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Chronic obstructive pulmonary disease and periodontitis - Unwinding their linking mechanisms

Authors:
  • Saveetha Institute of Medical and Technical Sciences
  • Saveetha institute of medical and technical sciences

Abstract

Background Chronic obstructive pulmonary disease (COPD) and periodontitis are severe debilitating disorders of inflammatory origin. COPD manifests as inflammation of the lung connective tissue caused by irritants such as smoking and dust particles, resulting in narrowing of the airway. Periodontitis follows the same inflammatory course with the resultant destruction of the local connective tissue, and several irritants are well-documented risk factors for this disease. Highlights Neutrophilic dominance is well established in both of these conditions, and some evidence suggests that periodontopathogens play a role in causing respiratory infections. Given the similarities in the etiopathogenesis and the risk factor profiles of these diseases, a common foundation exists to suggest an inter relationship between the two diseases. Conclusion The present article briefly reviews the interlinking mechanisms between the two diseases, starting with the role of periodontal pathogens, innate immunity, and, ultimately, imbalances in oxidative stress and the protease-antiprotease system. Although epidemiological evidence provides no clear association between these two diseases, the striking commonalities should not be overlooked. Hence, future research should be targeted to this area in order to obtain constructive information. © 2015 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved.
Review
Chronic obstructive pulmonary disease and periodontitis unwinding
their linking mechanisms
Asha Ramesh
n
, Sheeja S. Varghese
1
, N.D. Jayakumar
2
, Sankari Malaiappan
3
Department of Periodontics, Saveetha Dental College and Hospital, No. 162, Poonamallee High Road, Velappanchavadi 600077, Chennai, India
article info
Article history:
Received 25 August 2015
Received in revised form
11 September 2015
Accepted 15 September 2015
Available online 3 October 2015
Keywords:
Periodontitis
COPD
Neutrophil
Oxidative stress
Association
abstract
Background: Chronic obstructive pulmonary disease (COPD) and periodontitis are severe debilitating
disorders of inammatory origin. COPD manifests as inammation of the lung connective tissue caused
by irritants such as smoking and dust particles, resulting in narrowing of the airway. Periodontitis follows
the same inammatory course with the resultant destruction of the local connective tissue, and several
irritants are well-documented risk factors for this disease.
Highlights: Neutrophilic dominance is well established in both of these conditions, and some evidence
suggests that periodontopathogens play a role in causing respiratory infections. Given the similarities in
the etiopathogenesis and the risk factor proles of these diseases, a common foundation exists to suggest
an inter relationship between the two diseases.
Conclusion: The present article briey reviews the interlinking mechanisms between the two diseases,
starting with the role of periodontal pathogens, innate immunity, and, ultimately, imbalances in oxi-
dative stress and the proteaseantiprotease system. Although epidemiological evidence provides no clear
association between these two diseases, the striking commonalities should not be overlooked. Hence,
future research should be targeted to this area in order to obtain constructive information.
&2015 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved.
Contents
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
2. Role of periodontal pathogens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
2.1. Neutrophilic predominance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
2.2. Neutrophil extracellular traps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
2.3. Protease/anti-protease imbalance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
2.4. Oxidative stress in the midst . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
3. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
Ethical approval. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
Conict of interest. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
References.............................................................................................................. 26
1. Introduction
Periodontitis is a chronic inammatory disease that results in the
destruction of the supporting structures of the teeth. The etiology is
multifactorial, with periodontopathogens being the major crux in the
initiation and progression of the disease. Plaque build-up allows the
growth of anaerobic bacteria [1], which eventually leads to the
recruitment and activation of neutrophils. This results in the up-
regulation of pro-inammatory cytokines, leading to the release of
neutrophilic enzymes to combat the invaders. Prolonged exposure of
Contents lists available at ScienceDirect
journal homepage: www.elsevier.com/locate/job
Journal of Oral Biosciences
http://dx.doi.org/10.1016/j.job.2015.09.001
1349-0079/&2015 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved.
Abbreviations: COPD, Chronic obstructive pulmonary disease; Fmlp, N-formyl-
Met-Leu-Phe; NET, Neutrophil extracellular traps; GCF, Gingival crevicular uid;
MMP, Matrix metalloproteinase
n
Corresponding author. Tel.: þ91 9841722113.
E-mail addresses: ash.periopg@gmail.com (A. Ramesh),
drsheeja@rediffmail.com (S.S. Varghese),
principaldental@saveetha.com (N.D. Jayakumar),
msankari@gmail.com (S. Malaiappan).
1
Tel.: 9884042252.
2
Tel.: 9444071930.
3
Tel.: 9840285905.
Journal of Oral Biosciences 58 (2016) 2326
the connective tissue to these insults results in its degradation and the
subsequent loss of ligamentous support and alveolar bone, eventually
leading to tooth loss [2].
The focal infection theory proposed by William Hunter in the
1800s suggested that the oral cavity was the root cause of all sys-
temic diseases; however, this theory was widely disregarded in the
1930s. This theory has been revisited in the modern era because of
the multitude of systemic inuences exerted by periodontal infec-
tions, which are a current focus of research [3]. Recent evidence has
established that periodontitis could be a probable risk factor for
cardiovascular diseases such as atherosclerosis, stroke, myocardial
infarction, diabetes, adverse pregnancy outcome, and respiratory
disorders. This paradoxical shift has been studied extensively and is
now termed periodontal medicine.
Respiratory disorders rank high in the leading causes of mor-
tality and morbidity globally, with upper respiratory infections
affecting over 2 billion people and chronic respiratory infections
causing an increase in years lived with disability (YLD) [4]. Chronic
obstructive pulmonary disease (COPD) is a generic term that is
dened by the chronic obstruction of airow. The pathological
subtypes include emphysema, chronic bronchitis, and small airways
disease; although these are distinct entities, they can occur together
in a single patient. This is also a predominantly neutrophil-
mediated inammatory disease, and an increased number of neu-
trophils has been reported in the airways of patients with COPD [5].
Periodontitis and COPD share a common risk factor prole,
with both diseases showing increased susceptibility of the host to
environmental and genetic factors. Both of these diseases are
bacterial in origin, with a neutrophilic predominance, and they
manifest as chronic inammation with underlying connective
tissue destruction of the respective areas. Further, an imbalance is
present in the redox system and in proteaseantiprotease activity,
which are prime targets in the pathogenesis of the two diseases.
Several epidemiological studies have attempted to nd an asso-
ciation between the two diseases [6,7]. A randomized clinical trial
showed that non-surgical periodontal therapy improved lung
function in COPD patients with chronic periodontitis [8]. In addi-
tion, a recent meta-analysis by Zeng et al. of 14 observational
studies showed that populations with periodontal disease had an
overall increased risk of developing COPD (odds ratio, 2.40); these
authors concluded that periodontal disease signicantly increased
the risk of COPD, but the mechanisms remain unclear [9]. Since the
oral cavity physically continues into the respiratory tract, and
because these two diseases share innumerable contributory
mechanisms, elucidating the connecting links is necessary in order
to deduce the association between these two chronic diseases.
This review will focus on the role of periodontal pathogens and
various other mechanisms through which these conditions are
inter-connected.
2. Role of periodontal pathogens
Scannapieco elucidated various mechanisms by which oral
bacteria can contribute to the pathogenesis of respiratory infec-
tions [10]:
1. The aspiration of oral pathogens, such as Porphyromonas gingi-
valis (P. gingivalis), Aggregatibacter actinomycetemcomitans (A.
actinomycetemcomitans), etc., into the lung can cause infection.
2. Periodontal disease-associated enzymes in saliva may modify
the mucosal surfaces to promote adhesion and colonization by
respiratory pathogens, which are then aspirated into the lung.
3. Periodontal disease-associated enzymes may destroy salivary
pellicles on pathogenic bacteria to hinder their clearance from
the mucosal surface.
4. Cytokines originating from the periodontal tissues may alter the
respiratory epithelium to promote infection by respiratory
pathogens.
Laboratory studies have suggested that oral anaerobes such as
P. gingivalis can cause marked inammation when instilled into
the lungs of laboratory animals [11]. Further, the colonization of
the Prevotella species (a periodontopathogen) in patients may be
associated with an infectious process leading to ventilator-
associated pneumonia and a systemic humoral response [12].
As previously mentioned, oral bacteria can modulate the adhe-
sion of respiratory pathogens on epithelial cell lines. Oral bacterial
products or cytokines in the oral/pharyngeal aspirate may stimulate
cytokine production from respiratory epithelial cells, resulting in
the recruitment of inammatory cells. The resulting inamed epi-
thelium may be more prone to respiratory infection. A study by
Scannapieco et al showed that A. actinomycetemcomitans was the
stronger stimulant in the production of pro-inammatory cytokines
from epithelial cells when compared with P. gingivalis [13].A. acti-
nomycetemcomitans has been established as the most prominent
pathogen in human periodontal disease [14].
2.1. Neutrophilic predominance
Although many immune cells like macrophages and dendritic
cells have been proposed to play a role in the pathogenesis of
periodontitis and COPD, neutrophils are considered the most
important because of their high preponderance in both diseases.
Neutrophil counts are high in COPD, and this does not correlate
with effective elimination of the microbes. This results in collateral
lung tissue damage due to the release of enzymes and reactive
oxygen species (ROS). The amount of neutrophil elastase present
in the lung tissue has been correlated with the severity of
emphysema [15]. Further, neutrophilic function is impaired in
COPD patients. A previous study reported that neutrophils isolated
from the blood of individuals with moderate-to-severe COPD
showed decreased chemotaxis in response to classical chemoat-
tractants such as bacterial protein N-formyl-Met-Leu-Phe (fMLP)
and the pro-inammatory cytokine interleukin (IL)-8, with a cor-
relation between the reduced chemotaxis of neutrophils to fMLP
and the degree of airow limitation [16]. Moreover, neutrophils
from individuals with COPD migrate faster than those from heal-
thy subjects, but the accuracy of migration toward known che-
moattractants, such as fMLP and IL-8, is markedly reduced [17].
Cigarette smoke, which is an exogenous source of oxidants, free
radicals, and neutrophils have been shown to induce oxidative
stress in the lung tissue of COPD patients.
The role of neutrophils in periodontitis has not been clearly
elucidated since both qualitative and quantitative differences
have been observed. Neutrophil function shows both hyper and
hypo activity in response to bacterial stimuli in various forms of
periodontitis. Evidence suggests that neutrophil defects generally
lead to a predisposition for aggressive forms of periodontitis and
hyperactivity or that elevated function is associated with an
increased respiratory burst of the neutrophils [18]. Thus, under-
standing the role of neutrophils in periodontitis and COPD is
necessary to ascertain the common pathophysiological pathway
between these two diseases.
2.2. Neutrophil extracellular traps
Neutrophil extracellular traps (NETs) are web-like extracellular
structures of decondensed chromatin associated with histones and
enzymes such as neutrophil elastase (NE) and myeloperoxidase
(MPO), which are both antimicrobial and cytotoxic. They are
released by activated neutrophils, mainly during a distinct process
A. Ramesh et al. / Journal of Oral Biosciences 58 (2016) 232624
of cell death termed NETosis [19]. The triggers of NETosis are the
bacterial cell wall components that activate complement recep-
tors, Fc receptors, or toll-like receptors on neutrophil surfaces [20].
Once in the extracellular space, these components have the ability
to trap micro-organisms and to expose them to high local con-
centrations of degradative enzymes [21]. This is a type of adaptive
mechanism, wherein the bacterial elimination occurs even after
the death of the neutrophil. These mechanisms form an important
part of innate immunity and they are associated with the release
of ROS and degradative enzymes that play a crucial role in bacteria
elimination and the concomitant tissue damage in chronic dis-
eases like periodontitis and COPD.
A study performed by using the sputa of patients with both the
stable and exacerbated forms of COPD showed that this is char-
acterized by the presence of large amounts of NETs and NET-
forming neutrophils [22]. In addition, studies have shown that an
abundance of NETs contain trapped bacteria in the periodontal
pocket (pocket surface, gingival crevicular uid [GCF], and pus)
[2325]. The knowledge that NETs are involved in both diseases
invokes the possibility of developing new therapeutic strategies
that target the host immune defense mechanisms.
2.3. Protease/anti-protease imbalance
Neutrophils are the prime source of proteolytic enzymes such as
matrix metalloproteinase (MMP) and elastase. The neutrophil elastase
present in the azurophilic granules has been shown to play a pivotal
role in the pathogenesis of COPD. This hypothesis was proposed in the
1960s, when patients with deciency of
α
1
-antitrypsin (AAT) were
noted to be specically susceptible to the development of early onset
emphysema, disproportionate to smoking history [26].AATwaslater
foundtohaveaninhibitoryactiononneutrophilelastase.Insupportof
this mechanism, a relationship between the elastase and anti-elastase
imbalance and the extent of emphysema was evident in the broncho
alveolar lavage uid from patients with COPD [27]. This tilt in the
balance in favor of proteases is associated with connective tissue
destruction, in which components like collagen, laminin, and elastin
are targeted by neutrophil elastase.
MMPs are endogenous enzymes with proteolytic activity
against all components of the extracellular matrix and basement
membrane, leading to subsequent periodontal destruction.
Pathogens in microbial dental plaque are capable of stimulating
host cells to increase MMP release, which is considered one of the
indirect mechanisms of tissue destruction observed in period-
ontitis [28]. Vernooy et al. reported increased MMP-8 and MMP-9
activity in the airway compartment of patients with mild-to-
moderate COPD and suggested that an impaired proteinase-
antiprotease balance exists in COPD [29].
Since all of these enzymes comprise the host response compo-
nent in the pathogenesis of these diseases, therapeutic strategies
such as host modulation have been implemented. For periodontitis,
the FDA has approved the use of the host modulatory agent Periostat
(a sub antimicrobial dose of doxycycline) in conjunction with non-
surgical periodontal therapy. In a landmark study by Canton et al, the
usage of a sub antimicrobial dose of doxycycline in conjunction with
scaling and root planing resulted in a signicant improvement in
clinical parameters like probing depth and the clinical attachment
level in adult periodontitis patients [30].Thelong-termuseofmac-
rolides such as azithromycin was shown to reduce the risk of acute
exacerbations in patients with COPD. This was highlighted in a study
where 1142 patients at an increased risk of COPD exacerbation were
randomly assigned at a 1:1 ratio to receive azithromycin (n¼570) at
a dose of 250 mg daily or placebo (n¼572) for 1 year in addition to
their usual care [31]. The median time to acute COPD exacerbation
was 266 days in the azithromycin group compared with 174 days in
the placebo group.
2.4. Oxidative stress in the midst
Excessive production of free radicals and ROS occurs when oxida-
tive stress increases. The lungs are the site of the majority of redox
reactions with exposure to free radicals derived from tobacco smoke
and air pollution [32]. Immune cells such as macrophages and neu-
trophils are endogenous producers of free radicals, which are released
because of bacterial stimulation or environmental insults [33].ROS
may damage the tissues of the body, depending on the amount and
duration of exposure, and may further act as triggers for enzymatically
generated ROS released from respiratory, immune, and inammatory
cells. The body is equipped with antioxidant defense mechanisms
with enzymes such as superoxide dismutase, glutathione peroxidase,
catalase, and peroxiredoxins. These antioxidants function by degrading
the free radicals and ROS and nullifying their harmful effects.
A positive relationship exists between sputum neutrophils and
hydrogen peroxide levels in patients with severe COPD, suggesting
that these cells are the major source of oxidants [34]. Further,
neutrophils from COPD patients were shown to have greater oxi-
dant production than those of smokers with normal lung function
and non-smoking control individuals [35]. The levels of protective
antioxidants are signicantly depleted in the alveolar macro-
phages of COPD patients, and recent studies indicate that anti-
oxidative mechanisms are not sufciently adapted in inamma-
tory respiratory diseases such as COPD; therefore, the oxidants
may subsequently take on the leading role under these conditions.
Polymorphonuclear neutrophils (PMNs) have an established role in
periodontitis, but whether their hyperactivity is responsible for period-
ontal destruction remains a controversial topic. This is because neu-
trophil defects have been associated with localized aggressive period-
ontitis, which is a more rampant and severe form of the disease;
therefore, the pathogenic mechanism remains to be elucidated. Never-
theless, oxidative stress markers have been routinely studied in period-
ontal research. In chronic periodontitis, even unstimulated neutrophils
had greater spontaneous ROS production, as detected by chemilumi-
nescence, than cells from control individuals [36].Anotherstudyshowed
that antioxidant enzymes like superoxide dismutase, catalase, and glu-
tathione reductase are signicantly lower in chronic periodontitis sub-
jects when compared to healthy controls [37]. Thus, cumulative evidence
suggests that oxidative stress plays a major role in both diseases.
3. Conclusion
Since these two diseases have many features in common, i.e., they
follow the same inammatory course with the resultant destruction
of the local connective tissue, it is reasonable to suppose that a
holistic treatment approach is required to combat these two condi-
tions. Neutrophils, with their oxidants and proteases, play a pre-
dominant role in the pathogenesis of both disorders. The future
scope of research should be targeted towards nding the triggers
that cause the imbalance within neutrophils and initiate the disease
process. Although current epidemiologic studies have provided little
evidence to support an association between these two diseases, the
striking similarities in the disease processes suggest that such a
relationship exists. Clinical trials analyzing the causality and patho-
logical basis of these diseases are a necessity.
Ethical approval
Ethical approval was not obtained since this is a review article.
Conict of interest
None.
A. Ramesh et al. / Journal of Oral Biosciences 58 (2016) 2326 25
Acknowledgments
The authors wish to thank the staff and students of the
Department of Periodontics, Saveetha Dental College, for their
assistance with this manuscript.
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A. Ramesh et al. / Journal of Oral Biosciences 58 (2016) 232626
... Some diseases of the respiratory tract also share molecular and other factors with periodontitis [140][141][142]; such as asthma [143][144][145][146], pneumonia [147][148][149], sleep apnea [150][151][152][153][154], and chronic obstructive airway disease (COAD/COPD) [155][156][157][158]. We can notice, however, that most studies in the current literature (with some exceptions such as in COAD/COPD) consider these associations to have epidemiological origins rather than relying on their molecular and mechanistic origins, which gains support in view of our results presented above. ...
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Periodontal disease, a multifactorial inflammatory condition affecting the supporting structures of the teeth, has been increasingly recognized for its association with various systemic diseases. Understanding the molecular comorbidities of periodontal disease is crucial for elucidating shared pathogenic mechanisms and potential therapeutic targets. In this study, we conducted comprehensive literature and biological database mining by utilizing DisGeNET2R for extracting gene–disease associations, Romin for integrating and modeling molecular interaction networks, and Rentrez R libraries for accessing and retrieving relevant information from NCBI databases. This integrative bioinformatics approach enabled us to systematically identify diseases sharing associated genes, proteins, or molecular pathways with periodontitis. Our analysis revealed significant molecular overlaps between periodontal disease and several systemic conditions, including cardiovascular diseases, diabetes mellitus, rheumatoid arthritis, and inflammatory bowel diseases. Shared molecular mechanisms implicated in the pathogenesis of these diseases and periodontitis encompassed dysregulation of inflammatory mediators, immune response pathways, oxidative stress pathways, and alterations in the extracellular matrix. Furthermore, network analysis unveiled the key hub genes and proteins (such as TNF, IL6, PTGS2, IL10, NOS3, IL1B, VEGFA, BCL2, STAT3, LEP and TP53) that play pivotal roles in the crosstalk between periodontal disease and its comorbidities, offering potential targets for therapeutic intervention. Insights gained from this integrative approach shed light on the intricate interplay between periodontal health and systemic well-being, emphasizing the importance of interdisciplinary collaboration in developing personalized treatment strategies for patients with periodontal disease and associated comorbidities.
... Some diseases of the respiratory tract share also molecular and other factors with Periodontitis [134][135][136]; Such is for instance the case of Asthma [137][138][139][140], Pneumonia [141][142][143], Sleep apnea [144][145][146][147][148] and Chronic obstructive airway disease (COAD/COPD) [149][150][151][152]. We can notice, however, that most studies in the current literature (with some exceptions such as in COAD/COPD) consider these associations based on epidemiological rather than relying on their molecular and mechanistic origins which gain support in view of our results presented above. ...
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Full-text available
Periodontal disease, a multifactorial inflammatory condition affecting the supporting structures of the teeth, has been increasingly recognized for its association with various systemic diseases. Understanding the molecular comorbidities of periodontal disease is crucial for elucidating shared pathogenic mechanisms and potential therapeutic targets. In this study, we conducted comprehensive literature and biological database mining utilizing tools such as DisGeNET2R, Romin, and Rentrez R libraries to identify diseases sharing associated genes, proteins, or molecular pathways with periodontitis. Our analysis revealed significant molecular overlaps between periodontal disease and several systemic conditions, including cardiovascular diseases, diabetes mellitus, rheumatoid arthritis, and inflammatory bowel diseases. Shared molecular mechanisms implicated in the pathogenesis of these diseases and periodontitis encompassed dysregulation of inflammatory mediators, immune response pathways, oxidative stress pathways, and alterations in the extracellular matrix. Furthermore, network analysis unveiled key hub genes and proteins that play pivotal roles in the crosstalk between periodontal disease and its comorbidities, offering potential targets for therapeutic intervention. Insights gained from this integrative approach shed light on the intricate interplay between periodontal health and systemic well-being, emphasizing the importance of interdisciplinary collaboration in developing personalized treatment strategies for patients with periodontal disease and associated comorbidities.
... Previously our team had conducted various studies on treatment modalities for periodontal diseases and periodontal procedures [13][14][15][16][17][18][19][20][21][22], studies correlating various diseases and factors related to periodontal diseases [23][24][25] and in-vitro & radiological studies [26,27] over the past five years. Now we are focussing on epidemiological studies. ...
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To the Editor: In the excellent article by Weiss on tissue destruction by neutrophils (Feb. 9 issue),¹ there is an implicit assumption that neutrophils lack endogenous reducing substances that could quench intracellular or extracellular oxidants. We would therefore like to emphasize that ascorbic acid is present in human neutrophils, in concentrations 20 to 30 times higher than in plasma.² Although the function of ascorbic acid in neutrophils is unknown, it has been proposed that it quenches free radicals,³ either within or perhaps outside neutrophils. However, before this or other functions of neutrophil ascorbic acid can be addressed, it is of…
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This study assessed the activities of antioxidant enzymes superoxide dismutase (SOD), glutathione reductase (GR), and catalase (CAT) and free radical damage marker malondialdehyde (MDA) levels in saliva of 30 patients with chronic periodontitis (CP) compared to 30 healthy controls by spectrophotometry. MDA levels were significantly elevated in the CP group, whereas the SOD, CAT, and GR activities were significantly reduced compared to healthy controls. MDA levels demonstrated a significant direct correlation with all periodontal parameters, whereas all antioxidant enzymes studied (SOD, CAT, and GR) showed an inverse correlation. These findings support the idea that oxidative stress has a role in periodontal disease pathogenesis.
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