Associations Between Periodontal Diseases

8/14/2019 Associations Between Periodontal Diseases

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Lan-Chen Kuo, Alan M. Polson,Taeheon Kang


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Summary

The aim of this review article is to examine the associationsbetween periodontal diseases and common systemicdiseases, namely diabetes, respiratory diseases,cardiovascular diseases and osteoporosis.

A substantial number of review articles have been published toelucidate the relationships between these diseases; however,none provide a complete overview on this topic from theaspects of definition, classification, clinical characteristics andmanifestations, inter-relationships and interactions,proposed schematic mechanisms, clinical implications andmanagement of periodontal patients with these systemicdiseases.

The aim of this article is to provide an overall understandingand general concepts of these issues in a concise and inter-


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Periodontal diseases and diabetes

Periodontal diseases are a group of bacterial infectiousand inflammatory diseases that result in the destructionof tooth-supporting tissue, including the gingiva,alveolar bone and the teeth themselves, which mayeventually cause tooth loss. (Mealey BL, RethmanMP.,2003)

Diabetes mellitus represents a group of metabolicdiseases that are characterized by hyperglycaemiaresulting from defects in insulin secretion, insulin actionor both.

Worldwide, more than 18 million people suffer from

diabetes itself and its severe complications, i.e.blindness, leg amputation, renal dialysis, impairedwound healing, cardiovascular diseases (CVD) anddeath.


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Type 2 diabetes has many causes; however, 8090% of patients with Type 2 diabetes are obese.

An episodic form of diabetes is termed gestational

diabetes. (Mealey BL, Rethman MP.,2003) Pregnant women who have never had diabetes

before but who have high blood glucose levels

during pregnancy are classified into this category.

Approximately 4% of pregnant women are affectedby gestational diabetes. (Mealey BL, RethmanMP.,2003)


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Clinical characteristics and manifestations of

diabetes

Clinical symptoms of diabetes include polyuria,polydypsia, weight loss and polyphagia.

(Loe H..1993, American Diabetes Association positionstatement,2007)

These symptoms are the direct result of hyperglycaemiaand the resultant osmotic imbalance.

The five major complications of diabetes are retinopathy(leading to blindness), nephropathy, neuropathy,macrovascular disease and altered wound healing,

which are the result of hyperglycaemia. (Mealey BL, Rethman MP.,2003, American Academy ofPeriodontology position paper,2000)


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Other oral manifestations of diabetes include: A burning sensation (burning mouth syndrome),

Fungal infection (candidiasis),

Dental caries and xerostomia(dry mouth) due to a

diminished saliva flow, increased saliva thicknessor medications.

Diabetic ketoacidosis is another serious acutemetabolic complication caused by a profound lack

of effective insulin. (American Academy of Periodontology positionpaper,2000, Stegeman CA.,2005)


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Inter-relationships and interactions between

periodontal diseases and diabetes mellitus

Effects of diabetes on periodontal health Prolonged exposure to hyperglycaemia is the

primary factor responsible for diabeticcomplications.

The biochemical basis for the mechanism ofdiabetic complications is the chemically irreversibleproduction of advanced glycation end products(AGEs).

AGEs are formed by the non-enzymatic glycation(addition of hexoses) to proteins or lipids underhyperglycaemic conditions.


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A pro-inflammatory state could occur when AGEs bindto AGE receptors on critical target cell surfaces.

Such proinflammatory cytokines include interleukin-1-(IL-1), tumour necrosis factor-(TNF-) andprostaglandin E (PGE2).

Accumulation of AGEs would also affect migration andphagocytic activity due to vascular occlusion resultingfrom the thickened endothelial basement membrane,which triggers an infection-mediated pathway ofcytokine upregulation, and further aggravates the

concentration of pro-inflammatory cytokines, resultingin destruction of connective tissue.

(Grossi SG, Genco RJ..1998, Mealey BL, Moritz AJ.,2000)


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Simultaneously, periodontal infection may induce achronic state of insulin resistance, contributing tothe cycle of hyperglycaemia and formation of AGEs,thus amplifying the pathways of degradation and

destruction of connective tissue.(Grossi SG, Genco RJ..1998) In 2001, Taylor conducted a comprehensive

Medline search for studies examining periodontaldiseases as a complication of diabetes and theeffect of periodontal therapy on glycaemic control.


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Forty-four of 48 reports (published since 1960)indicated that subjects with diabetes haveincreased prevalence, extent, severity orprogression (more frequent and advancedattachment or bone loss) of periodontal diseases.

Two surveys showed that diabetic individuals aretwice as likely to have severe attachment losscompared with individuals without diabetes.

(Grossi SG, Zambon JJ, Ho AW, et al.,1994, DolanTA, Gilbert GH, et al,1997)


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Cianciola et al. (1992) reported that Type 1 diabeticpatients have an increased risk of developingperiodontal diseases with age, and that the severityof periodontal diseases increases with the

increased duration of diabetes.

Deep pockets (4 mm) and gingival inflammationwere also found to be more common in diabetic

patients.


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Effects of periodontal infection on glycaemic

control

Several studies have shown that acute bacterialinfections can provoke insulin resistance innondiabetic individuals that may last for up to 3months after resolution of the infection.

(Sammalkorpi K.,1989, Sammalkorpi K, Koivisto VA,et al.,1989) Insulin resistance in such infections is

characterized by hyperglycaemia and

hyperinsulinaemia. Porphyromonas gingivalis is thought to play an

important role in periodontal diseases.


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A lipopolysaccharide (LPS) produced by P. gingivalisis a potent inducer of IL-1, TNF-and PGE2.

TNF-has been suggested as the mediator of

insulin resistance in infection, thus impairinginsulin action. (Mealey BL, Rethman MP.,2003)

Also, bacterial infections can decrease insulin

mediated glucose uptake by skeletal muscle andproduce whole-body insulin resistance.

(Grossi SG, Genco RJ.,1998)


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Based on Taylors review in 2001, there is evidencefrom numerous studies to support the concept thatperiodontal infection in severe periodontal diseaseshas an adverse effect on glycaemic control.

A longitudinal study of Pima Indians showed thatType 2 diabetic subjects with severe periodontaldiseases were six times as likely to have poor

glycaemic control after 2-year follow-up.(Taylor GW, Burt BA, Becker MP. et al.,1996)


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According to the American Diabetes Associationsrecommendation in 2005, the goal of maintaining awell-controlled HbA1c level for adults with diabetesshould be below 7%.(Mealey BL, Rethman MP.,2003)

One striking finding is that studies involving mechanicalperiodontal treatment alone reported improvedperiodontal status but no change in glycaemic control,(Taylor GW.,2001).

While studies involving adjunctive use of systemic

antibiotics (especially tetracycline and doxycycline) andmechanical periodontal treatment reported animprovement in both periodontal status and glycaemiccontrol.


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The putative mechanism is that doxycyclineinhibits the non-enzymatic glycation ofproteins via a nonanticollagenasemechanism, which then decreases the levelsof AGEs within the bloodstream.

(Taylor GW.,2001 Grossi SG.,2001 )


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Clinical implications and management in

treating periodontal patients with diabetes

Since periodontal diseases occur more frequently indiabetic patients with elevated blood glucose levels

than in non-diabetic patients, it is important toteach populations and patients to look for the

following signs and symptoms in order to preventperiodontal infections due to poor oralhygiene,such as: (Harmel AP, Mathur R,2004)

red, swollen and easily bleeding gums, which are

indicators for inflammation; dental plaque and calculus accumulation;

increased space between teeth, receding gums

and loose teeth; and

early loss of teeth due to gum disease.


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Useful preventive measures for diabetic

individuals

Maintain good control of blood glucose level; Clean teeth well at least twice daily and use

Dental floss frequently;

Visit a dentist regularly at least every 6 months;

Visit the dentist immediately if experiencingbleeding gums, any sores or swelling in the mouth.

(Harmel AP, Mathur R,2004)


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Recommendations for dental professionals who

treat diabetic individuals

Ensure the patient has consumed adequate foodbefore the dental procedures; if not, the risk ofhypoglycaemia is significant.

Procedures should be short, atraumatic and as

stress-free as possible. Early appointments areoften preferred because levels of endogenouscorticosteroids are generally higher at that timeand stressful procedures may be better tolerated.


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For many dental procedures, no change in insulin regimen isnecessary. Type 2 diabetic patients may reduce or omit oralhypoglycaemic medications on the day of the procedure,followed by a return to normal dosage the following day.

Antibiotics are not necessary for routine dental procedures indiabetic patients but may be considered in the presence ofovert oral infections due to lower host resistance and delayedwound healing.

The combination of mechanical debridement and systemicantibiotic use (such as tetracycline or doxycycline) mayprovide better glycaemic control in some diabetic patients.

(American Academy of Periodontology position paper,2000)


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Periodontal diseases and respiratory

diseases

Introduction Respiratory diseases cause significant morbidity

and mortality in the population, especially in thehospital environment.

Lower respiratory infection and chronic obstructivepulmonary disease were ranked as the third andsixth most common causes of mortality worldwidein 1990, causing 4.3 and 2.2million deaths,

respectively. (Murray CJ, Lopez AD.,1997)


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Definition, classification and clinical

characteristics of respiratory diseases

Respiratory infection can be divided into two majorcategories:

Community-acquired and

Hospital acquired types of bacterial pneumonia.

(Toews GB.,1986) Community-acquired pneumonia is typically

caused by bacteria that normally reside on the

oropharyngeal mucosa, such as Streptococcuspneumonia, Haemophilus influenza, Candidaalbicans and anaerobic species.


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Hospital-acquired pneumonia is usually caused bypathogens which are not normally resident in theoropharynx, but that enter this area from otherenvironments, including Gram negative bacilli,

Pseudomonas aeruginosa andStaphylococcusaureus.

(Scannapieco FA.,1999 ) Another severe respiratory disease affecting a

significant proportion of the elderly population isCOPD.

(Toews GB.,1986 Scannapieco FA.,1999 )


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This is characterized by chronic obstruction of air

flow through the airways or out of the lungs, withexcess production of sputum.

The obstruction is usually permanent andprogressive over time.

Chronic bronchitis and emphysema are the mostcommon forms of COPD.


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Risk factors of respiratory diseases

Cigarette smoking is by far the most commoncause of chronic bronchitis and emphysema.

Genetic predisposition (such as the presence of adefective 1-antitrypsin gene) and otherenvironment factors (including chronic exposure totoxic atmospheric pollutants, i.e. second-handsmoke) could also be risk factors for thedevelopment of respiratory diseases.

(Scannapieco FA.,1999 Sandford AJ, Joos L, ParePD.,2002)


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periodontal diseases and respiratory

diseases

Effects of periodontal diseases on respiratorydiseases

Lower respiratory infection begins bycontamination of the lower airway epithelium by

microorganisms contained in aerosol droplets or byaspiration of saliva containing bacteria.

A critical step is the colonization of oropharyngealmucosal surfaces by respiratory pathogens and theshedding of attached bacteria from these surfaces

into oral secretions that subsequently contaminatethe lower respiratory tree.

(Scannapieco FA., 1999)


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Teeth and periodontium may serve as a reservoirfor respiratory infection.

Dental plaque could be the important local sourceof these anaerobic bacteria that cause pneumonia

or other types of respiratory infection. Once bound to the host surface, the bacteria

multiply and colonize the upper respiratory airway.

These bacteria can be aspirated into the lower

airway to cause subsequent lower respiratoryinfection.

(Scannapieco FA, Wang B, Shiau HJ.,2001)


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Several mechanisms have been proposed to explainhow oral bacteria can participate in thepathogenesis of respiratory infection:

Oral pathogens (e.g. P. gingivalis, A.actinomycetemcomitans) may be aspirated into the

lung. Periodontal-disease-associated enzymes in saliva

may modify mucosal surfaces to promote adhesionand colonization by respiratory pathogens.

Periodontal-disease-associated enzymes maydestroy salivary pellicles, thus diminishing theprotection of non-specific host defence againstrespiratory pathogens.


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Cytokines (such as IL-1, IL-1, IL-6, IL-8 and TNF-)released from periodontal tissues may alter respiratoryepithelium and increase its susceptibility to colonizationby respiratory pathogens. Subsequent inflammatoryresponses also contribute to break down the pulmonary

tissues.(Scannapieco FA., 1999 Sandford AJ, Joos L, ParePD.,2002 Scannapieco FA, Wang B, Shiau HJ.,2001) Increased bacterial load of the dental plaque due to

poor oral hygiene may be a major risk factor forrespiratory diseases in elderly institutionalizedindividuals.


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Data from the National Health and NutritionExamination Survey I (NHANES I) of 23,808individuals were analysed.

Of these, 464 individuals reported a suspectedrespiratory infection. Patients who had the highest

oral hygiene index (OHI) values were 4.5 timesmore likely to have COPD than patients with an OHIof 0. (Scannapieco FA, Papandonatos GD, DunfordRG.,1998)

Although this study was crosssectional in design,the result is supported by a longitudinal studyperformed by Hayes et al. (1998)


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They defined patients with a history of periodontaldiseases as assessed by radiographic alveolar bone loss(ABL) and found that ABL at baseline is an independentrisk factor for COPD, and increased ABL is associatedwith increased risk for COPD.

Travis et al.(1994) described a biologically plausiblemechanism to explain the theoretical associationbetween emphysema and periodontal diseases.

Both diseases share very similar pathological processesthat are characterized by the recruitment of neutrophilsto inflammatory sites. Destruction of connective tissueis a common result in both diseases.


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Some studies have indicated that oral bacteria(such as P. gingivalis, A. actinomycetemcomitansand S. aureus) may enhance the risk of respiratorydiseases.

Other factors that inhibit the normal lung defence

systems and increase susceptibility to respiratoryinfections must be taken into consideration.

Currently, there is no direct, strong evidence for acausal relationship between periodontal diseases

and respiratory diseases. (Garcia RI, Nunn ME, Vokonas PS.,2001 PageRC.,2001)


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Effects of respiratory infection on periodontal

health

Regarding the impact of respiratory infection onperiodontal health, no studies to date haveindicated a direct or indirect association in thisrespect.


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treating periodontal patients with

respiratory diseases

As oropharyngeal bacterial colonizationplays a key role in the pathogenesis ofrespiratory diseases, it has beenhypothesized that improved oral hygiene in

the hospital setting may decrease the riskof respiratory infection. Several methods have been proposed to

reduce bacterial colonization in susceptible

individuals, such as patients withmechanical ventilation devices. (Scannapieco FA, Mylotte JM..1996)


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One of the methods, called selective digestivedecontamination (SDD), used topicaloropharyngeal antibiotics applied to the surfaces ofthe gastrointestinal tract (including the oral cavity)

to reduce the bacterial load and prevent respiratoryinfection.

However, SDD may foster the selection ofantibiotic-resistant pathogens.


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Methods of maintaining good oral hygiene inmechanically ventilated patients or nursing homeresidents (with or without periodontal diseases), ifas effective as SDD, may be much less expensive,

reduce the risk of developing antibiotic resistanceand reduce the use of antibiotics.


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Periodontal diseases and cardiovascular

diseases

Introduction CVD accounts for approximately 50% of deaths in the

USA each year and 29% of deaths worldwide; it ranks asthe second leading cause of death after infectious andparasitic disease. (Libby P, Geng YJ,et al,1997)

CVD is a large group of diseases that include congestiveheart failure, cardiac arrhythmias, coronary arterydisease [such as atherosclerosis, angina pectoris,myocardial infarction (MI)], Valvular heart disease andstroke.

Among these, atherosclerosis, which is a majorcomponent of CVD, affects one in four people andcontributes to 39% of deaths in the USA each year.

(American Heart Association.,2004)


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The characteristics of both periodontal diseasesand CVD are very similar; they are common, usuallychronic and multifactorial.

Since the 1980s, several epidemiological studies

have indicated that periodontal diseases may be animportant risk factor for coronary heart disease(CHD) and stroke.


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Definition, classification and clinical

characteristics of cardiovascular diseases

Among the cardiovascular disorders, CHD (such asischaemic heart disease due to atherosclerosis),stroke and Valvular heart disease (such as infectiveendocarditis) are more likely to be related toperiodontal diseases than other types of CVD.

Atherosclerosis is a major form of coronary arterydisease that is commonly referred to as ahardening of the blood vessels.

It is a condition in which atheromata (oratherosclerotic plaques) are deposited on theinnermost layer of walls of large- and medium-sized arteries.


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periodontal diseases and cardiovascular

diseases

Effects of periodontal infection on cardiovasculardiseases Several plausible mechanisms have been proposed to

explain the relationship between periodontal diseasesand CVD.

In general, the host response to a long-term systemicexposure to periodontal pathogens may play a centralrole.

The local inflammatory state in periodontal disease sitescould lead to systemic pro-atherogenic effects.

Periodontal patients with poor oral hygiene are at high

risk of frequent episodes of bacteraemia, whichincreases with increasing severity of gingivalinflammation. (American Academy of Periodontologyacademy report.,2002)


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Periodontal pathogens, release oflipopolysaccharide (LPS) and the resultantinflammatory response may systemically triggerseveral pro-inflammatory cytokines and tissue-

destructive mediators, such as C-reactive protein(CRP), TNF-, PGE2, IL-1and IL-6.

(Pussinen PJ, Mattila K.,2004)

These cytokines can recruit additional monocytesand T-lymphocytes to the lesion sites.

(Craig RG.,2004)


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The host inflammatory responses have both localand systemic manifestations.

Transient bacteraemia and endotoxaemiasecondary to periodontal infection may also affectatherogenesis indirectly by stimulating the normal

host responses. (Paquette DW.,2004) During episodes of dental bacteraemia, viridans

group streptococci encounter platelets.

Herzberg and Meyer(1996) used a rabbit model toshow that S. sanguis and P. gingivalis can induceplatelet aggregation through the expression ofplatelet aggregation-associated proteins.


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During infection or inflammation, alterations inlipoprotein metabolism could occur due to the acutephase response.

Pro-inflammatory cytokines may be pro-atherogenic,resulting in hypertriglyceridaemia, increased low-

density lipoprotein and decreased high-densitylipoprotein cholesterol.

The impacts of these events make vascular endotheliummore susceptible to injury. Since endothelialdysfunction or injury is an early event in atherogenesis,

this suggests the association between periodontal diseases and CVD. (Pussinen PJ,Mattila K.,2004)


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Mattila et al.(2004) first reported this associationbased on epidemiological data in a randomizedcontrolled study comparing 100 patients with acutemyocardial infarction (AMI) and 102 controls in the

community. Their results showed that poor oralhealth correlated positively with AMI.

A prospective cohort study by DeStefano etal.(1993) indicated that patients with periodontaldiseases had a 225% increased risk of CHD, and

that men with periodontal diseases under the ageof 50 years had a relative risk for CHD of 1.72.


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Arbes et al.(1999) investigated 5564 adults in acrosssectional study and found that the odds ratiofor self-reported history of heart attacks was 3.8among patients who had periodontal attachment

loss greater than 3mm at 67% or more of the sites. Wu et al.(2000) examined 9962 adults and

suggested a relative risk of 2.11 forcerebrovascular accidents among patients withperiodontal diseases and 1.41 among edentulous

patients.


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A recent systematic review by Scannapieco et al.(1998) accessed papers assessing the associationbetween periodontal diseases and atherosclerosis,MI, CVD and stroke from 1966 to 2002.

Conversely, several studies failed to show thispositive connection.

Joshipura et al. (1996) reported that, overall, noassociations were found between periodontaldiseases and CHD in a study of 44,119 US adultmales.


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Hujoel et al. ( 2002) looked at NHANES data for 636adults with pre-existing CVD and concluded thatgingivitis or periodontal diseases did not increasethe risk of CVD.

At present, although the majority of studies on thissubject support a positive association betweenperiodontal diseases and CVD, evidence is stillinsufficient to state that periodontal infection has acausal link to CVD.


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Effects of cardiovascular diseases on periodontal

health

Meurman et al.(2003) found poorer oral healthstatus in patients with CHD than in 250 controlswithout CHD. Serum inflammatory markers (CRPand fibrinogen concentrations) were significantly

higher in the CHD group. They suggested thatacute soft tissue inflammation, such as gingivitis,pericoronitis or remaining root tips, may contributemore to the cytokine levels than a single chronicpathology, such as periodontal diseases, which are

often low-grade subclinical inflammatoryprocesses. The CHD group also included a highproportion of hypertensive patients, and manyantihypertensive medications cause xerostomia,

which may increase oral mucosal inflammation and

l l l d


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cardiovascular diseases

Recent studies have indicated that endogenousadrenaline levels peak during morning hours, and mostsudden cardiac arrests occur between 8 a.m. and 11a.m. Therefore, late morning or early afternoonappointments are recommended.

Profound local anaesthesia is necessary to prevent therelease of large amounts of endogenous adrenaline inresponse to pain. Oral or inhalation sedation can beprovided if needed.

Only minimal treatment is advised within 6 months ofan MI, after consultation with the patients doctor.Selective dental treatment can be rendered 6 monthsafter an MI.


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Periodontal diseases and osteoporosis

Introduction Osteoporosis is the most common type of

metabolic bone disease, characterized bycompromised bone strength that predisposes an

individual to increased risk of fracture, with bonestrength determined by both bone density andbone quality.

As the population ages, an increasing number of

men and women are affected by this skeletaldisorder.

(Iqbal MM.,2000)


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Definition, clinical characteristics and

manifestations of osteoporosis

Osteoporosis has been described as thin bones orbrittle bones, and, at one time, the diagnosis ofosteoporosis relied on the occurrence of a low-trauma fracture.

In 1994, the World Health Organization (WHO)declared that the level of bone mineral density(BMD) should be used as a clinically applicable andconsistent measurement to define osteoporosis.

Since loss of bone mass itself does not cause anyobvious symptoms until fractures actually occur,osteoporosis is often viewed as a silent disease.


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There are some signs that may accompany thedevelopment of Osteoporosis.

(DAiuto F Parkar M Tonetti MS. 2007)These include:

Decreased height (due to collapsing vertebrae)

Back pain (typically in the lower thoracic and

lumbar areas)

Development of a curved upper back Fracture after a minimal trauma.


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Risk factors for osteoporosis have been studied extensively. Some of the risk factors are modifiable and others are not.

Age and gender are two major non-modifiable factors.

Older females are considered to be at high risk for thedevelopment of osteoporosis.

Modifiable risk factors, which affect the development ofosteoporosis to some extent, include :

smoking, alcohol, low intake of calcium or vitamin D

physical inactivity (lack of exercise)

medications (such as glucocorticoids) and certain diseases(such as hyperparathyroidism).

(Jeffcoat MK, Lewis CE, et al.,2000)


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Osteoporosis and periodontal diseases have severalrisk factors in common, such as increased diseaseprevalence with increased age, negative impacts ofsmoking on disease development and severity, andimpaired tissue healing as a result of the disease.


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periodontal diseases and osteoporosis

Effects of osteoporosis on periodontal health Several potential mechanisms by which

osteoporosis and periodontal diseases may beassociated have been proposed.

First, osteoporosis results in loss of BMDthroughout the body, including the maxilla and themandible.

The resulting low density in the jawbones leads toincreased alveolar porosity, altered trabecular

pattern and more rapid alveolar bone resorptionfollowing invasion by periodontal

pathogens.


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Second, systemic factors affecting boneremodelling may also modify the local tissueresponse to periodontal infection, such asincreased systemic release of IL-1 and IL-6.

Osteoporosis and clinical attachment level


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Osteoporosis and clinical attachment level,

alveolar crestal bone height loss, tooth loss and

mandibular bone density

Crosssectional studies, such as Wactawski-Wendeet al.(1996) and Tezal et al.(2000), reported thatseverity of osteoporosis or skeletal BMD is relatedto interproximal alveolar bone loss.

A 2-year longitudinal study by Payne et al(2000).

showed that both smoking and osteoporosis havenegative influences on alveolar bone.

A cross-sectional study by Hirai et al(1993).focused on the relationship between osteoporosisand the height of the mandibular residual ridge inelderly edentulous patients and found thatosteoporosis strongly affected the reduction of theresidual ridge


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Effects of periodontal infection on systemic bone

loss

Increased local production of cytokines associatedwith periodontal diseases could accelerate systemicbone resorption by modulating the host response.

Pro-inflammatory cytokine IL-6, produced byosteoblasts, may play a pivotal role in this potential

mechanism. (Reddy MS.,2001) Genetic factors that predispose an individual to

systemic bone loss may also predispose them toperiodontal destruction.

(Ershler WB, Keller ET.,2000) Among several factors that downregulate IL-6 gene

expression are oestrogen and testosterone.


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After menopause, IL-6 levels are elevated, even inthe absence of infection, trauma or stress.

The increased gene expression of IL-6 with agemay be the reason why both osteoporosis and

chronic periodontal diseases are age related. Certain lifestyle factors, such as smoking and low

calcium intake, may influence the risk ofdeveloping osteoporosis and periodontal diseases.

(Payne JB, Reinhardt RA, et al,2000)



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osteoporosis

There are some preventive measures that can andshould be taken earlier in life, especially duringadolescence, to stop or slow down bone loss.These include:

A diet rich in calcium and vitamin D

Exercise

No use of tobacco products

Careful use of medications, such as calcitonin,sodium fluoride, bisphosphonates or hormone-replacement therapy.


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Some studies have addressed the clinical andradiographic effects of bisphosphonates onperiodontal diseases.

Investigators have demonstrated a statisticallysignificant decrease of alveolar bone loss at 9

months after use of alendronate. Rocha et al.(2001) reported an improvement of

alveolar bone crest height favouring thealendronate group.

Takaishi et al.(2001) indicated that there wasclinical and radiographic improvement when abisphosphonate was used in combination withperiodontal treatment.


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Bisphosphonates used for the treatment ofosteoporosis may have a potential adjunctive effectin periodontal therapy.(Reddy MS, Geurs NC, et al.2003)

Additional studies are needed to establish if there

is a definite benefit of using bisphosphonates inperiodontal patients.

In most women, bone mass reaches its peak in thethird decade of life and declines thereafter.

Oestrogen deficiency seems to be a major factor inthe period of rapid bone loss, as oestrogen levelsdecline dramatically after menopause.


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Hormone replacement therapy after menopausehas been suggested to be protective against loss ofbone minerals.


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Conclusions

The focus of this non-systematic review was toexplore and clarify the inter-relationships andinteractions between periodontal diseases and fourcommon systemic diseases, na

Knowledge and information on the association

between periodontal diseases and systemicdiseases, as well as the biological effect of theseinflammatory and immunological mediators on acellular basis, may lead to interventions on thepharmacological and therapeutical regimens, which

will reduce the incidence, morbidity and mortalityof systemic diseases with infectious origins.

(Beck JD, Offenbacher S.,2001)


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Overall, further understanding of the links betweenperiodontal diseases and systemic diseases canraise societys awareness of the connectionsbetween oral health and inflammatory diseases.

This could lead to extensive general medical

benefits through periodontal treatment, such asimproving glycaemic control in diabetes patients,potentially reducing morbidity and mortality insusceptible individuals with respiratory diseases,improving endothelial function in CVD patients and

potentially reducing the risk of alveolar bone lossin osteoporosis patients.


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Therefore, dental professionals are encouraged toplay an active role in the public healthcare system,and prevention and treatment of periodontaldiseases should be an important initiative in thisrespect.

Associations Between Periodontal Diseases

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