effects of systemic diseases on periodontis. … · metabolic and endocrine disorders – glycogen...

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EFFECTS OF SYSTEMIC DISEASES ON PERIODONTIS. PERIODONTITIS AS A

MANIFESTATION OF SYSTEMIC DISEASES

Assoc. Prof. Theodora Bolyarova, MD

The current Classification of periodontal and peri-implant diseases and conditions (2018)

includes three main groups of diseases that have an impact on periodontal supporting tissues:

1.Systemic disorders that have a major impact on the loss of periodontal tissues by

influencing periodontal inflammation.

1.1. Genetic disorders

1. 1. 1.Diseases associated with immunologic disorders – Down syndrome, Leukocyte

adhesion deficiency syndromes, Papillon-Lefevre syndrome ect.

1.1. 2. Diseases affecting the oral mucosa and gingival tissue – Epidermolysis bullos,

Dystrophic epidermolysis bullosa ect.

1.1. 3. Diseases affecting the connective tissues – Ehlers-Danlos syndromes ect.

1.1. 4. Metabolic and endocrine disorders – Glycogen storage disease, Gaucher disease,

Hypophosphatasia ect.

1.2. Acquired immunodeficiency diseases – Acquired neutropenia, HIV infection.

1.3. Inflammatory diseases – Epidermolysis bullosa acquisita, Inflammatory bowel disease.

2.Other systemic disorders that influence the pathogenesis of periodontal diseases.

Diabetes mellitus (type 1), (type 2), Obesity, Osteoporosis, Arthritis (rheumatoid arthritis,

osteoarthritis), Emotional stress and depression, Smoking (nicotine dependence),

Medications.

3.Systemic disorders that can result in loss of periodontal tissues independent of

periodontitis.

3.1. Neoplasms

3. 2. Other disorders that may affect the periodontal tissues.

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Group III includes systemic diseases that can lead to loss of periodontal tissue, regardless of

periodontitis. These are neoplastic diseases that can affect the periodontal complex irrespective of

plaque-induced disease and such clinical findings should be classified on the basis of primary

systemic disease and should be placed in the category "Systemic diseases or conditions affecting

supporting tissues of periodontium".

Group I includes mainly rare diseases that affect periodontium (e.g., Papillon-Lefevre

Syndrome, Leucocyte adhesion deficiency, and Hypophosphatasia). Many of these diseases have

a major impact resulting in the early presentation of severe periodontitis. Such conditions are

defined as “Periodontitis as a Manifestation of Systemic Diseases”. Now this diagnosis is made

when systemic diseases are the main factor in the disease, and the role of local factors (plaque

and dental calculus) is not so significant. The Consensus Report for this contains a list of

systemic diseases in which periodontitis is a manifestation.

Periodontitis as a manifestation of systemic diseases

The Consensus Report for this portion of the workshop contains of list of systemic diseases in

which periodontitis is a manifestation.

Some are inborn defects such as the leukocyte adhesion deficiencies (LAD). Others are

acquired following exposure to pharmacological agents such as drug-induced granulocytopenia.

Positive confirmed history of a significant systemic condition results in the diagnosis of

periodontal manifestation of systemic disease. The major gene disease are associated with

prepubertal periodontitis. These syndromic disorders are characterized either by immune or

structural deficiencies.

Papillon-Lefevre (PLS) is relatively unique, in that periodontitis forms a significant

component of the disease along with hyperkeratosis of the palms of the hands and soles of the

feet. Prepubertal periodontitis is clinical diagnosis with genetically heterogeneous condition. In

some cases representing variant of PLS.

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Papillon-Lefevre syndrome. Severe generalized periodontitis in a 13-year-old boy.

Hyperkeratosis of the palms.

Hyperkeratosis of the soles.

(Laskaris, G., C. Scully. Periodontal Manifestations of Local and Systemic Diseases, 2003.)

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One hypothesis for PLS is: The gene mutated in PLS was mapped to a specific band on

the long arm of chromosome 11. Subsequently, this location was refined and a candidate gene

within this region was identified that encoded for the lysosomal protease cathepsin C: the CTSC

gene. Cathepsin C is a proteinase, which is found in neutrophils and lymphocytes as well as in

epithelial cells. Toomes et al. (1999) elucidated its genomic organization, demonstrated

mutations in the CTSC gene in eight families, and showed that these mutations result in an almost

complete loss of function of the enzyme. Periodontal lesions are due to multiple leukocyte

dysfunctions, and a specific bacterial infection of dental plaque origin (Aggregatibacter

actinomycetemcomitans). Periodontal involvment present always.

Leukemias which give excessive numbers of leukocytes and their precursors in the blood

and tissues also cause a greatly decrease of bone marrow function with concomitant anemia,

thrombocytopenia, neutropenia, and reduced range of specific immune cells which give some

characteristic periodontal features: anemic gingival pallor; gingival bleeding; gingival ulceration.

Leukemic features are further complicated by the potential for the proliferating leukocytes to

infiltrate the gingiva and result in gingival enlargement.

Cyclic neutropenia. Leukemic infiltrates.

(Lindhe, J. Clinical periodontology and implant dentistry. 4-th Edition, 2003.)

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Familial neutropenia. Fiery red oedematous gingivitis.


Cyclic neutropenia. Diffuse gingival erythema and oedema.


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Aplastic anaemia. Early necrotic ulceration on the upper gingiva.


Aplastic anaemia. Early necrotic ulceration on the upper gingiva.


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Acute myeloid leukemia (AML).


Hematologic disorders

The polymorphonuclear leukocyte (PMN cell) is undoubtedly crucial to the defense of the

periodontium. To exert this protective function several activities of PMNs must be integrated,

namely chemotaxis, phagocytosis, and killing or neutralization of the ingested organism or

substance. Individuals with either quantitative (neutropenia) or qualitative (chemotactic or

phagocytic) PMN deficiencies, exhibit severe destruction of the periodontal tissues. Quantitative

deficiencies are generally accompanied by destruction of the periodontium of all teeth, whereas

qualitative defects are often associated with localized destruction affecting only the periodontium

of certain teeth.

More severe cases affecting the primary dentition and leading to tooth exfoliation early in

life are usually interpreted as periodontal manifestations of systemic (hematologic) diseases, such

as leukocyte adhesion deficiency. Since patients with these diseases frequently lose teeth early in

life they often have extensive prosthetic needs with total protheses and with dental implants.

Treatment considerations of hematologic disorders/leukemia

Hemorrhagic gingival enlargement with or without necrosis is a common early

manifestation of acute leukemia. Patients with chronic leukemia may experience similar but less

severe periodontal changes. Chemotherapy or therapy associated with bone marrow

transplantation may also adversely affect the gingiva.

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Considerations for patients with hematologic disorders and periodontal disease should

include:

1. Coordination of treatment with the patient’s physician.

2. Minimization of sites of periodontal infection by means of appropriate periodontal

therapy prior to the treatment of leukemia and/or transplantation.

3. Avoidance of elective periodontal therapy during periods of exacerbation of the

malignancy or during active phases of chemotherapy.

4. Consideration of antimicrobial therapy for emergency periodontal treatment when

granulocyte counts are low.

5. Monitoring for evidence of host-versus-graft disease and of drug-induced gingival

overgrowth following bone marrow transplantation.

6. Periodontal therapy, including surgery, for patients with stable, chronic leukemia.

Group II includes systemic diseases that influence the pathogenesis of periodontal diseases.

There are common systemic diseases, such as uncontrolled diabetes which have various effects,

modifying course of periodontitis. They are part of the multifactorial nature of complex diseases

as periodontitis and are included in the new clinical classification of periodontitis as grading of

periodontitis.

Diabetes and smoking were cited as risk factors for periodontitis and the epidemiological

evidence for their association with periodontitis was dealt with.

Diabetes is an important modifying factor of periodontitis, and should be included in a

clinical diagnosis of periodontitis as a descriptor. According to the new classification of

periodontitis, the level of glycemic control in diabetes influences the grading of periodontitis.

It is well established that smoking has a major adverse effect on the periodontal

supporting tissues, increasing the risk of periodontitis by 2- to 5-fold. There are no unique

periodontal phenotypic features of periodontitis in smokers. On this basis smoking-associated

periodontitis is not a distinct disease. Nevertheless, tobacco smoking is an important modifying

factor of periodontitis, and should be included in a clinical diagnosis of periodontitis as a

descriptor. According to the new classification of periodontitis, the current level of tobacco use

influences the grading of periodontitis.

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Diabetes mellitus can be a significant modifier of all forms of periodontitis but there are

insufficient data to conclude that there is a specific diabetes mellitus-associated form of

periodontitis. For example, the presence of uncontrolled diabetes mellitus can alter the clinical

course and expression of chronic and aggressive forms of periodontitis. Similarly, the new

classification does not contain a separate disease category for the effects of cigarette smoking on

periodontitis. Smoking was considered to be a significant modifier of multiple forms of

periodontitis.

Diabetes and tobacco smoking have profound and far-reaching effects on the host,

including effects on the:

1. Physiological response

2. Vascular system

3. Inflammatory response

4. Immune system

5. Tissue repair.

They therefore have the potential to modify the:

1. Susceptibility to disease

2. Plaque microbiota

3. Clinical presentation of periodontal disease

4. Disease progression

5. Response to treatment.

Recent meta-analyses consistently show a statistically significant positive association

between obesity and periodontitis.

A recent systematic review concluded that postmenopausal women with osteoporosis or

osteopenia exhibit a modest but statistically significant greater loss of periodontal attachment

compared with women with normal bone mineral density.

A recent meta-analysis found a statistically significant positive association between

rheumatoid arthritis and periodontitis. There is some evidence that periodontitis may contribute to

the pathogenesis of rheumatoid arthritis.

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Diabetes mellitus (DM) is a complex disease with varying degrees of systemic and oral

complications, depending on the extent of metabolic control, presence of infection, and

underlying demographic variables.

DM is categorized as type 1 and type 2 DM. Type 1 DM develops due to impaired

production of insulin, while type 2 DM is caused by deficient utilization of insulin. Type 1 DM

results from destruction of the insulin-producing β cells of the pancreas.

Type 2 DM results from insulin resistance.

The complications of DM include retinopathy, nephropathy, neuropathy, macrovascular

disease, microvasculopathy and impaired wound healing. The treatment of DM is aimed at

reducing blood glucose levels to prevent such complications.

There is good evidence to support the concept that there is an association between poorly

controlled diabetes mellitus and periodontitis. Any differences in periodontal health between type

1 and type 2 DM patients may relate to differences in management of glycemic control, age,

duration of disease, utilization of dental care, periodontal disease susceptibility, and habits such

as smoking. Diabetics with more advanced systemic complications present with a greater

frequency and severity of periodontal disease. Periodontal attachment loss has been found to

occur more frequently in moderate and poorly controlled diabetic patients, of both type 1 and

type 2 DM, than in those under good control.

Initial phase periodontal treatment comprising motivation and debridement of periodontal

pockets in type 2 diabetic patients resulted in improved metabolic control of diabetes and

significant improvement in glycaemic control (Stewart et al. 2001). Total cholesterol,

triglyceride, and low density lipoprotein levels also decreased in the test group (with initial

periodontal treatment) and increased in the control group (without initial periodontal treatment).

The status of periodontal disease control can contribute to metabolic control of DM (Faria-

Almeida et al. 2006).

The most classic description of the undiagnosed or poorly controlled diabetic is the

patient presenting with multiple periodontal abscesses, leading to rapid destruction of periodontal

support. DM was a predisposing factor for periodontal and periapical abscess formation due to

suppression of neutrophil function (Ueta et al. 1993).

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A localized palatal periodontal abscess associated with a periodontal pocket in a 42-year-old

poorly controlled diabetic patient (Lindhe, 2009).

Influence of infection

The presence of infection seen in periodontal disease can predispose to insulin resistance

(Atkinson & Maclaren 1990). This can occur independently of a diabetic state and persist for up

to 3 weeks after resolution of the infection (Yki-Jarvinen et al. 1989). Reduced insulin dosage in

type 1 diabetics following periodontal treatment has also been reported (Sastrowijoto et al. 1990).

Significant inflammatory lesions in severe periodontal disease could contribute to exacerbation of

diabetes. Markers of inflammation common to diabetes and periodontal disease are an indication

of disease control (Soory 2002, 2004).

Hyperglycemia in uncontrolled diabetics has implications on the host response and affects

the regional microbiota (Gugliucci 2000). Capnocytophaga species have been isolated as the

predominant cultivable organisms from periodontal lesions in type 1 diabetics. A similar

distribution of the predominant putative pathogens, Prevotella intermedia, Campylobacter rectus,

Porphyromonas gingivalis, and Aggregatibacter actinomycetemcomitans, to those associated

with periodontal disease was detected in periodontal lesions of type 2 diabetics (Zambon et al.

1988).

Effects on the host response

Mechanisms underlying the accelerated periodontal disease associated with diabetes

appear to reflect primarily abnormal host responses, rather than microbial shifts, resulting from

diabetes.

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Page & Kornman (1997)

Diabetes mellitus is in group of Environmental and acquired risk factors. DM has far-

reaching effects on the host response.

Polymorphonuclear leukocytes

Reduced PMN function and defective chemotaxis in uncontrolled diabetics can contribute

to impaired host defenses and progression of infection. Crevicular fluid collagenase, beta-

glucuronidase and elastase activity, originating from PMNs, was found to be increased in poorly

controlled diabetic patients.

Chronic hyperglycemia results in non-enzymatic glycosylation of numerous proteins,

leading to the accumulation of advanced glycation end products (AGE), which play a central role

in diabetic complications (Brownlee 1994). Increased binding of AGEs to macrophages and

monocytes can result in a destructive cell phenotype with excessive release of cytokines. Diabetic

patients with periodontitis have significantly higher levels of interleukin (IL)-1β and

prostaglandin E2 (PGE2), TNF-α in crevicular fluid compared to non-diabetic controls with a

similar degree of periodontal disease.

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Connective tissue

A hyperglycemic environment, due to decreased production or utilization of insulin, can

reduce growth, proliferation, and matrix synthesis by gingival and periodontal ligament

fibroblasts and osteoblasts. Several oral and extraoral diabetes-induced collagen abnormallities

have been identified, including a large reduction in collagen synthesis and solubility in gingiva,

skin and bone.

Vascular changes, such as thickening of the capillary basement membrane in a

hyperglycemic environment, can impair oxygen diffusion, metabolic waste elimination, PMN

migration, and diffusion of antibodies. Binding of AGE to vascular endothelial cells can trigger

responses that induce coagulation, leading to vasoconstriction and microthrombus formation,

resulting in impaired perfusion of tissues.

Effects of diabetes mellitus on the host response.( Lindhe, 2009)

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Bacterial challenge in an environment of enhanced RAGE expression leads to

exaggerated inflammation and impaired repair. This in turn cause accelerated and severe

periodontal destruction. RAGE – receptor for advanced glycation end products.

(Lalla, E. & Papapanou, P. N. (2011) Diabetes mellitus and periodontitis: a tale of two common

interrelated diseases. Nat. Rev. Endocrinol.)

Effects on healing and treatment response

Wound healing is impaired due to the cumulative effects on cellular functions:

1. Decreased synthesis of collagen by fibroblasts

2. Increased degradation by collagenase

3. Glycosylation of existing collagen at wound margins

4. Defective remodeling and rapid degradation of newly synthesized, poorly cross-linked

collagen.

We present a patient 54-years old, with diabetes mellitus for more than 3 years, on oral

antidiabetics. We diagnosing periodontitis with PD up to 5 mm and periodontal pocket on tooth

15 with PD=5 mm, with purulent exudates, and periodontal pocket on tooth 16 with PD=6 mm.

Examination of preprandial Blood glucose level and Glycated hemoglobin.

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Clinical appearance in April 2016

Rö-gr of tooth15 – March 2016

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Rö-gr of tooth 15 – March 2013 г. Rö-gr of tooth 15 – March 2016 г.

Treatment: An endocrinologist is consulted. After changing the antidiabetic therapy and the

established control of diabetes, periodontal treatment was performed, including supragingival and

subgingival plaque and calculus removal of entire dentition, root planing of teeth 15 and 16.

The goal of systemic phase of periodontal treatment is: to eliminate or decrease the

influence of systemic conditions on the outcomes of therapy and to protect the patient and the

dental care providers against infectious hazards. Contact with a physician or specialist should

enable appropriate preventive measures to be taken, if necessary. All possible attempts should be

made to alleviate the effects of systemic diseases, such as blood disorders and diabetes mellitus,

as much as possible before definitive periodontal treatment is initiated.

Treatment considerations

Treatment considerations for patients with periodontitis associated with diabetes should include:

1. Identification of signs and symptoms of undiagnosed or poorly controlled diabetes

mellitus.

2. Consultation with the patient’s physician as necessary.

3. Consideration of diagnosis and duration of diabetes; level of glycemic control; and

medications and treatment history.

4. Recommendation that diabetic patients take medication as prescribed and maintain an

appropriate diet on the day of periodontal therapy.

5. Consideration of adjunctive systemic antibiotics for periodontal procedures if the

diabetes is poorly controlled.

6. Attempts to reduce stress/anxiety.

7. Preparation to diagnose and manage medical emergencies associated with diabetes.

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Good glycemic control is: HbA1c (glycated hemoglobin) of 6% to 7.0% and Preprandial

blood glucose: 3.9 to 7.2 mmol/L (70 to 130 mg/dl). Degree of glycemic control as measured by

the levels of HbA1c is:

Good (HbA1c ≤7)

Fair (HbA 1c = 7-8) and

Poor (HbA1c> 8). (American Diabetes Association (Jan, 2014)

When worsened glycemic control (glycated hemoglobin >9%, blood glucose over 8

mmol/L) there were no indications of periodontal treatment.

Palliative treatment of advanced periodontitis should not be undertaken for such patients.

Rather the involved teeth with repeated abscesses and pus formation should be extracted if

needed to accomplish infection control. However, diabetics may have angiopathic changes

associated with a lowered resistance to infection that requires consideration of using of antibiotics

following periodontal treatment or surgery.

The treatment of well controlled DM patients would be similar to that of non-diabetic

patients for most routine dental procedures. The short-term nonsurgical treatment response of

stable diabetics has been found to be similar to that of non-diabetic controls, with similar trends

in improved probing depths, attachment gain, and altered subgingival microbiota. A less

favorable treatment outcome may occur in long-term maintenance therapy of poorly controlled

diabetics, who may recur to initially deep pockets.

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Cigarette smoking

Cigarette smoke is a very complex mixture of substances with over 4000 known

constituents. These include carbon monoxide, hydrogen cyanide, reactive oxidizing radicals, a

high number of carcinogens, and the main psychoactive and addictive molecule – nicotine.

Many of these components could modify the host response in periodontitis.

Periodontal disease in smokers

The lingual aspects of the lower incisors showing gross supragingival calculus formation and

relatively little gingival inflammation in a female patient who has smoked 20 cigarettes per day

for over 20 years. (Richard Palmer and Mena Soory. Modifying Factors. in Jan Lindhe. Clinical

Periodontology and Implant Dentistry, 2008).

Early studies showed that smokers had higher levels of periodontitis, but they also had

poorer levels of oral hygiene and higher levels of calculus. Later studies which took account of

oral hygiene status and employed more sophisticated statistical analyses showed that smokers had

more disease regardless of oral hygiene. A large number of studies have established that in

comparing smokers and non-smokers with periodontitis, smokers have:

1. Deeper probing depths and a larger number of deep pockets.

2. More attachment loss including more gingival recession.

3. More alveolar bone loss.

4. More tooth loss.

5. Less gingivitis and less bleeding on probing.

6. More teeth with furcation involvement.

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Clinical appearance:

The finding of less gingival bleeding on probing is associated with less inflamed marginal

tissue and lower bleeding scores when probing the depth of the pockets. The typical clinical

appearance of the smoker‘s gingival tissue demonstrates relatively low levels of marginal

inflammation and a tendency to a more fibrotic appearance with little edema. Despite the clinical

appearance of the gingival tissue, the patient has deep pockets, advanced attachment loss, and

bone loss.

Effects of smoking on plaque bacteria

Smokers may have higher levels of plaque than nonsmokers, which may be accounted by

poorer levels of oral hygiene rather than higher rates of supragingival plaque growth. Several

studies have shown that smokers harbor more microbial species which are associated with

periodontitis than non-smokers, including P. gingivalis, A.actinomycetemcomitans, Tanerella

forsythia. Changes in the pocket environment secondary to the effect of smoking on the host

tissues could result in a different microflora in smokers.

Effects of smoking on the host response

The development of inflammation was very much retarded in the smoking group with less

sites exhibiting redness or bleeding on probing. The experimental studies also showed lower

amounts of gingival crevicular fluid (GCF) during the development of gingivitis. The reduced

bleeding has previously been proposed to be caused by nicotine-induced vasoconstriction, but

more recent evidence has failed to show a reduction in blood flow to the gingiva following

smoking a cigarette in regular smokers.

Histological comparisons of the lesions from smokers and non-smokers have shown fewer

blood vessels in the inflammatory lesions of smokers. Alterations in the expression of adhesion

molecules within the endothelium and within the inflammatory lesion. Smoking has a profound

effect on the immune and inflammatory system. Smokers have an increased number of

leukocytes in the systemic circulation, but fewer cells may migrate into the gingival

crevice/pocket. Studies in vitro have shown a direct inhibition of neutrophil and monocyte–

macrophage defensive functions by high concentrations of nicotine that may be achieved in

patients using smokeless tobacco. In patients group with refractory periodontitis, smokers are in

high proportion. It is proposed that smoking causes alterations to PMN function. There are

abnormal PMN phagocytosis associated with a high level of cigarette smoking.

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A potential destructive mechanism is the release of elastase from neutrophils. Within

tissues of smokers release more elastase compared to non-smokers. Levels of IL-1beta and IL-1ra

are significantly lower in GCF from diseased sites in smokers compared to nonsmokers.

Generation of oxygen radicals from stimulated neutrophils, is higher in neutrophils from

smokers, compared to neutrophils from non-smokers. Thus activation of periodontal neutrophils

is thought to contribute to the degradation of gingival tissues and the progression of inflammatory

periodontal disease.

The effects of smoking on lymphocyte function and antibody production are very

complex. Acute or chronic exposure to hydrocarbons may stimulate or inhibit the immune

response, the net effect being dependent upon the dose and duration of the exposure to

components of tobacco smoke. Smoking appears to affect both B and T cell function, inducing

functional unresponsiveness in T cells. It has been reported that serum IgG levels in smokers may

be reduced.

Effects of tobacco smoking on the host response. (Lindhe, 2009)

Effects on healing and treatment response

Tobacco smoke and nicotine undoubtedly affect the microvasculature, the fibroblasts and

connective tissue matrix, the bone and also the root surface itself. It has been shown in in vitro

studies that fibroblasts are affected by nicotine in that they demonstrate reduced proliferation,

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reduced migration and matrix production, and poor attachment to surfaces. Smoking has a direct

effect on bone and is an established risk factor in osteoporosis. It has also been proposed that it

may have a direct affect on bone loss in periodontitis. Tobacco smoking has been implicated in

poorer responses to periodontal surgical treatment.

Smoking cessation

Cigarette smoking constitutes the second most important risk factor in the pathogenesis of

periodontal diseases after poor oral hygiene standards.

Depending on the duration of the exposure to tobacco smoking, daily consumption, and

the patient’s periodontal status, smoking counseling has to be undertaken as one of the primary

measures. For smoking cessation during the initial phase of periodontal therapy motivational

techniques may be included or professional cessation programs may be the appropriate for heavy

smokers.

Medication

Many patients – over 90% over the age of 60 years regularly take medications for various

systemic conditions. Overgrowth of gingiva is a significant side effect which may be associated

with acceptance of:

• Anticonvulsant (e.g. phenytoin, sodium valproate, etc.)

• Immunosuppressant (e.g. cyclosporine A)

• Calcium channel blocking agents (e.g. nifedipine, verapamil, etc.). (Hassell & Hefti 1991;

Seymour et al. 1996; Seymour 2006)

Overgrowth of gingiva can be found in a periodontium with or without bone loss, it is not

always associated with attachment loss or tooth mortality. It does appear that the severity of the

lesion is affected by the oral hygiene of the patient.

One prominent theory of the etiology of phenytoin-associated gingival enlargements

suggests that the accumulation of genetically distinct populations of gingival fibroblasts results in

the accumulation of connective tissues resulting from reduced catabolism of the collagen

molecule.

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Gingival overgrowth induced by phenytoin.

(Rateitschak, 1985).

Calcium channel blockers may directly influence gingival connective tissues by

stimulating an increase of gingival fibroblasts as well as an increase in the production of the

connective tissue matrix. In our study (Dzhemileva, Bolyarova, 2000) involved 144 adult patients

on long-term therapy with three types of calcium channel blockers – nifedipine, verapamil,

diltiazem. With gingival overgrowth are 54,9% of all patients who were examined. All the

patients receiving the calcium antagonists and examined by us have chronic periodontitis by the

presence of periodontal pockets. The depth of the pockets promotes the retention of the dental

plaque, the inflammation, and possibly the proliferation of the tissue.

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A patient, 77 years with gingival enlargement.

Gingival overgrowth (GOI = 2) induced by Corinfar.

Hypotheses explaining why cyclosporine A affects the gingiva are diverse but a leading

theory suggests that the principal metabolite of cyclosporine A, hydroxycyclosporine (M-17), in

conjunction with the main compound, stimulates fibroblast proliferation. This increase in cell

number linked with a reduction in the breakdown of gingival connective tissues is the cause of

excessive extracellular matrix accumulation in cyclosporine A associated gingival enlargements.

Effects of hormonal status on periodontal tissues.

Alteration of circulating hormone levels may increase the severity of plaque-induced

gingival inflammation, but does not increase sensitivity to periodontitis.

Hormonal changes following menopause have been associated with osteoporosis, but

there is no evidence of an association of estrogen deficiency with increased susceptibility to

periodontitis.

effects of systemic diseases on periodontis. … · metabolic and endocrine disorders – glycogen...

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