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that good oral hygiene and regular professional dental cleaning can attenuate cardiovascular
risk by 9– 14%(78).
Traces of genetic material and antigens of periodontal bacteria, such as P. gingivalis, Aggregatibacter
actinomycetemcomitans and Tannerella forsythia, have been found in atherosclerotic tissues (50,
79– 81). Interestingly, P. gingivalis was found to be one of the most abundant oral bacteria (representing nearly 80% of all bacterial species) found in non- diseased coronary and femoral arteries in
people with atherosclerosis undergoing coronary artery bypass surgery whose periodontal status
was unknown(82). Similarly, meta- analysis identified P. gingivalis as the most frequently detected
periodontal bacterial species in coronary atherosclerotic plaques from individuals post- MI with
periodontal disease(83). However, only two papers have identified viable periodontal bacteria
(P. gingivalis and A. actinomycetemcomitans) within atherosclerotic plaques(84, 85). It is unclear at
present whether bacteria within an atherosclerotic plaque are mere bystanders or whether they play
an active role in the development and/or progression of atheromas.
Elevated plasma levels of triglycerides, low- density lipoproteins (LDL) and very low- density
lipoproteins (VLDL) are proatherogenic(86). A meta- analysis of 29 studies revealed that triglycerides, total cholesterol and LDL levels were 19.4, 15.4 and 11.7 mg/dl higher in individuals with
periodontitis than controls(87). In contrast, high- density lipoproteins (HDL), which have a protective effect (mainly through their ability to remove excess cholesterol from cells and prevent the
oxidation of LDL), are significantly reduced by 4.5 mg/dl in individuals with periodontitis compared to controls(87). Periodontitis may promote dyslipidaemia through various mechanisms. For
example, LPS from periodontal bacteria can boost hepatic de novo fatty acid synthesis and lipolysis, which increases triglyceride and LDL formation (88). In addition, increased circulating
cytokines such as TNFα and IL- 1in periodontitis inhibit lipoprotein lipase activity, thereby reducing LDL clearance(89).
Endothelial cells form a single cell layer that lines the coronary arteries. Damage to these cells is
an essential step in the development of atherosclerosis(90). This is because endothelial cell damage results in the permeation of lipids into the artery wall(91). In health arteries, endothelial cell
integrity and continuity are maintained in part by adhesion molecules such as platelet endothelial
cell adhesion molecule (PECAM- 1), and vascular endothelial cadherin (VE- cadherin)(92). P. gin-
givalis can both degrade PECAM- 1 and VE- cadherin and infect the endothelial cells, resulting in
increased endothelial permeability, oedema and vascular inflammation (93– 95) as shown in
Figure20.5. This process may accelerate the permeation of lipids into the artery wall in individuals
with periodontitis.
P. gingivalis also promotes the expression of adhesion molecules by endothelial cells, which enable adhesion and invasion of monocytes to the site of endothelium damage(96, 97). Monocytes are
essential as they can migrate into the artery wall, differentiate into macrophages and ingest the
retained lipid (98). Macrophages containing ingested lipids are called foam cells (due to their
frothy appearance) and these cells become pro- inflammatory and contribute to the development of
atherosclerotic plaques(98). P. gingivalis has been found to infect macrophages and oxidise lipids,
processes which accelerate foam cell formation resulting in larger atherosclerotic plaques in people
with periodontitis (Figure20.5)(99– 102).
P. gingivalis has also been found to promote atherosclerosis in numerous other ways as
illustrated in Figure20.5:
349
● It can activate platelets which promotes coagulation and inflammation(95).
● Promote the calcification of vascular smooth muscle cells in the artery wall, causing the arteries
to become stiff and hardened(103).
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350
● It can increase the expression of MMP- 9 from blood monocytes and MMP- 1 and MMP- 9 in
plaque macrophages, all of which can encourage degradation, destabilisation and possible
rupture of vulnerable plaques which can lead to MI(104, 105).
● Induce autoimmunity, for example, the production of autoantibodies that cross- react with
antigens in cardiovascular tissues(106) (Figure20.5).
20.4.2 AssociationBetweenPeriodontitisandDiabetesMellitus
Type 1 diabetes mellitus (T1DM) usually develops as an autoimmune condition whereby
thedestruction of pancreatic β- cells results in absolute insulin deficiency. T2DM is a chronic
inflammatory condition characterised by increased insulin resistance and deficits in
insulin secretion, resulting in abnormal glucose metabolism and glucose accumulation in
the bloodstream. Both T1 and T2 DM result in long- term vascular complications such as
CVD, cerebrovascular disease, peripheral vascular disease, retinopathy, neuropathy and
nephropathy(107, 108).
There is a bidirectional relationship between DM and periodontitis. Individuals with T1DM
or T2DM have increased prevalence and severity of periodontitis compared to healthy
individuals(38). The risk of periodontitis is approximately three to four times higher in people
with T2DM than in non- diabetic individuals (109). Interestingly, there is also evidence that
periodontitis can promote the onset of diabetes, and people with periodontitis have more diabetic
complications than those with good periodontal health(110). Findings from 14 studies involving
31,988 individuals with diabetes showed that those with periodontitis had significantly more
renal and CVD, diabetic foot ulceration and overall mortality(110). A recent Cochrane review
showed moderate- certainty evidence from 30 studies consisting of 2443individuals, that treatment of periodontitis resulted in an absolute reduction of HbA1c of 0.43% (4.7 mmol/mol)
3– 4months after treatment, while one study involving 264 participants showed a total reduction
of 0.5% (5.4 mmol/mol) 12 months after treatment (111). This reduction is indicative of the
bidirectional relationship between these two diseases.
Hyperglycaemia in individuals with T2DM augments an inflammatory response in periodontal
tissues and may contribute to accelerated periodontal disease (112). One way this can occur is
through the formation of advanced glycation end products (proteins that become glycated after
exposure to sugar) (AGEs) that can then activate the pro- inflammatory receptor for AGE (RAGE).
Elevated expression of AGEs and RAGE are found in the periodontium of individuals with diabetes; blocking RAGE in diabetic animals resulted in less inflammation and reduced periodontal
bone loss(113, 114).
Mechanistic evidence to support a link between periodontitis and diabetes is limited, and some
of the evidence is conflicting. Some studies have shown that the presence of circulating periodontal pathogens and inflammatory mediators (such as IL- 6, TNF- α and oxygen free radicals) nega-
tively impact insulin signalling, and give rise to insulin resistance(112, 114). Indeed, P. gingivalis
has been found to translocate from the oral cavity to islet β- cells in the pancreas of mice and
humans(115). Here, P. gingivalis has been shown to alter the pancreatic architecture, promote
hyperinsulinemia (seen in pre- diabetes in response to insulin resistance) and cause apoptosis of
pancreatic β- cells(116). Finally, P. gingivalis and other periodontal pathogens have been found to
degrade incretins in the gut (hormones that stimulate a decrease in blood glucose levels), resulting
in elevated glucose levels, as seen in DM(117).
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20.4.3 AssociationBetweenPeriodontitisandAlzheimer’sDisease
Alzheimer’s disease is a chronic progressive neurodegenerative disorder that affects the whole
cerebral cortex and hippocampus resulting in cognitive decline(118). Alzheimer’s disease is the
most common cause of dementia and is characterised by the formation of extracellular amyloid
β- peptide (Aβ) plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau pro-
tein(119). These plaques and tangles cause inflammation, driven by resident macrophages called
microglia, as well as cytokine and complement activation, resulting in neuronal degeneration,
atrophy, synaptic injury and cell death(118, 120).
A recent meta- analysis consisting of five studies shows that periodontitis is associated with
Alzheimer’s disease (OR 1.69, CI: 1.21– 2.35) (121), and the presence of periodontitis is coupledwith a sixfold increase in cognitive decline(122). Clinical studies have also shown that
antibodies to periodontal bacteria such as Fusobacterium nucleatum and Prevotella intermedia
are significantly increased in people with Alzheimer’s disease compared to controls, suggesting
that periodontal disease could potentially contribute to Alzheimer’s disease onset and
progression(123).
Periodontal bacteria can cross the blood– brain barrier and have been found in the human
hippocampus, brain cortex and cerebrospinal fluid (CSF)(124). Gingipains are also found in the
AD brain, a group of proteinases recognised as a major virulence factor of P. gingivalis(125).
Gingipains independently correlate with tau load in the AD brain. They can cleave tau, thereby
contributing to the accumulation of neurofibrillary tangles of aggregated tau that are seen in
Alzheimer’s disease(126).
Low- grade systemic inflammation resulting from periodontitis can increase blood– brain- barrier
permeability, enabling the transmigration of P. gingivalis, peripheral immune cells and inflammatory mediators into the brain tissue of mice. This results in neuroinflammation and neurodegeneration(127). Furthermore, P. gingivalis has been shown to increase levels of tau proteins and Aβ
peptides within brain tissue invivo(124, 128). It has been hypothesised that Aβ peptide has antimicrobial properties, and it is produced in response to oral bacteria in the brain to encapsulate and
prevent further invasion of periodontal pathogens(124). The presence of P. gingivalis in the brain
and the subsequent accumulation of Aβ peptide is lost when mice are infected with gingipain deficient P. gingivalis or administered gingipain inhibitors, thereby highlighting the virulent effect of
these proteinases(126).
Finally, the apolipoprotein E 4 gene (APOE4) is associated with the risk of developing Alzheimer’s
disease by promoting Aβ plaque formation and increasing tau phosphorylation(129). Fragments
of APOE are considered neurotoxic, and P. gingivalis gingipains have been found to cleave
APOE4into fragments. This suggests another potential mechanism of how periodontitis might
contribute to Alzheimer’s disease(130).
351
20.4.4 AssociationBetweenPeriodontitisandRheumatoidArthritis
Rheumatoid arthritis is a chronic autoimmune inflammatory condition characterised by erosive
arthritis of the small joints of the hands and feet(131). A meta- analysis of 13 studies involving
706,611individuals with periodontitis and 349,983 controls, showed that those with periodontitis
had a 69% greater risk of rheumatoid arthritis than the control group (OR 1.69, CI: 1.31– 2.17)(132).
Current evidence also suggests that periodontal treatment improves rheumatoid arthritis disease
activity and circulating inflammatory markers(133). However, there is a lack of randomised
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352
control trials investigating the effect of periodontal treatment on rheumatoid arthritis, and these
results should be interpreted cautiously.
The pathophysiology of rheumatoid arthritis is not fully understood, but a central component is the citrullination of proteins. Citrullination occurs when the amino acid arginine is
converted to citrulline by the enzyme peptidyl arginine deiminase enzyme (PAD)(134). The
immune system is not able to recognise citrullinated proteins as self- structures, and this results
in an inflammatory response that includes auto- antibody production (Rheumatoid factor and
anti- citrullinated protein antibodies are the most synonymous auto- antibodies in rheumatoid
arthritis)(135). An influx of inflammatory cells into the synovium of a joint and the release
ofvarious inflammatory cytokines such as IL- 1, IL- 6, IL- 17 and TNF- α promotes inflamma-
tion and ultimately stimulates osteoclast activity that leads to joint swelling and bone
erosion(135).
Periodontitis can contribute to rheumatoid arthritis pathogenesis. For example, P. gingivalis
expresses its unique PAD (PPAD) that can citrullinate bacterial and host peptides (136).
Furthermore, P. gingivalis gingipains can augment this effect by cleaving peptides, exposing the
arginine component for citrullination by PPAD. This generates more autoantigens and subsequent
autoantibody production that drives inflammation in rheumatoid arthritis(137). Another periodontal pathogen, A. actinomycetemcomitans, can induce hypercitrullination in neutrophils through
the secretion of the pore- forming toxin leukotoxin- A (LtxA)(138). The LtxA also causes neutrophil
cell death, releasing the citrullinated proteins and generating another pool of rheumatoid arthritis
autoantigens(138).
Finally, P. gingivalis can promote bone loss in rheumatoid arthritis by increasing the expansion
of osteoclast precursor cells (bone- resorbing cells) in the bone marrow(44). This expansion is
driven by increased circulating IL- 6 due to P. gingivalis infection. These osteoclast precursor cells
can travel from the bone marrow and populate areas of bone resorption such as a rheumatoid
arthritis joint, where they differentiate into mature osteoclasts in response to locally produced
receptor activator of NF- κB ligand (RANKL)(139).
20.4.5 BriefOverviewofAssociationsBetweenPeriodontitisandOther
SystemicConditions
Pregnancy
● Weak evidence of an association between periodontal disease and adverse pregnancy outcomes
(APOs) such as low birth weight, preterm delivery (PTD) and preeclampsia(140).
● Limited evidence suggests that periodontal treatment during pregnancy improves pregnancy
outcomes(141).
● Periodontal pathogens have been found in the foetal– placenta unit. However, the exact role of
these pathogens in APOs is unclear(142).
● Inflammatory mediators induced by periodontitis may impact the foetal– placenta unit(142). For
example, IL- 1, IL- 6 and TNF- α can stimulate prostaglandin E2 (PGE2) production, and PGE2
can cause cervical ripening and uterine contraction thereby increasing the risk of PTD(143).
Chronic Kidney Disease (CKD)
● CKD is defined as kidney structure or function abnormalities present for ≥ three months and
associated health consequences.
● Strong evidence from a meta- analysis of an association between periodontal disease and
CKD(144).
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● Insufficient evidence to suggest that periodontal treatment may benefit renal function in people
with CKD and periodontitis(145).
● No evidence of periodontal bacteria disseminating to and infecting renal tissue(146).
● Increased systemic inflammation, oxidative stress and dyslipidaemia from periodontal disease
may accelerate CKD but the exact mechanism is still unclear(146).
Cancer
● There is a positive association between periodontitis and a range of cancers, in particular head
and neck, upper gastrointestinal, oesophageal and pancreatic cancers(147).
● The underlying mechanism linking periodontal disease to cancer risk is unclear, but chronic
inflammation seems to play an important role(147).
● Chronic inflammation may lead to DNA damage, mutations and/or interfere with DNA repair
mechanisms, which can drive malignancy(148).
Non- periodontal inflammatory mucosal diseases have also been associated with an increased
risk of CVD, independent of common risk factors(10). For example, people with infectious oral
mucosal diseases such as oral candidiasis and herpes simplex infection are 1.33 times more likely
to have a history of angina compared to controls(10). Similarly, those with inflammatory oral
mucosa diseases like OLP(149, 150). The association between common oral mucosal diseases,
including recurrent aphthous stomatitis (RAS), and CVD history is also evident (10). This is
biologically plausible as these conditions can give rise to chronic systemic inflammation which
previously discussed may promote CVD.
353
20.5 Summary
In conclusion, oral bacterial infection and inflammation are linked to the initiation and/or
exacerbation of systemic diseases. In the case of periodontitis and OLP, the relationship is not
necessarily causal, and further studies are needed to clarify exactly how these conditions are
associated with systemic diseases. Nonetheless, current research does indicate that various plausible cellular mechanisms are at play which account for the close correspondence between oral
and systemic conditions.
Educating both medical and dental professionals and patients about the possible links between
oral and systemic disease will be essential. There will be numerous benefits. The first is to emphasise the importance of a comprehensive medical history in the dental setting to identify, educate
and manage those at risk. Secondly, interdisciplinary collaboration will benefit patient care, as
medical physicians will refer patients with certain systemic diseases to dentists to investigate and
manage their oral disease. Finally, the prevention and early management of oral disease may
reduce the morbidity, mortality and economic cost associated with numerous systemic diseases,
while at the same time promoting good oral health.
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