influence_of_systamic_conditionn[1].pptx

1. Relationship between Periodontal
Disease and Systemic Heath
Dr. Samah Omer Musa
BDS,MSC,MD,MHPE

2. • There is clear evidence for a bacterial etiology
and there are specific bacteria (periodontal
pathogens) associated with destructive
periodontal disease, the presence of these
pathogens does not invariably cause disease

3. • The most significant advance in our
understanding of the pathogenesis of
periodontitis is that the host response varies
among individuals and that an altered,
deficient, or exaggerated host immune
response to bacterial pathogens may lead to
more severe forms of the disease.

4. • Furthermore, systemic diseases, disorders, and
conditions alter host tissues and physiology,
which may impair the host's immune defense
against periodontal pathogens, lead to
progression of destructive periodontal disease.
• Evidence also suggests that periodontal
infections can adversely affect systemic health

5. Influence of Systemic
Conditions

6. • Endocrine Disorders and
Hormonal Changes

7. 1/Diabetes Mellitus
• Characterized by chronic hyperglycemia.
• Diminished insulin production, impaired insulin action,
or a combination of both result in the inability of
glucose to be transported from the bloodstream
into the tissues, which in turn results in high blood
glucose levels and the excretion of sugar in the urine

8. • There are two major types of diabetes:
• a) Type 1 diabetes mellitus, (insulin-dependent
diabetes mellitus)
• b)Type 2 diabetes mellitus (non– insulin-
dependent diabetes mellitus)
• c)An additional category of diabetes is
hyperglycemia secondary to other diseases or
conditions, (Gstational diabetes associated with
pregnancy, Endocrine diseases, Tumors,
Pancreatectomy, and Drugs or chemicals that
cause altered insulin levels

9. • Symptoms associated with diabetic patients
polyphagia, polydipsia, polyuria, fatigue and
predisposition to infections.
• Periodontal disease is considered to be the sixth
complication of diabetes

10. Oral Manifestations
• (not always present, not specific, not
pathognomonic for diabetes)
• Cheilosis,
• Mucosal drying
• Cracking,
• Burning mouth and tongue,
• Diminished salivary flow,
• Alterations in the flora of the oral cavity, with
greater predominance of Candida albicans,

11. • Influence of diabetes on the periodontium
• Severe gingival inflammation
• Deep periodontal pockets, rapid bone loss ,
periodontitis
• Frequent periodontal abscesses
• loosened teeth

12.  Periodontitis in patients with type 1diabetes appears to
start after the age of 12 years, and it has fivefold
increased prevalence in teenagers.
 Patients who have had overt diabetes for more than 10
years have a greater loss of periodontal support than
those with a diabetic history of less than 10 years.
 Diabetes mellitus dose not cause gingivitis or
periodontitis ,but it alters the response of periodontal
tissue to local factors , hastening bone loss and delaying
postsurgical healing

13. • 1/Bacterial Pathogens
• The increased glucose in the gingival fluid and
blood of patients with diabetes could change
the environment of the micro-flora, thereby
inducing qualitative changes in bacteria.
Capnocytophaga, and Actinomyces species.
+ Black-pigmented species— especially
P. gingivalis, P. intermedia, and C. rectus

14. • 2/Polymorphonuclear Leukocyte Function
• The increased susceptibility of patients with
diabetes to infection can be due to-
PMN deficiencies that result in impaired
chemotaxis, defective phagocytosis, or impaired
adherence

15. • 3/Altered Collagen Metabolism
• 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 non-
enzymatic glycosylation, thereby resulting
in accumulated glycation end-products
(AGEs).

16. • The formation of AGEs occurs at normal
glucose levels as well; however, in
hyperglycemic environments, AGE formation
is excessive.
• Collagen is cross-linked by AGE formation,
which makes the collagen less soluble and less
likely to be normally repaired or replaced.

18. 2/Metabolic Syndrome
• Metabolic syndrome is a term used to describe
a condition of abdominal obesity combined
with two or more of the following metabolic
disturbances: hypertension, dyslipidemia, and
hyperglycemia.
Subjects who became overweight and obese
had a higher risk of developing periodontitis
when compared with those who did not gain
weight.

19. The association between periodontitis and metabolic
syndrome is thought to be the result of systemic
oxidative stress and an increased inflammatory
response.
It may be explained by common risk factors such as
obesity and obesity-related habits including diet,
exercise, and poor oral hygiene.
Obesity is associated with increased cytokine production
as well as T-cell and monocyte/macrophage
dysfunction,

20. 3/Female Sex Hormones
• 1/ Puberty is often accompanied by an
exaggerated response of the gingiva to plaque.
• 2/Menstruation During the menstrual period, the
prevalence of gingivitis increases.
• 3/ Hormonal contraceptives aggravate the
gingival response to local factors in a manner
similar to that seen during pregnancy; when these
drugs are taken for longer than 1.5 years, there is
an increase in periodontal destruction.

21. • 4/Pregnancy The hormonal changes of
pregnancy accentuate the gingival response to
plaque and modify the resultant clinical picture
 pregnancy it self does not cause gingivitis.
 No notable changes occur in the gingiva
during pregnancy in the absence of local
factors.
5/Menopause Menopausal gingivostomatitis
(chronic desquamative gingivitis)

22. • It has been suggested that the accentuation of
gingivitis during pregnancy has two peaks: during
the first trimester, when there is an over
production of gonadotropins, and during the third
trimester, when estrogen and progesterone levels
are highest.
P. intermedia appears to be the only
microorganism that increases significantly during
pregnancy.

23. The destruction of gingival mast cells by the
increased sex hormones and the resultant release
of histamine and proteolytic enzymes may
also contribute to the exaggerated inflammatory
response to local factors.
 A depression of the maternal T-lymphocyte
response may be a factor in the altered tissue
response to plaque

24. 4/Hyperparathyroidism
• Generalized demineralization of the skeleton.
• Increased osteoclasis with proliferation of the
connective tissue in the enlarged marrow
spaces.
• Formation of bone cysts and giant cell tumors.

25. • Oral changes:
• Malocclusion and tooth
mobility.
• Radiographic evidence of
alveolar osteoporosis with
closely meshed trabeculae ,
widening of the periodontal
ligament space, absence of
the lamina dura at late
stage

26. Hematologic Disorders
and Immune Deficiencies

27. 1/Leukocyte (Neutrophil) Disorders
• ***PMNs (i.e., neutrophils) particular play a
critical role in bacterial infections, because PMNs
are the first line of defense.
• Neutropenia
• Neutropenia is a blood disorder that results in low
levels of circulating neutrophils.
• It may be caused by diseases, medications,
chemicals, infections, idiopathic conditions, or
hereditary disorders.
• It affects as many as one in three patients who are
receiving chemotherapy for cancer.

28. • An absolute neutrophil count (ANC) of 1000
to 1500 cells/µL is diagnostic for mild
neutropenia.
• An ANC of 500 to 1000 cells/µL is considered
moderate neutropenia.
• An ANC of <500 cells/µL indicates a severe
neutropenia

29. • Agranulocytosis
• Agranulocytosis is a more severe neutropenia that
involves not only neutrophils but also basophils and
eosinophils.
• It is defined as an ANC of <100 cells/µL
• Oral signs :
• Gingival hemorrhage, necrosis, increased
salivation, and fetid odor are accompanying clinical
features.
• Also occurrence of generalized aggressive periodontitis
has been described.

30. 2/Leukemia
• leukemias are malignant neoplasias of WBC precursors.
• All leukemias tend to displace normal components of
the bone marrow elements with leukemic cells, thereby
resulting in the reduced production of normal RBCs,
WBCs, and platelets, which leads to anemia,
leukopenia (a reduction in the number of nonmalignant
WBCs), and thrombocytopenia.

31. • The Periodontium in Leukemic Patients:
• 1/Leukemic Infiltration
Leukemic cells can infiltrate the gingiva and, less
frequently, the alveolar bone , often results in leukemic
gingival enlargement.
• The highest incidence seen in patients with acute
monocytic leukemia.

32. The abnormal accumulation of leukemic cells
in the dermal and subcutaneous connective
tissue is called leukemia cutis (on the right
cheek).

33. Gingival enlargement in leukemic patient

34. • 2/ Bleeding:
• Bleeding gingiva can be an early sign of leukemia
even in the absence of clinically detectable
gingivitis.
• It is caused by the thrombocytopenia that results
from the replacement of bone marrow cells with
leukemic cells.
• Bleeding may also be a side effect of the
chemotherapeutic agents used to treat leukemia.

35. • 3/ Oral Ulceration and Infection:
• Granulocytopenia (diminished WBC count)
results from the displacement of normal bone
marrow cells by leukemic cells, which
increases the host susceptibility to
opportunistic microorganisms and leads to
ulcerations and infections.

36. 3/Anemia
• Anemia is a deficiency in the quantity or
quality of the blood as manifested by a
reduction in the number of erythrocytes and in
the amount of hemoglobin.
• Anemia may be the result of blood loss,
defective blood formation, or increased RBC
destruction.

37. • Anemias are classified according to cellular
morphology and hemoglobin content as follows:
(1) macrocytic hyperchromic anemia (pernicious
anemia).
• (2) microcytic hypochromic anemia (iron
deficiency anemia.
• (3) sickle cell anemia.
• (4) normocytic–normochromic anemia(hemolytic
or aplastic anemia).

38. • Oral manifestations :
• The tongue appears red, smooth, and shiny
• Marked pallor of the gingiva
• In iron deficiency anemia (Plummer–Vinson
syndrome) :A syndrome that consists of glossitis
and ulceration of the oral mucosa and oropharynx
and that induces dysphagia.
• Sickle cell anemia :Generalized osteoporosis of
the jaws with pallor and yellowish discoloration
of the oral mucosa, and great possibility for
periodontal infections .

39. • Oral manifestations :
 The tongue appears red, smooth,
and shiny.
• Marked pallor of the gingiva.
 Chronic iron deficiency anemia
(Plummer–Vinson syndrome) :
A syndrome that consists of
glossitis and ulceration of the oral
mucosa and oropharynx and that
induces dysphagia.
 Sickle cell anemia: Generalized
osteoporosis of the jaws with
pallor and yellowish discoloration
of the oral mucosa, and great
possibility for periodontal
infections . Glossitis

40. 4/Thrombocytopenia
• Is a term that is used to describe the condition
of a reduced platelet count that results from
either a lack of platelet production or an
increased loss of platelets.
• Thrombocytopenic purpura is characterized by
a low platelet count, a prolonged clot retraction
and bleeding time, and a normal or slightly
prolonged clotting time.

41. • Oral manifestaions :
• Petechiae and hemorrhagic
vesicles occur in the oral
cavity, particularly in the
palate, the tonsillar pillars,
and the buccal mucosa.
• The gingivae are swollen,
soft, and friable. Bleeding
occurs spontaneously or
with the slightest
provocation, and it is
difficult to control.
• Gingival changes represent
an abnormal response to
local irritation
Petechia
Ecchymosis

42. 5/Antibody Deficiency Disorders
• Agammaglobulinemia, is an immune
deficiency that results from inadequate
antibody production caused by a deficiency in
B cells.
• It can be congenital or acquired.
• Aggressive periodontitis is a common finding
in children who are diagnosed with
agammaglobulinemia

43. • Genetic Disorders

44. • Systemic conditions that are associated with or
that predispose an individual to periodontal
destruction include genetic disorders that
result in an inadequate number or reduced
function of circulating neutrophils

45. • 1/Chédiak–Higashi Syndrome
A rare disease that affects the production of
organelles found in almost every cell.
• 2/Lazy Leukocyte Syndrome
Characterized by susceptibility to severe
microbial infections, neutropenia, defective
chemotactic response by neutrophils, and an
abnormal inflammatory response.

46. • 3/Leukocyte adhesion deficiency (LAD)
• A rare genetic disorder, categorized as a primary
immunodeficiency that is most often diagnosed at birth.
• Many children with LAD do not survive.
• LAD results from an inability to produce or a failure to
normally express an important cell surface integrin
(CD18), which is necessary for leukocytes to adhere to
the vessel wall at the site of infection.
• Cases of periodontal disease that are attributed to LAD
begin during or immediately after the eruption of the
primary teeth.

47. • 4/Papillon–Lefèvre Syndrome
It is a very rare inherited condition that appears to
follow an autosomal-recessive pattern.
• Characterized by hyperkeratotic skin lesions,
severe destruction of the periodontium, and, in some
cases, calcification of the dura.
• 5/Down Syndrome (mongolism, trisomy 21)
• It is a congenital disease caused by a chromosomal
abnormality and is characterized by mental deficiency
and growth retardation.
• The prevalence of periodontal disease in patients with
Down syndrome is high, occurring in almost 100% of
patients who are younger than 30 years of age.

48. • 6/Hypophosphatasia:
is a rare familial skeletal disease that is
characterized by rickets, poor cranial bone
formation, craniostenosis, and the premature loss
of the primary teeth, particularly the incisors.
• Patients have a low level of serum alkaline
phosphatase, and phosphoethanolamine is present
in serum and urine.

49. • Stress and Psychosomatic Disorders

50. • Psychologic conditions, particularly stress,
have been implicated as risk indicators for
periodontal disease.
• The most notable example is the documented
relationship between stress and acute
necrotizing ulcerative gingivitis (ANG).

51. • 1/ Psychosocial Stress, Depression, and Coping:
• Stable lifestyles and minimal negative life events had less
periodontal disease destruction than individuals with less
stable lifestyles (e.g., unmarried, unemployed) and more
negative life events.
• The effect is not simply a matter of the presence or absence of
stress; rather, the type of stress and the ability of the individual
to cope with stress correlate with destructive periodontal
disease.
• Chronic stress and inadequate coping could lead to changes in
daily habits, such as poor oral hygiene, clenching, and
grinding, as well as physiologic changes such as decreased
saliva flow and suppressed immunity

52. • 2/Stress-Induced Immunosuppression:
•
Stress stimulate pituitary gland to release
adrenocorticotropic hormone which increase cortisol
production from the adrenal cortex.
• Increased cortisol suppresses the immune response
directly through the suppression of neutrophil activity,
immunoglobulin G production, and salivary IgA secretion.
• All of these immune responses are critical for the normal
immunoinflammatory response to periodontal pathogens.

53. • 3/ Psychiatric Influence of Self-Inflicted Injury
• Neurotic habits such as grinding or clenching the
teeth, nibbling on foreign objects (e.g., pencils,
pipes), nail biting, and excessive use of tobacco
are all potentially injurious to the teeth and the
periodontium.
• Self-inflicted gingival injuries, such as gingival
recession, have been described in both children
and adults

54. •
• Nutritional Influences

55. • 1. There are no nutritional deficiencies that by
themselves can cause gingivitis or periodontitis.
• Nutritional deficiencies can affect the condition of
the periodontium and thereby may accentuate the
effects of plaque-induced inflammation in
susceptible individuals.
• 2. There are nutritional deficiencies that produce
changes in the oral cavity.
• These alterations are considered to be the
periodontal and oral manifestations of nutritional
disease.

56. 1/Fat-Soluble Vitamin Deficiency
Vit A,D,and E
• Vitamin A Deficiency:
• A major function of vitamin A is to maintain
the health of the epithelial cells of the skin and
mucous membranes.
• Vitamin A may play an important role in
protecting against microbial invasion by
maintaining epithelial integrity.

57. • Vitamin D Deficiency:
Vitamin D or calciferol is essential for the absorption of
calcium from the gastrointestinal tract and for the
maintenance of the calcium–phosphorus balance.
• A deficiency of vitamin D and an imbalance in
calcium–phosphorus intake result in rickets in young
children and osteomalacia in adults.
• No studies have demonstrated a relationship between
vitamin D deficiency and periodontal disease, but in
young dogs it results in osteoporosis of alveolar bone.

58. • Vitamin E Deficiency
Vitamin E serves as an antioxidant to limit free-
radical reactions and to protect cells from lipid
peroxidation.
• No relationship has been demonstrated between
deficiencies in vitamin E and oral disease,
but systemic vitamin E may accelerate gingival
wound healing .

59. 2/Water-Soluble Vitamin Deficiency
Vitamins B and C
• B-Complex Deficiency:
• Oral disease is rarely caused by a deficiency in just one
component of the B-complex group; the deficiency is
generally multiple.
• The symptoms of riboflavin deficiency (ariboflavinosis)
and Niacin deficiency include glossitis, angular cheilitis.
• The most common finding in Niacin deficiency is
necrotizing ulcerative gingivitis, usually in areas of local
irritation.
• Folic acid deficiency results in macrocytic anemia with
megaloblastic erythropoiesis accompanied by oral changes,
gastrointestinal lesions, diarrhea, and intestinal
malabsorption.

60. • Vitamin C Deficiency
Severe vitamin C (ascorbic acid) deficiency in
humans results in scurvy, a disease that is
characterized by hemorrhagic diathesis and
delayed wound healing.
• Scurvy results in the defective formation and
maintenance of collagen, the impairment or
cessation of osteoid formation, and impaired
osteoblastic function.

61. Ascorbic acid may play a role in periodontal disease
through one or more of the following suggested
mechanisms:
 1. Low levels of ascorbic acid influence the
metabolism of collagen within the periodontium,
thereby affecting the ability of the tissue to regenerate
and repair itself.
 2. Ascorbic acid deficiency interferes with bone
formation and leads to the loss of periodontal bone.
 3.Optimal levels of vitamin C would maintain the
epithelium's barrier function to bacterial products.

62. 4. Increasing levels of ascorbic acid enhance the
chemotactic and migratory actions of leukocytes.
5.An optimal level of ascorbic acid is apparently
required to maintain the integrity of the
periodontal microvasculature as well as the
vascular response to bacterial plaque and
wound healing.
6. Depletion of vitamin C may interfere with the
ecologic equilibrium of bacteria in plaque and
thus increase its pathogenicity.

63. •
• Medications

64. • Some medications may have adverse effects on
periodontal tissues, wound healing, or the host
immune response.
• For example :
• Bisphosphonates and Corticosteroids

65. 1/ Bisphosphonates
• Bisphosphonates have a high affinity for
hydroxyapatite. They are rapidly absorbed in bone
• They act by inhibiting osteoclastic activity, which
leads to less bone resorption, less bone
remodeling, and less bone turnover.
• Primarily used to treat cancer (intravenous [IV]
administration) and osteoporosis (oral
administration).

66. • The use of bisphosphonates in cancer treatment is
aimed at preventing the often lethal imbalance of
osteoclastic activity.
• During the treatment of osteoporosis, the goal is
simply to harness osteoclastic activity to
minimize or prevent bone loss and , to increase
bone mass by creating an advantage for
osteoblastic activity.

67. • Bisphosphonates may contribute to ONJ via
acting on oral keratinocytes to impair wound
healing by inhibiting epithelial migration and
wound closure.
• Osteonecrosis of the jaw (ONJ), a serious
condition that is characterized by non-healing and
often painful exposure of non-vital and often
sequestrating bone in the jaws

68. • Necrotic bone exposure of the
jaw (ONJ) is a condition with
multiple possible etiopathogenic
factors, including systemic
medications, radiation, infection,
trauma, direct chemical toxicity,
and other idiopathic
mechanisms; clinicians should
carefully consider all factors
before making a diagnosis of
bisphosphonate-related ONJ
(BRONJ)

69. The condition of BRONJ has been defined as
the exposure and necrosis of portions of the
jaw bone in patients who have been exposed to
bisphosphonates that has persisted for longer
than 8 weeks with no history of radiation
therapy to the jaws.

70. 2/Corticosteroids
• In humans, the systemic administration of cortisone and
adrenocorticotropic hormone appears to have no effect on the
incidence or severity of gingival and periodontal disease.
• While systemic administration of cortisone in experimental
animals resulted in the osteoporosis of alveolar bone.
• Stress increases circulating endogenous cortisol levels through
stimulation of the adrenal glands. This increased exposure to
endogenous cortisol may have adverse effects on the
periodontium by diminishing the immune response to
periodontal bacteria.

71. • Congenital Heart Disease

72. Clinical Features
• 1/Cyanosis caused by the shunting of deoxygenated
blood from the right to the left, which results in the
return of poorly oxygenated blood to the systemic
circulation.
• 2/Polycythemia (i.e., an increase in RBCs and
hemoglobin).
• 3/Clubbing edema of toes and fingers .
• 4/At risk for infective endocarditis.

73. • 5/ Oral signs :
 Obvious cyanosis of the lips and the oral mucosa.
 Delayed eruption of both primary and permanent dentitions.
 Increased positional abnormalities, and enamel hypoplasia.
 The teeth often have a bluish-white appearance with an
increased pulp vascular volume.
 Reports seem to indicate more severe caries and periodontal
disease
*However, the apparent increase in dental disease may be
attributed to poor oral hygiene and a general lack of dental
care rather than a disease-related etiology

74. • Metal Intoxication

75. • The ingestion of metals such as mercury, lead,
and bismuth in medicinal compounds and
through industrial contact may result in
oral manifestations caused by either
intoxication or absorption without evidence of
toxicity

76. Conclusion
• Genetic, environmental, physical, and
psychosocial factors have the potential to alter
periodontal tissues and the host immune response,
thereby resulting in more severe periodontal
disease.
• Systemic diseases, disorders, or conditions
themselves do not cause periodontitis; rather, they
may predispose, accelerate, or otherwise increase
disease progression.

77. Good luck