle’s Law of gas behavior

15. • Henry’s Law(Edward et al.2010)
“states that the concentration of a dissolved gas
(Concgas) equals the pressure (P) times the
solubility coefficient (Sol) of that gas.”
Concgas=P(sol)
• The 3 main gases of concern in HBOT are oxygen,
carbon dioxide, and nitrogen
Oxygen 0.024
Carbon dioxide 0.57
Nitrogen 0.012
solubility coefficients normal body temperature

16. • Fick’s law (Edward et al,2010)
describes the rate of diffusion of a gas through tissues or
fluids.
• “the gas flow (volume of gas per unit time [Vgas]) through a
tissue or membrane is equal to the area (A) divided by the
thickness (T) multiplied by the diffusion constant (D) times the
difference in partial pressures (P1–P2) of the gas across the
tissue or membrane.”
• The diffusion constant is proportional to the solubility of the
gas (Sol) divided by the square root of the molecular weight
(MW) of the gas.
Vgas =D(P1 - P2)

17. • Boyle’s law (Edward et al,2010)
relates to how volumes of gas behave under pressure.
• “with increasing pressure (P) the volume (V) of a gas
decreases proportionately.”
• Significance-This becomes important when gases are trapped
in various cavities during compression and decompression of
the patient
if there is air trapped
within a body cavity the
volume will contract and
may alleviate some
clinical conditions
when the patient is
decompressed the trapped
gas will expand and may
cause complications.

18. PHYSIOLOGY
• The air that we normally breathe contains 21% O2 at
sea level pressure.
• The tissues that are in need of oxygen obtain it from
the oxygen combined to hemoglobin(oxy Hb)which is
95% saturated.
• Oxygen is needed to provide energy and support
cellular respiration.

19. • Any injury or disease
decreases the body’s ability to transport
oxygen to the tissues,
• Eg – hemolytic anemia, toxin exposure, and
hemorrhage

20. Increases the tissue demands for oxygen
Eg- infections,tissue healing
 may increase the distance that the oxygen must travel
from the capillary to reach the cell.
Eg-Edema,decreased perfusion and microthrombosis

21. To brush up ………
• Oxygen is carried by blood mainly in 2 ways-
1. Hemoglobin
2. Plasma
• Hemoglobin carries majority of oxygen
• Plasma carries only minute amounts of
oxygen

22. 100 ml of blood 19ml O2 + Hb
0.32ml in plasma
At the same pressure
100 % O2 inspired O2 + Hb 20ml
Plasma 2.09ml
The higher pressure during
HBO treatment pushes more oxygen
into solution
2ATA pressure
3ATA pressure
4.4 ml/dl
6.8ml/dl
PLASMA
This additional O2 in solution is sufficient to meet tissue needs without
contribution from O2 bound to hemoglobin and is responsible for most of the
beneficial effects of this therapy.

23. MECHANISM OF ACTION
(Bhutani et al,Ind Jr Plastic Surgery,2012)
• 2 primary MOA –
1. hyperoxygenation
2. decrease in bubble size

24. Hyperoxygenation
• an application of Henry's law
• results from an increase in dissolved oxygen in
plasma as a result of increased partial pressure of
arterial oxygen(pO2).
• management of crush injury, compartment
syndrome, flap salvage and acute blood loss
anaemia.
A pressure of 3 ATA results in 6 ml of
O2being dissolved per 100 ml of plasma,
thus rendering as much O2 delivery as by
haemoglobin bound O2.

25. Decrease in bubble size
• application of Boyle's law
• High oxygen (100%) intake saturates the blood
plasma with oxygen.
• volume of a bubble decreases directly in
proportion to increasing pressure and is the
primary mechanism at work in management
of decompression sickness and arterial gas
embolism. (Latham E et al. Hyperbaric oxygen
therapy. eMedicine. Medscape).

26. Secondary MOA –
• include vasoconstriction,
• angiogenesis,
• fibroblast proliferation,
• leukocyte oxidative killing,
• toxin inhibition& antibiotic synergy

27. Vasoconstriction
• Hyperoxia in normal
tissues causes
vasoconstriction which reduces post-traumatic tissue
oedema.
• This contributes to the treatment of crush injuries,
compartment syndromes and burns.
• Vasoconstriction, however, does not cause hypoxia as
this is more than compensated by increased plasma
oxygen content and microvascular blood flow.

28. Collagen formation
Oxygen is vital for
• hydroxylation of lysine and proline residues
during collagen synthesis
• for cross linking and maturation of collagen
which is required for strong wound healing.
• Lack of oxygen is corrected during HBOT,
leading to adequate amounts of mature
collagen formation.

29. Angiogenesis
Hypoxia is a vital stimulant for angiogenesis, but
development of adequate capillary network requires
adequate amounts of tissue oxygen concentration..
This along with fibroblastic proliferation leads to
increased neovascularisation.
HBOT increases the oxygen gradient between the
centre and periphery of the wound, thus creating a
strong angiogenic stimulus.

30. What is hypoxia???
Hypoxia or hypoxiation is a pathological condition in
which
• the body as a whole (generalized hypoxia)
• or a region of body (tissue hypoxia) is deprived of
adequate oxygen supply.

31. Hypoxia v/s Hypoxemia

32. • Generalized hypoxia
• occurs in healthy people when they ascend to
high altitude, where it causes altitude sickness
leading to potentially fatal complications:
• High altitude pulmonary edema and high
altitude cerebral edema.

33. • Hypoxia also occurs in healthy individuals when
breathing mixtures of gases with low oxygen
content,
e.g. while diving underwater especially when using
closed-circuit re-breather systems that control
the amount of oxygen in the supplied air.

34. • Hypoxia is also a serious consequence of preterm birth in
the neonate.
• The main cause for this is that the lungs of the human
fetus are among the last to develop during pregnancy.
• To assist the lungs to distribute oxygenated blood
throughout the body ,infants at risk of hypoxia are often -
• placed inside an incubator capable of providing continuous
positive airway pressure (also known as a humidicrib).

35. MECHANISM -HYPOXIA
• Hypoxia extends beyond the local wound
environment.
• Reactive oxygen species are produced, including
oxygen free radicals.
• these cause vasoconstriction followed by vasodilatation.
• Endothelial cell damage and release of prostaglandins, pro-
inflammatory cytokines (tumor necrosis factor-α and
interleukin-6) and nitric oxide from vascular endothelium
occurs

36. • capillaries become leaky, interstitial edema
occurs.
• Circulation is further compromised with
compounded injury
• The surgical or medical reestablishment of
interrupted circulation sends blood to the
ischemic area, providing new oxygen substrate
for the formation of more free radicals.
In massive injury the release of inflammatory cytokines and
free radicals escape the normal regulatory mechanisms
and can lead to multiple organ failure. Hence, a long
and catastrophic chain of events can be initiated by O2
deprivation.

37. • HBO 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.

38. •Hypoxia reduces this function.
•Significant reductions in the killing capacity of leukocytes occur
when tissue pO2 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.
Indirect effect of HBO 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.

39. Hyperoxia and HBO 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 and Pseudomonas and also for a
range of enteric bacteria (Salmonella, Shigella
and Proteus).

40.  Improved leukocyte killing activity
 Promotion of fibroblast
 proliferation, collagen formation,
 angiogenesis in problem wounds,
flaps, and irradiated tissues.
 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.

41. Mechanism References Clinical Application
Hyperoxygenation
Boerema I
Bassett BE
Bird AD
•DCS
•CO poisoning
•Central retinal artery
occlusion
•Crush
injury/compartment
syndrome
•Compromised grafts and
flaps
•Severe blood loss
anemia
Decrease gas bubble
size
Boyle law •Air or gas embolism
Vasoconstriction
Nylander G
Sukoff MH
•Crush
injury/compartment
syndrome
•Thermal burns

42. Angiogenesis
Knighton DR
Tal S
•Problem wounds
•Compromised grafts
and flaps
•Delayed radiation
injury
Fibroblast
proliferation/collagen
synthesis
Hunt TK
•Problem wounds
•Delayed radiation
injury
Leukocyte oxidative
killing
Mader JT
Park MK
Mandell GL
•Necrotizing soft tissue
infections
•Refractory
osteomyelitis
•Problem wounds

43. Reduces intravascular
leukocyte adherence
Zamboni WA
Thom SR
•Crush
injury/compartment
syndrome
Reduces lipid
peroxidation
Thom SR
•CO poisoning
•Crush
injury/compartment
syndrome
Toxin inhibition Van Unnik A •Clostridial myonecrosis
Antibiotic synergy
Mirhij NJ
Keck PE
Mendel V
Muhvich KH
•Necrotizing soft tissue
infections
•Refractory
osteomyelitis

44. Dosage and Delivery
• All regimens use 100% oxygen
• Pressures are more variable-
 Mostly used 2.4 atm
 Maximum tolerated is 3 atm
 4 atm induces seizures

45. Compression
10min
Decompression
10min
90 min on Oxygen + Two 5min- “Air Breaks”
Treatment Phase – 100min

46. • Dives between 30 and 120 minutes
• May be daily or BID
• Total number varies by indication
• Most treatments include 30 dives
• Optional addition of 10 or more dives are accepted.
HBOT is carried out in 2 chambers-
1. Monoplace chamber
2. Multiplace chamber

47. Monoplace chambers
•Small and designed to accommodate only one adult individual,
usually in a supine or semi-recumbent position
•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.

48. •Cost efficient delivery of
HBO2.
• No risk of decompression
sickness.
• Portable, less space, less
equipments, no hood or
mask.
•No risk of iatrogenic
decompression sickness in
patient or staff
Advantages
•Relative patient isolation.
•Associated fire hazard.
• Inability to use certain
diagnostic and/or
therapeutic equipment.
•Limited access to the
patient inside chamber
with only visual and
auditory communication
available to the patient
and observers.
Disadvantages

49. Multiplace chambers
• These units can accommodate between 2 and 18 or
more patients and commonly incorporate a
minimum pressure capability of 6.0 ATA.

50. •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.
•Reduced fire risk
•More room available, which
allows medical personnel to
enter to deal with acute
problems, e.g., pneumothorax
•Higher capitalization
requirements.
•risk of cross infection when
used to treat wounds
• Major space requirements;
basement and/or ground
floor level limitations.
•Higher operating costs.
Advantages Disadvantages

51. Other chambers
• Two other types of chambers are mentioned,
although they are not considered HBOT.
1. Topical oxygen, or Topox, is administered
through a small chamber that is placed over an
extremity and pressurized with oxygen.
• The patient does not breathe the oxygen, nor is
the remainder of the body pressurized.
• The patient cannot benefit from most of the
positive effects of HBOT, which are systemic or
occur at a level deeper than topical oxygen can
penetrate

52. • Topox is based on the concept that oxygen
diffuses through tissue at a depth of 30-50
microns.
• This method does not treat DCS, arterial gas
emboli (AGE), or carbon monoxide (CO)
poisoning.

53. 2. portable "mild" hyperbaric chamber
• These soft vessels can be pressurized to 1.5-1.7
atmospheres absolute (ATA).
• They are only approved by the FDA for the treatment
of altitude illness.
• The number of these chambers has increased, as
they are being used more commonly in off-label
indications.

54. INDICATIONS
• According to Undersea and Hyperbaric Medicine Society
(UHMS)-
1.Air or gas embolism.
2. Carbon monoxide poisoning or carbon monoxide poisoning
complicated by cyanide poisoning.
3. Clostridal myositis and myonecrosis (gas gangrene).
4. Crush injury, compartment syndrome, and other acute
traumatic ischemia.
5. Decompression sickness.
6. Enhancement of healing in selected problem wounds;
a. Diabetically derived illness, such as diabetic foot,
diabetic retinopathy, diabetic nephropathy.

55. 7. Exceptional blood loss (anemia)
8. Intracranial abscess.
9. Necrotizing soft tissue infections (necrotizing fasciitis).
10. Osteomyelitis (refractory).
11. Delayed radiation injury (soft tissue and bony necrosis).
12. Skin grafts and flaps (compromised).
13. Thermal burns.
Additional indications recommended by European Concensus
Conference 2004 –
1. Surgery and implant in irradiated tissue(Preventive action)
2. Sudden deafness
3. Neuroblastoma stage IV
4. Post anoxic encephalopathy
5. Limb replantation

56. Figure shows sequential photographs of a 53-year-old male
diabetic suffering from spontaneous gangrene of the thigh
who was managed successfully with HBOT at a tertiary care
hospital of the Armed Forces.

57. CONTRAINDICATIONS
Absolute
Contraindications
Reason
Contraindicated
Necessary
Conditions Prior to
HBOT
Untreated
pneumothorax
Gas emboli
Tension pneumothorax
Pneumomediastinum
Thoracostomy
Bleomycin
Interstitial
pneumonitis
No treatment for
extended time from
use of medication
Cisplatin
Impaired wound
healing
No treatment for
extended time from
use of medication

58. Disulfiram
Blocks superoxide
dismutase, which is
protective against
oxygen toxicity
Discontinue
medication
Doxorubicin Cardiotoxicity
Discontinue
medication
Sulfamylon
Impaired wound
healing
Discontinue and
remove medication

59. • Relative
a. Upper respiratory tract infection
b. Chronic pulmonary obstructive disease
c. Congenital spherocytosis
d. Eustachian tube dysfunction
e. Asthma
f. Pregnancy
g. Claustrophobia
h. Seizure disorder
i. Hyperthermia

60. PREPARATIONS BEFORE HYPERBARIC
OXYGEN THERAPY
1. Medication
• The HBO 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

61. 2.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 treatments may need to be postponed until
symptoms have subsided.

62. 3.Smoking
• 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.
4. Cosmetics
• Cosmetics, hair spray, nail polish, perfume, or
shaving lotion containing petroleum, alcohol or oil
base are not allowed while in the HBO chamber.
• It is important to discuss all skin care products with
the HBO technician, so they may assure safety.

63. 5. Clothing (Moon & Grande)
• Patients are provided with
100% cotton gowns to wear
during treatment.
• No articles containing nylon
or polyester can be
worn in the chamber.

64. Negative affects after therapy??
• A “cracking” sensation in their ears
between treatments as a pressure
difference develops between their
middle ear and the chamber atmosphere.
(Lehm JP, Bennett MH. Predictors of middle ear
barotrauma associated with hyperbaric oxygen
therapy.)
• Feeling of light headedness for a few minutes
immediately following a treatment.

65. Potential complications after HBO
1.Oxygen toxicity - Seizures, dry cough, chest
pain or burning.
2.Visual refraction changes - Cataract,
progressive myopia with prolonged number of
treatments.
3. Barotrauma - In ears, sinus, lungs, tooth
caries/fillings.

66. Complication Presentation Treatment
Barotrauma
Middle ear (URI,
Eustachian tube
dysfunction)
Ear pain,
fullness
Muffled hearing
•Autoinflation
technique
•Pseudoephedri
ne/oxymetazoli
ne
•Tympanostomy
tubes
•Wait for URI
resolution
Sinus
Sinus pain or
bleeding
•Oxymetazoline
/pseudoephedri
ne
•Antihistamines
•Steroid nasal
spray

67. Dental Tooth pain
Replacement of
filling or crown
(allows trapped
air bubble to
escape)
Pulmonary
•Dry cough
•Chest pain or
burning
•Decreased vital
capacity
•No breath-
holding
•Thoracostomy (if
pneumothorax)
•Increase
decompression
time
Round or oval window blowout
•Immediate
deafness
•Tinnitus
•Nystagmus,
vertigo, or both
Discontinue
Valsalva
Refer to ENT

68. Visual
refraction
change
Lens
morphology
Progressive
myopia with
prolonged
number of
treatments
Most resolve
spontaneously
when
treatment
finished
Cataracts
Clouding of
vision
•Prescreen for
existing
cataracts
•HBOT generally
does not
influence
cataract
formation,
except after
prolonged
(>100)
treatments

69. Oxygen toxicity
CNS (Incidence
0.7 per 10,000
treatments at 2.4
ATA)
Seizure
•Removal from
oxygen source
•Resume HBOT
with shorter
oxygen treatment
periods
•Does not require
medication
•Treat
hypoglycemia if
present
•Treat fever if
present
Pulmonary
•Dry cough
•Chest pain or
burning
•Decreased vital
capacity
•Decrease total
oxygen exposure
time (including
outside HBOT)

70. APPLICATIONS IN DENTISTRY
hyperbaric oxygen therapy is used in
• Osteoradionecrosis
• Osteomyelitis of jaws
• Aggressive periodontitis
• Adjunctive therapy for the placement of the
implants in irradiated jaws.

71. Osteoradionecrosis
complication of the jaws which occurs
after head and neck radiotherapy
Patients are subjected to HBOT to
prevent the necrosis of the bone after
extraction in irradiated patients.
Necrosis occurs since blood supply is
compromised after radiotherapy
characterized by hypocellularity,
hypovascularity and hypoxia
Mode of action of HBOT
•Increases the oxygen tension in the
region and promotes angiogenesis and
wound healing

72. Osteomyelitis
chronic, unresponsive bone infection
which is caused by bacteria that may
remain dormant for years.
treatment of osteomyelitis is surgical
debridement and antibiotic prophylaxis
main complication in osteomyelitis is
the presence of a barrier between the
host and the infection.
This barrier can be suppuration,
necrotic bone, but it can limit the action
of the host’s immune system.
Mode of action of HBOT
Increases the host response by
favouring the action of inflammatory
cells.

73. Implants in irradiated
bone
Dental implants are directly inserted into the bone which
replaces the missing teeth.
in an individual who has already undergone radiation therapy,
the implant is likely to fail, because the bone formation is
compromised after radiation
In an experimental study done on implants inserted into
irradiated bone, to assess the effects of hyperbaric oxygen
therapy on the capacity of bone formation, hyperbaric oxygen
therapy was found to stimulate effective bone formation .

74. • Implants when placed in the irradiated bone
lead to failure because of increased
susceptibility to infection and compromised
bone formation.
Mode of action of HBOT
• Stimulates effective bone formation and
increases host defense mechanism

75. Periodontitis
• The effect of hyperbaric oxygen on aggressive periodontitis
and subgingival anaerobes in Chinese patients,
documented the effect of hyperbaric oxygen therapy.
• This assessment was done by measuring plaque index,
gingival index, probing depth and attachment loss, two
years after hyperbaric oxygen therapy was indicated.
• It was concluded in this study, that HBO could inhibit the
growth of subgingival obligate anaerobes, facultative
anaerobes and Bacteroides melaninogenicus,
• thus promoting healing of peridontium, which could help
in the treatment of aggressive periodontitis.( Tie-lou Chen,et
al.2012)

76. • The use of hyperbaric oxygen as a adjunct to scaling and
root planning in patients with generalized chronic
periodontitis, is found to improve the clinical parameters
like probing depth and attachment level, thus indicating the
beneficial effects of hyperbaric oxygen on the
periodontium .(Getulio R et al 2010)
• Microorganisms and their toxins affect the periodontium
Mode of action of HBOT
• Inhibits the growth of subgingival obligate anaerobes and
facultative anaerobes and promotes healing of the
peridontium

77. HBO and Periodontitis
Mechanism
• 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.
• HBO 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.

78. Studies
AUTHOR STUDY
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.

79. 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 P. intermedia, T.
forsythia, and T. 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 combination of HBO2 and SRP substantially reduced (by up to
99.9%) the Gram-negative anaerobe loads of the subgingival
microflora. In addition, molecular detection of the main
periodontopathogenic bacteria significantly reduced in the
number of dental sites, which harbored them.
Nogueira-Filho et
al.
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. concluded that HBO2 inhibits the growth of subgingival obligate
anaerobes and facultative anaerobes and B. melaninogenicus thus
promoting healing of peridontium, which will be of help in the
treatment of AgP.

80. HBO and Implant
Mechanism
• The exact mechanisms at the cellular level where
HBO2 act remain obscure.
• It has been recently shown that HBO2 and basic
fibroblast growth factor (bFGF) acts synergistically in
irradiated bone.
• Factors that could be involved in bone protection by
bFGF and HBO2 are bone marrow radioprotection,
induction of oxygen radical scavengers and
production of different cytokines.

81. • 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.
• HBO2 has furthermore been shown to affect the interface
between the titanium implant and bone, which could be
different from cellular effect.(Johnson k et al,1993.)
• 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.

82. Biological effect on periodontium
• Animal studies showed that HBO can increase the amounts
of opened blood vessels, and increase the gingival blood flow
and blood current velocity, decrease the blood
concentration.
• HBO may regulate the microcirculation by changing the
opened blood vessels and endoepithelial cell metabolism.
• The value of PGE2 in alveolar bone and gingiva reduce
markedly after HBO exposure in experimental periodontitis.
• HBO is effective in treating periodontitis after periodontal
flap surgery.(Lai SP, Huang F. Observation of the therapeutic
effects of hyperbaric oxygen on periodontitis after
periodontal flap surgery. )

83. CONCLUSION
 HBOT was started as a treatment modality for
management of decompression sickness and, with the
passage of time, its scope has gradually increased to
include numerous indications.
 Hyperbaric oxygen has been successfully used in several
medical applications.
 The therapeutic effect is related to elevated partial
oxygen pressure in the tissues.
 Dental patients too could be benefited with this
treatment approach along with the advancement in the
medicines and technical equipment’s used in the patient
care.

84. • 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.

85. REFERENCES
• Hyperbaric Oxygen Therapy – Can It Be the New Era in Dentistry? Divya Devarajand D.
Srisakthi
• www.mayoclinic.org/testsprocedures/hyperbaric-oxygen-therapy/about/pac-20394380
• Hyperbaric Oxygen Therapy, Medscape
• Hyperbaric oxygen and wound healing Sourabh Bhutani,Guruswamy Vishwanath
• Hyperbaric oxygen therapy. Part 1: history and principles Melissa L. Edwards, DVM,
DACVECC
• Applications of hyperbaric oxygen therapy in dentistry: A mini review Nalini Jain, D.
Deepa
• Biological effec ts of hyperbaric oxygen in human severe periodontitis,T chen Y zhou
• Hyperbaric oxygen therapy in periodontal diseases Swapna A. Mahale, Pankaj K.
Kalasva, Sunil Vinayak Shinde
• Microbiological evaluation of the effects of hyperbaric oxygen on periodontal disease
Caterina Signoretto, Franco Bianchi, Gloria Burlacchini, Pietro Canepari
• Role of hyperbaric oxygen therapy in the treatment of periodontitis Ravi Prakash Popat,
Parita Ravi Popat1
• Neelima Malik 3° edition
• Internet sources