1. INFLUENCE OF SYSTEMATIC DISEASES
ON PERIODONTIUM
By:
- Abdallah Abdelnabi Aref
- Huda Mohamed Hashem
- Musaab Mohammed Hassan
- Omar Essam Eldin Elsayed Shehab
- Ahmed Shaker Ahmed Taha
- Zeyad Khaled
2. • Clinical and basic science research over the past several decades has led to an
improved understanding of and appreciation for the complexity and pathogenesis of
periodontal diseases.
(Page RC, 1998)
• Many systemic diseases, disorders, and conditions have been implicated as risk
indicators or risk factors in periodontal disease.
• The individual host immune response to periodontal pathogens is very important
and likely explains many of the differences in disease severity observed from one
individual to the next.
3.
4.
5. A. Endocrine System and Periodontal diseases:
- Diabetes Mellites
- Female sex hormones
- Hyperparathyroidism
- Cortisol and Priodontitis
14. • the majority of well-controlled studies show a higher prevalence and severity of
periodontal disease in individuals with diabetes compared with nondiabetic persons
with similar local factors. (Campbell MJ, 1972) (Bernick SM,
1975)
• They show a greater loss of attachment, increased bleeding on probing, and increased
tooth mobility.
• Adults who are 45 years of age or older with poorly controlled diabetes (i.e., with a
glycated hemoglobin level >9%) were 2.9 times more likely to have severe
periodontitis than those without diabetes. The likelihood was even greater (4.6 times)
among smokers with poorly controlled diabetes.
(Centers for Disease Control and Prevention: National diabetes fact sheet: national
estimates and general information on diabetes and prediabetes in the United States, 2011,
Atlanta, GA, 2011, U.S. Department of Health and Human Services, Centers for Disease
Control and Prevention.)
15.
16. Diabetes mellitus does not cause gingivitis or periodontitis, but
evidence indicates that it alters the response of the periodontal
tissues to local factors, thereby hastening bone loss and
delaying postsurgical healing.
17. • Mechanism of Diabetic influence on Periodontium:
• 1. Bacterial Pathogens
• 2. Polymorphonuclear Leukocyte Function :
• 3. Altered Collagen Metabolism
(Newman and Carranza’s Clinical Periodontology 13th edition)
18. 1. Bacterial pathogens
• The increased glucose in the gingival fluid and blood of patients with diabetes could
change the environment of the microflora, thereby inducing qualitative changes in
bacteria that may contribute to the severity of periodontal disease observed in those
with poorly controlled diabetes.
19. • Periodontally healthy individuals but, with diabetes mellitus, are at risk for
periodontitis due to a decrease in the relative abundance and prevalence of species
compatible with health (such as Atopobium and Corynebacterium) and an increase
in the pathogenic content of the hyperglycemic microbiota
(including Porphyromonas, Prevotella, Campylobacter, and Fusobacterium)
(Ganesan SM et al., 2017) ( Long J et al., 2017)
• Some authors report evidence that type 2 diabetes mellitus reduces the diversity
and richness of the subgingival microbiome, and this decrease is even associated
with inadequate glycemic controls. (Longo PL et al., 2018) (Saeb ATM et al., 2019)
(Demmer RT et al., 2017)
20. • A consensus report from the American Academy of Periodontology and
the European Federation of Periodontology stated that there was no
compelling evidence that diabetes mellitus significantly impacted the
oral microbiota. This conclusion was based on several human studies
that reported inconsistent and contradictory findings on whether
diabetes mellitus altered the bacterial composition in the oral cavity.
(Chapple IL Genco R working working group 2 of the joint EFPAAPw. Diabetes
and periodontal diseases: consensus report of the Joint EFP/AAP Workshop on
Periodontitis and Systemic Diseases. J Periodontol. (2013) 84(4 Suppl):S106–12.
doi: 10.1902/jop.2013.1340011)
21.
22. 2. Polymorphonuclear Leukocyte (PML) Function :
Neutrophils act as first-line-of-defense cells and the reduction of their functional
activity contributes to the high susceptibility to and severity of infections in diabetes
mellitus.
23. • Studies show that the chemotactic activity of neutrophils from
diabetic patients is significantly lower than in cells from healthy
controls.
• Studies of the phagocytic and microbicidal activities of diabetic
patients reveal, with few exceptions, an impairment of these
functions. (Mowat A, Baum J, 1971) Decreased bactericidal activity (Tan JS
et al., 1975), impairment of phagocytosis and decreased release of
lysosomal enzymes (Bagdade JD et al., 1972), and reduced production of
reactive oxygen species (Nielson CP et al., 1989) by neutrophils of diabetic
patients have been described.
24. 3. Altered Collagen Metabolism:
• Chronic hyperglycemia impairs collagen structure and function, which may directly
impact the integrity of the periodontium.
• Chronic hyperglycemia adversely affects the synthesis, maturation, and
maintenance of collagen and extracellular matrix.
• In the hyperglycemic state, numerous proteins and matrix molecules undergo a
nonenzymatic glycosylation, thereby resulting in accumulated glycation end-
products (AGEs).
25. • The formation of AGEs occurs at normal glucose levels as well; however, in
hyperglycemic environments, AGE formation is excessive. Many types of molecules are
affected, including proteins, lipids, and carbohydrates.
• Collagen is cross-linked by AGE formation, which makes the collagen less soluble and
less likely to be normally repaired or replaced. Cellular migration through cross-linked
collagen is impeded, and, perhaps more importantly, tissue integrity is impaired as a
result of damaged collagen that remains in the tissues for longer periods (i.e., collagen
is not renewed at a normal rate)
• As a result, collagen in the tissues of patients with poorly controlled diabetes is older
and more susceptible to pathogenic breakdown (i.e., less resistant to destruction by
periodontal infections).
26.
27. • AGEs and receptors for AGEs (RAGEs) play a central role in the
classic complications of diabetes,34 and they may play a signiicant
role in the progression of periodontal disease as well. Poor glycemic
control, with the associated increase in AGEs, renders the periodontal
tissues more susceptible to destruction.
31. Parathyroid gland
• consists of four small glands, are paired and located
behind the thyroid gland in the neck.
• They produce and release parathyroid hormone
(PTH), which is involved in regulating the
metabolism of calcium and phosphorus.
32. • It plays an important role in tooth and bone
mineralization.
• Increases the bone resorption,
• Stimulates formation of active metabolite of
Vitamin D in the kidneys,
• promotes the intestinal absorption of calcium and
decreases renal reabsorption of phosphate.
33. • Hyperparathyroidism
• is characterized by hypersecretion of PTH.
• HPT occurs in three categories:
• primary secondary tertiary
• Primary Usually caused by a tumor (adenoma in 85% of
all cases) or hyperplasia of the gland that produces an
increase in PTH secretion resulting in hypercalcemia and
hypophosphatemia.
In primary HPT, about 50% of patients
have no symptoms and the problem is
picked up as an incidental finding (via
raised calcium or characteristic X-ray
appearances )
34. • Secondary
• Glands are stimulated to produce increased
amounts of hormones to
• correct abnormally low serum calcium levels
in different physiologic or pathologic
conditions like
Renal failure,
Intestinal malabsorption syndrome,
Decrease of Vitamin D production, lead to
parathyroid hyperplasia.
Tertiary
When long-standing secondary hyperplasia becomes autonomous in spite of correction of
the underlying stimulant (renal transplant).
35. • Main clinical manifestations of HPT
bone disease( The ribs, clavicles, pelvic girdle
and mandible )are the bones most involved.
A pathologic fracture may be the first symptom of
the disease.
Bone pain and joint stiffness may be present.
Renal calculi are a common finding in this
condition.
Almost all patients with HPT have skeletal
lesions in the advanced stages.
The loss of calcium in this condition results in
generalized osteoporosis
36. There is radiographic evidence of alveolar
osteoporosis with closely meshed trabeculae,
widening of the periodontal ligament space, absence
of the lamina dura, and radiolucent cyst like spaces .
The most common intraoral manifestations of
pHPT have been described as
loss of bone density in the maxillomandibular area
and brown tumor.
Periapical
radiograph of a
brown tumor in a
patient with
hyperparathyroidis
m
37. Bone cysts become filled with fibrous
tissue with abundant hemosiderin
laden macrophages and giant cells.
These cysts have been called brown
tumors. More accurately, they are
reparative giant cell granulomas.
In some cases, these lesions appear in
the periapical region of teeth, and they
can lead to a misdiagnosis of a lesion of
endodontic origin
Occlusal radiographic
view of the brown
tumor. Note the
expansion of the
lingual cortical plate
and the movement of
the premolar
38. IN HPT:
Increased osteoclasis with proliferation
of the connective tissue in the enlarged
marrow spaces, and the formation of
bone cysts and giant cell tumors.
The disease is called osteitis fibrosa
cystica or von Recklinghausen bone
disease.
Loss of the lamina dura and giant cell
tumors in the jaws are late signs of
hyper parathyroid bone disease.
•Fibrous replacement of
marrow, cysts in trabecular
bone that looks like “brown
tumors” (fibrosis and
organized hemorrage)
39. NOTE:
High levels of PTH cause a reduction of the
mandibular cortical bone, and its anabolic
effect, combined with biomechanical forces
of the oral cavity, allows the expansion of
the trabecular bone.
HPT could also be involved in the
development of periodontal disease.
Considering that poor oral hygiene and
insufficient professional dental care can
contribute to the development of periodontal
disease.
40. The presence of hyposalivation and
high calcium concentrations can
contribute to dental plaque
accumulation and gingival calculus
formation which lead to
periodontitis.
There is an association between
osteoporosis/osteopenia and risk of
periodontal attachment loss.
Secondary hyperparathyroidism in
a 35- year-old woman with
advanced kidney disease. This
periapical radiograph shows the
ground-glass appearance of the
bone and the loss of lamina dura
41. A possible association between
osteoporosis/osteopenia and periodontal disease
has been suggested.
Bone loss is a common feature of osteoporosis
and periodontal disease.
Both diseases share common etiologic factors,
such as smoking, nutritional deficiencies,
increasing age, corticosteroid use, and immune
dysfunction.
several studies that evaluated this association
used differing periodontal measures, including
clinical attachment loss (AL), loss of alveolar
crestal height (ACH), and tooth loss.
Studies have shown low BMD to be
independently and consistently associated with
loss of ACH and tooth loss.
42. So, if we dealing with
hyperparathyroidism, we are deal with
hyper calcemia
Classic sign and symptoms
Kidney stones, painful bones,
abdominal groans and psychiatric
moans
Brown tumors
genialized loss of lamina dura
Salt and pepper appearance
Elevated alkaline phosphate level
43. The clinical management of these patients
does not require any special consideration.
We should know that there is a higher risk
of bone fracture.
It is important to recognize the presence of
the brown tumor and to perform a correct
differential diagnosis so as not to conduct
an inadequate treatment.
The dentist plays important role in the
detection of HPT. Occasionally, the first sign
of the disease may be a cyst in the jaw.
46. PUBERTY
IS A COMPLEX PROCESS OF SEXUAL
MATURATION AND IT
IS RESPONSIBLE FOR CHANGES IN PHYSICAL
APPEARANCE AND BEHAVIOR THAT ARE
RELATED TO INCREASED LEVELS OF THE
STEROID SEX HORMONES, TESTOSTERONE IN
MALES, AND ESTRADIOL IN FEMALES
47. • Puberty gingivitis is characterized by
exaggerated response of the marginal and the
interdental papillae to plaque
• Clinically, Pronounced
inflammation, edema, and
gingival enlargement
48. • A peak prevalence of gingivitis has been determined at 12 years, 10 months in
females
• And 13 years, and 7 months in males
49.
50. • sex hormones alter microenvironment
along with the ability of certain species of
bacteria to capitalize on the higher
concentration of the hormones
A study showed that the severity of puberty
gingivitis was related more closely to plaque
build-up than to hormones. Tiainen et al.
The removal of local factors by oral hygiene
techniques was the key to the management
of hormone-related gingivitis, as it was
pointed. Oh et al.
51.
52. THE MENSTRUAL CYCLE AND
PERIODONTIUM
• The menstrual cycle is characterized by the
onset of increased production and secretion of
estrogen and progesterone in a cyclic pattern
coincident with the onset of puberty.
53. • Significant gingival inflammatory changes have
been documented and exaggarated by an
imbalance in sex hormones
• Women may complain of bleeding gums during
the days preceding menstrual flow, which
suggests that pre-existing gingivitis is
aggravated by menstruation.
• Inflammatory cytokines like (IL1β) levels were
also reported to have significant changes and
IL6 and TNF alpha may also contribute to the
inflammatory changes
54. • Klein (1934) reported a “gingivitis menstrualis”
• Mühlemann (1948) presented a “gingivitis inter-menstsrualis” which was
characterized by bright red hemorrhagic lesions of the interdental papilla
developed prior to the menstrual period.
55.
56. PREGNANCY
• Pregnant women are more prone to gingival inflammation due to:
• 1) significant endocrine alterations where both progesterone and
estrogen are remarkably elevated.
• 2) Alterations in the immune system so become more susceptible to
infections (e.g. periodontal infection)
57. PREGNANCY
• Pregnancy itself does not cause gingivitis.
• dental plaque is the primary cause of gingivitis, just similar to non
pregnant women.
• In absence of local factors, No changes occur in the gingiva
• The hormonal changes lead to changes in vascular permeability, which
leads to gingival edema and exaggerated inflammatory response.
58. Pregnancy gingivitis is extremely common
occurring in a range between 50 and 100%
of pregnant women.
Gingival inflammatory changes in
pregnancy usually begin during the 2nd
month and the severity of the disease
increases through the eight months
After which there is an abrupt decrease
related to a concomitant reduction in sex
steroid hormone secretion and generally
resolves following parturition.
59. • The subgingival microbiota may also
undergo changes, including an increase in
Prevotella intermedia
• Kornman and Loesche reported that 55-fold
of an increase in the proportion of P.
intermedia has been reported in pregnant
women compared to nonpregnant controls.
This increase appears to be associated with
elevations in systemic levels of estradiol and
progesterone
• There may also be a link between
periodontitis and adverse pregnancy
outcomes, including preterm delivery and
low birth weight babies
60. ORAL MANIFESTATIONS
• Marginal gingival enlargement
• The enlargement is usually generalized
• more prominent inter-proximally than on the
facial and lingual surfaces.
• The enlarged gingiva is bright red or magenta,
soft, and friable, and it has a smooth, shiny
surface.
• Spontaneous Bleeding or on slight
provocation.
61. PREGNANCY TUMOR
“PREGNANCY-ASSOCIATED PYOGENIC
GRANULOMA”
• Pinard first described this situation in 1877
• It is a localized gingival inflammatory condition in response to bacterial
plaque, It usually appears at the 2nd or 3rd month of pregnancy.
• It is hyperplastic, smooth surfaced mass that is either sessile or
pedunculated base extending from the gingival margin or, from the
interproximal tissues in the maxillary anterior region predominantly
• Clinically, it is painless, easily bleeding and may range in color from
purplish red to deep blue, although most commonly is red in color with
small fibrin spot.
• It is a superficial lesion that usually does not invade the underlying bone.
62.
63.
64. HORMONAL CONTRACEPTIVES
• Hormonal contraceptives show the exaggerated gingival response to local
factors (Plaque) similar to that seen during pregnancy.
• Women using contraceptives have poor periodontal and gingival health.
• The long-term use of oral contraceptives for more than 1.5 years may
cause gingivitis, gingival enlargement, attachment loss
65.
66. • Currently, there are new combination
of oral contraceptive formulations,
• if low plaque levels are established and
maintained during the period of
hormonal contraceptive usage, the
effects on the periodontium can be
minimized.
67.
68. MENOPAUSE
• Menopause usually begins between 45 and 55 years of age
• It is characterized by drop in estrogen levels
• Katz and Epstein suggested that conversion of androgens to estrogens might be
the main factor for protecting bone since estrogens have inhibitory effects on
osteoclastic functions.
• So, the most significant problem that develops during menopause is
osteoporosis.
69. • Oral manifestations are uncommon but,
• Menopause may be associated with important systemic and oral changes:
• 1)Osteoporosis affects jawbones, Reduction in bone density lead to
alveolar bone loss and progression of periodontal disease leading to tooth
loss
• 2) Reduction in epithelial keratinization and collagen formation in
connective tissue results in thinning of oral mucosa
• 3) Reduction in salivary flow and dryness of oral tissues
• If xerostomia is present, dental plaque may accumulate secondary to
reduced salivary function/flow, leading to caries and gingivitis
70. • Women may demonstrate menopausal gingivostomatitis
• clinical signs are:
1) drying of the oral tissues
2) abnormal paleness of the gingival tissues
3) bleeding on probing and brushing
4) Oral discomfort is also commonly reported by postmenopausal women with
burning sensation, xerostomia and bad taste
The signs and symptoms of postmenopausal gingivostomatitis are somewhat
comparable to those of chronic desquamative gingivitis.
72. ADRENAL GLAND HORMONES
• Glucocorticoids (e.g., cortisol).
• Mineralocorticoids (e.g.,
aldosterone).
• Adrenal androgen precursor
prohormones that are
converted in peripheral target
cells to become the sex
steroids.
76. IMMUNOSUPPRESSIVE EFFECT OF
CORTISOL
• Increased cortisol suppresses the immune response through
The suppression of neutrophil activity.
Decrease the production of lymphocytes.
Decrease immunoglobulin G production.
Decrease salivary IgA secretion.
80. • Periodontal examination (bleeding index, plaque index, probing depth and clinical
attachment loss)
• To assess stress in all patients, Depression, Anxiety, and Stress Scale-21 items (DASS-21)
was used.
• Salivary cortisol levels measured using ELISA kit.
81.
82.
83.
84. Conclusion
• Within the limits of the study, cortisol was associated with both periodontitis and
psychological stress. The levels of cortisol are higher in case of CP associated with stress
than in periodontitis or stress alone.
