Systemic diseases, or conditions themselves do not cause periodontitis but alter host tissues to increase the progression of periodontal disease. Systemic diseases and conditions can influence the course of periodontitis or affect the periodontal supporting tissues independent of the presence of dental plaque. Most commonly affecting diseases are diabetes, neoplasms.

1. Influence of Systemic Conditions
on the Periodontium
Dr.Oinam Monica Devi

2. INDEX
 Introduction
Endocrine Disorders
& Hormonal Changes
1. Diabetes Mellitus
2. Female Sex
Hormones
3. Hyperparathyroid
ism
Hematologic Disorders
& Immune Deficiencies
1. Leukemia
2. Anemia
3. Thrombocytopenia
4. Antibody
Deficiency
Disorders
5. Leukocyte
(Neutrophil)
Disorders
Genetic Disorders
1. Chédiak-Higashi
Syndrome
2. Lazy Leukocyte
Syndrome
3. Leukocyte
Adhesion
Deficiency
4. Papillon-Lefèvre
Syndrome
5. Down Syndrome

3.  Conclusion
 References
Stress & Psychosomtic
Disorders
1. Psychosocial Stress,
Depression, and
Coping
2. Stress-Induced
Immunosuppression
3. Influence of Stress
on Periodontal
Therapy
4. Outcomes
5. Psychiatric
Influence of Self-
Inflicted Injury
Nutritional Influences
1. Fat-Soluble
Vitamin Deficiency
2. Water-Soluble
Vitamin Deficiency
3. Protein Deficiency
Other Systemic
Conditions
1. Osteoporosis
2. Congenital Heart
Disease
3. Hypophosphatasia
4. Metal Intoxication
Medications
1. Bisphosphonates
2. Corticosteroids

4. INTRODUCTION
 Systemic diseases, or conditions themselves do not cause
periodontitis.
 Systemic diseases alter host tissues & physiology & predispose,
accelerate or increase the progression of periodontal disease.
 A variety of systemic diseases and conditions can affect the course of
periodontitis or have a negative impact on the periodontal attachment
apparatus.

5.  There are many diseases and conditions that can affect the periodontal
tissues either by
1) Influencing the course of periodontitis
2) Affecting the periodontal supporting tissues independently of dental
plaque biofilm-induced inflammation.
 These include:
1a. Mainly rare diseases that affect the course of periodontitis
 eg., Papillon Lefevre Syndrome, leucocyte adhesion deficiency, and
hypophosphatasia
 They have major impact resulting in the early presentation of severe
periodontitis.

6. 1b. Mainly common diseases and conditions that affect the course of
periodontitis
 e.g., diabetes mellitus
 The magnitude of the effect of these diseases and conditions on the
course of periodontitis varies .
 They result in increased occurrence and severity of periodontitis.
 It is as an important modifying factor rather than as a distinct disease.
2. Mainly rare conditions affecting the periodontal supporting tissues
independently of dental plaque biofilm induced inflammation
 e.g., Squamous cell carcinoma, Langerhans cell histiocytosis
 This is a more heterogeneous group of conditions which result in
breakdown of periodontal tissues .
 Some of the conditions may mimic the clinical presentation of
periodontitis.

7. Classificationofsystemicdiseasesandconditionsthataffecttheperiodontalsupporting
tissues( Jepsenetal,2018)

10. Diabetes Mellitus
 Complex metabolic disease characterized by chronic persistant
hyperglycemia
 Diminished insulin production and/or impaired insulin action
 Altered fat and protein metabolism
 In 2008, the American Diabetes Association (ADA) defined Periodontal
disease as a 6th complication of Diabetes.
 In 2018, ADA has included Periodontal disease as a comorbidity of
Diabetes.

11. chronic inflammatory response
 Periodontitis : symbiotic dysbiotic microbiome
 Diabetes pathogenesis : insulin underexpression / expression tolerance
 Periodontitis & Diabetes overlap by way of inflammation:
1. Diabetes may result in general impaired inflammatory and immune
responses as well as impaired healing.
2. Periodontitis is characterized by an unbalanced inflammatory and
immune response to the dysbiotic flora.
Periodontitis & Diabetes-possible mechanism of
comorbidity

12. Tonettietal,2018

13. Classification Of Diabetes Mellitus
Diabetes can be classified into the following general categories:
1. Type 1 Diabetes : due to autoimmune β-cell destruction
2. Type 2 Diabetes : due to progressive loss of β-cell insulin secretion
3. Gestational diabetes mellitus: diabetes diagnosed in the second or third
trimester of pregnancy that was not clear diabetes prior to gestation.
4. Specific types of diabetes due to other causes :
I. Monogenic diabetes syndromes ( neonatal diabetes & maturity-onset
diabetes of the young)
II. Diseases of the exocrine pancreas ( cystic fibrosis & pancreatitis)
III. Drug-or chemical-induced diabetes (such as with glucocorticoid use,
in the treatment of HIV/ AIDS, or after organ transplantation)
American Diabetes Association. 2. Classification and Diagnosis of Diabetes:
Standards of Medical Care in Diabetes-2020. Diabetes Care. 2020 ; 43 (1): S14 -31.

14. Staging ofType 1 Diabetes
American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in
Diabetes-2020. Diabetes Care. 2020 ; 43 (1): S14 -31.

15. Criteria for the diagnosis of Diabetes
American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in
Diabetes-2020. Diabetes Care. 2020 ; 43 (1): S14 -31.

16. Criteria fordefining Prediabetes
“Prediabetes” is a term used for individuals whose glucose levels do not
meet the criteria for diabetes but are too high to be considered normal.
American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-
2020. Diabetes Care. 2020 ; 43 (1): S14 -31.

17. Risk based screening fortype 2 diabetes or prediabetes in
asymtomatic children and adolescents in a clinical setting
American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-
2020. Diabetes Care. 2020 ; 43 (1): S14 -31.

18. Screening forand diagnosis of Gestational Diabetes Mellitus
American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-
2020. Diabetes Care. 2020 ; 43 (1): S14 -31.

20. Periodontal condition in patients with Diabetes Carranza, 13th ed SA

21. Fig:Glucose oxidation
and induced-oxidative
stress in hyperglycemic
conditions.
Ighodaro OM. Molecular pathways
associated with oxidative stress in diabetes
mellitus. Biomed Pharmacother 2018
;108:656-62.

22. Diabetes mellitus does not cause gingivitis or
periodontitis, but it :
A. Alters the response of the periodontal tissues to local
factor
B. Increased susceptibility to infections
C. Hasten bone loss
D. Delaying postsurgical healing

23. Important Studies
Llambés F, Arias-Herrera S, Caffesse R. Relationship between diabetes and periodontal infection.
World J Diabetes 2015; 6(7): 927-95
Knowler et al,1978 –
Approximately 40% of adult Pima Indians in Arizona have type 2 diabetes.
Risk of developing destructive periodontitis increases three fold in diabetic
individuals.
Llambés F et al, 2015
Periodontal treatment can be successful in diabetic patients, but more
recurrence of periodontal disease can be expected in non well controlled
diabetic individuals. HbA1c reduction after periodontal treatment is usually
less than 0.5%.

24. Periodontal disease & diabetes mellitus A two-way relationship
(Grossi et al,1998)

25. Potential mechanisms which link exacerbation of periodontitis with
uncontrolled diabetes

26. Effect of diabetes on the oral microbial flora
In 1989, Sastrowijoto et al examined A.actinomycetemcomitans,
black‐pigmented Bacteroides species, & Capnocytophaga species using culture
techniques of type 1 diabetes patients with near‐normal metabolic control
(HbA1c ≤ 7.7%) vs poor metabolic control (HbA1c ≥ 9.9%).
1. The study did not find a difference between the profile of the tested
microbes.
2. Periodontal diagnosis was overestimated as the sole criteria for diagnosis
was a pocket of 4 mm or more with BOP.
3. The tested microbes are not considered as key pathogens for chronic
periodontitis.
Most of the studies indicate that poor glycemic control has an impact on the
periodontal microbiota.
Studies also shows elevated numbers of periodontal pathogens in subjects with diabetes
and poor glycemic control.

27. Effect of diabetes on the inflammatory burden
in the periodontal tissues
Studies have shown an increased gingival crevicular fluid levels of tumor
necrosis factor‐alpha, interleukin‐6, and interleukin‐1beta in diabetes.
Hyperglycemic state can lead to increased expression of innate immunity
receptors such as toll‐like receptor‐2 and toll‐like receptor‐4.
1. Cytokines
2.Adipokines
Kardesler et al, found little difference in serum adiponectin and leptin
levels between subjects with periodontitis with well‐controlled and poorly
controlled diabetes.

28. 3. Hyperglycemia, Advanced glycation end products ( AGEs)
, and receptor for advanced glycation end products ( RAGEs)
AGEs are forrmed by nonenzymatic reaction of glucose & other
glycating compounds
Derived from the
1. Intracellular auto-oxidation of glucose to glyoxal
2. Decomposition of the amadori product
3. Fragmentation of glyceraldehade-3- phosphate &
dihydroxyacetone phosphate to methylglyoxal
Reactive intracellular dicarbonyls react with the amino groups
of intracellular and extracellular proteins to form AGEs.

29. AGEs form at normal glucose levels also
AGE formation is excessive in hyperglycemic environments
Accumulate in plasma ,tissues & gingiva of diabetic patients
Intracellular proteins & extracellular matrix components ,
modified by AGEs exhibit altered function

30. Receptor for advanced glycation end products (RAGE)
 Multiligand signaling receptor
 Member of the immunoglobulin superfamily of cell-surface
molecules
 Found on the surface :
1. Smooth muscle cells
2. Endothelial cells
3. Neurons
4. Monocytes
5. Macrophage

31. Polak D, Sanui T, Nishimura F, Shapira L. Diabetes as a risk factor for periodontal disease—plausible
mechanisms. Periodontol2000. 2020 ;83(1):46-58.

32. Llambés F, Arias-Herrera S, Caffesse R. Relationship between diabetes and periodontal
infection. World J Diabetes 2015; 6(7): 927-35

33. Altered Collagen Metabolism
Chronic
hyperglycemia
impairs collagen
structure (cross-
linking) &
function, which
affect the
integrity of the
periodontium
Decreased
collagen
synthesis,
osteoporosis,
reduction in
alveolar bone
height has been
demonstrated in
diabetic animals
Cross-linked
matrix
components
accumulate in
diabetic vessel
walls, lead to,
hardening of
arteries &
narrowing of
vascular lumina
Chronic
stimulus for this
matrix
proliferation are
growth factors
such as TNF- α,
IL-1, and
platelet-derived
growth factor
(PDGF)

34. 4. Bone Homeostasis
 Santos et al studied in their found that the total amounts of GCF’s
soluble RANKL & RANKL/osteoprotegerin ratios were higher in
subjects with poorly controlled diabetes than in subjects with
well‐controlled diabetes.
 Animal models generally indicate that osteoclast activity is increased
in diabetic animals.

35. 5.MicroRNAs
 Group of small, noncoding RNAs that regulate target gene
expression via post‐transcriptional regulation.
 They may have a biological role in the comorbidity
between periodontitis and diabetes by mechanisms :
(a) MicroRNAs have been shown to have immunomodulatory
properties.
(b) Several microRNAs have been reported to be involved in the
regulation of RANKL expression in various cell types.
(c) MicroRNAs were found to impact the AGEs/ RAGEs pathway.

36. Biological plausibility of the effect of treatment (controlling) of
diabetes on periodontitis
 The effects of diabetes treatment on periodontal tissues are
limited, periodontal disease will only improve with diabetes
treatment accompanied by periodontal treatment.
 Controlling diabetes will reduce the effect of the disease on the
inflammatory response and bone metabolism, & prevent the
progress & the recurrence of periodontitis.

37. Potential mechanisms which enable periodontal intervention to affect
diabetes control in diabetes patients with periodontitis
Polak D, Shapira L. An update on the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J
Clin Periodontol. 2018 ;45(2):150-66.

38. Effect of prediabetes on periodontitis
 In 2015, Demmer et al examined changes in oral microbiome in
diabetes‐free adults vs subjects with prediabetes. Their study found a
higher prevalence of A actinomycetemcomitans, P gingivalis, T
denticola, T forsythia,& A naeslundii in subjects with prediabetes.
 Limited available data regarding prediabetes and periodontitis to
indicate that a comorbidity between periodontitis and metabolic
“abnormalities” may even exist prior to the clinical diagnosis of
diabetes.

39. Wound Healing is Affected as cumulative
effect of:
1. Altered cellular activity
2. Decreased collagen synthesis
3. Glycosylation of existing collagen
4. Increase collagenase production readily degrade newly
synthesized, less completely cross linked collagen
5. Reduced Collagen solubility
6. Delayed remodelling of wound site.

40. FEMALE SEX HORMONES

41. Hormonal changes in the
female
Gingival alterations
During puberty
&pregnancy
Nonspecific
inflammatory reactions
Predominant vascular
component
Marked hemorrhagic
tendency.
Oral changes during
menopause
Thinning of the oral
mucosa, gingival
recession, xerostomia,
altered taste, and burning
mouth
Puberty,
Pregnancy, &
Menopause

42. Anand V, Gulati M, Anand B, Singh A, Daing A. Influence of Hormones in Periodontium – A review.
International Journal Of Research In Dentistry.2011;1(2):1-14.

43. Anand V, Gulati M, Anand B, Singh A, Daing A. Influence of Hormones in Periodontium –
A review. International Journal Of Research In Dentistry.2011;1(2):1-14.

44. I. GINGIVAIN PUBERTY
Raised levels of
testosterone in
males & estradiol
in females.
An exaggerated
response of the
gingiva to local
factors .
Pronounced
inflammation,
bluish-red
discoloration,
edema, &
enlargement
P. intermedia
substitute
progesterone and
estrogen for
menadione (vitamin
K) as an essential
nutrient
An association between pubertal
gingivitis, P. intermedia and serum
levels of testosterone, estrogen,
and progesterone has been
reported in a longitudinal study.
As adulthood is
approached, the
severity of the gingival
reaction diminishes,
even when local
factors persist.
Prevalence and severity
of gingival disease are
increased in puberty,
gingivitis is not a
universal.

45. II.GINGIVALCHANGESASSOCIATED WITH
THE MENSTRUALCYCLE
The prevalence of gingivitis increases
Bleeding gums or a bloated, tense feeling in the gums during the days preceding
menstrual flow
Exudate from inflamed gingiva is increased during menstruation
The crevicular fluid of normal, healthy gingiva is unaffected
Tooth mobility does not change significantly during the menstrual cycle (Friedman et
al .
The salivary bacterial count is increased during menstruation and at ovulation, which
occurs up to 14 days earlier.

46. III. GINGIVAL DISEASE IN PREGNANCY
Pregnancy itself does not cause gingivitis, but accentuates the
gingival response to plaque
No notable changes occur in the absence of local factors
Increase in the levels of both progesterone and estrogen which, by
the third trimester ( reaches levels 10-30 times than seen during
the typical menstrual cycle).
Prevalence of gingivitis 35% to 100%
Mechanism by which these steroids increase gingival
inflammation is not known.

47. Patients with slight
chronic gingivitis
before pregnancy
become aware of
the gingiva because
previously inflamed
areas become
enlarged,
edematous, and
more notably
discolored.
Patients with a slight
amount of gingival
bleeding before
pregnancy become
concerned about an
increased tendency
to bleed.
Loe H, 1965,
Gingivitis becomes
more severe by the
eighth month and
decreases during
the ninth, plaque
accumulation
follows a similar
pattern.
Loe H. Periodontal changes in pregnancy. J Periodontal Res.
1965;36:209.

48. Clinical features
 Pronounced ease of bleeding
 The gingiva is inflamed and bright red to
bluish red.
 The marginal and interdental gingivae
are edematous, appear smooth and
shiny, are soft and pliable, and
sometimes present a raspberry-like
appearance.
 Usually painless unless complicated by
acute infection.

49. Pregnancy granuloma or epulis
Combination of the vascular response induced by progesterone
& matrix stimulatory effects of estradiol contributes to the
development of pregnancy granulomas
Site- anterior papillae of the maxillary teeth & usually do not
exceed 2 cm in diameter.
Surface ulcerations, painless, often bleeds easily due to its
extreme vascularity.
Surgical removal of the granuloma during pregnancy avoided.
Careful oral hygiene and debridement during pregnancy are
important in preventing its occurrence.

51. Effects on the tissues and host response
 During pregnancy, progesterone is less actively catabolized to its inactive
products, resulting in higher levels of the active hormone.
 O’Leary et al, 1962, The aggravation of gingivitis in pregnancy has been
attributed principally to the increased levels of progesterone, which
produce
1.Dilation and tortuosity of the gingival microvasculature
2. Circulatory stasis
3. Increased susceptibility to mechanical irritation
all of which favor leakage of fluid into the perivascular tissues

52. IV. HORMONALCONTRACEPTIVESAND
THE GINGIVA
 Manner similar to that seen in pregnancy when taken for a period of
more than 1.5 years, increase periodontal destruction.
 Cumulative exposure to oral contraceptives apparently has no effect
on gingival inflammation or oral debris index scores

53. V. MENOPAUSALGINGIVOSTOMATITIS
(SENILEATROPHIC GINGIVITIS)
 Gingiva-dry and shiny, pale to red,and bleed easily.
 Dry, burning sensation throughout the oral cavity, associated with extreme
sensitivity to thermal changes; abnormal taste sensations "salty," "peppery"
or "sour"; and difficulty with removable partial prostheses.
 Microscopically, the gingiva exhibits atrophy of the germinal and prickle cell
layers of the epithelium
 Causes- occur after ovariectomy or sterilization by radiation in the treatment of
malignant neoplasms

54. Hyperparathyroidism
 Produces generalized demineralization of the skeleton.
 Formation of bone cysts and giant cell tumors.
 BROWN TUMOURS : Bone cysts become filled with
fibrous tissue with abundant hemosiderin-laden macrophages
& giant cells.
 25% to 50% of patients have associated oral changes.

55. Oral Manifestations of Patients with Hyperthyroidism
1. Dental abnormalities
-Widened pulp chambers
- Development defects
- Alterations in dental eruption
- Weak teeth
- Maloclussions
2. Brown tumor
3. Loss of bone density
4. Soft tissue calcifications
Carranza, 13th ed SA

56. HEMATOLOGIC DISORDERS
AND IMMUNE DEFICIENCIES

57. 1. Primary (inherited)
2. Secondary (acquired)-caused by
 Immunosuppressive drug therapy
 Pathologic destruction of the lymphoid system.
 e.g.Leukemia, Hodgkin’s disease, lymphomas, and multiple
myeloma

58. Leukemia
 Malignant neoplasias of WBC precursors characterized by :
(1) Diffuse replacement of the bone marrow with proliferating
leukemic cells
(2) Abnormal numbers and forms of immature WBCs in the
circulating blood
(3) Widespread infiltrates in the liver, spleen, lymph nodes, &
other body sites
 According to the Cell type- lymphocytic or myelogenous.
 According to their evolution, acute, (rapidly fatal), subacute, or
chronic.

59. Classification

60. Periodontium in Leukemic Patients
 Leukemic infiltration: Gingival Enlargement
 Highest incidence in Acute monocytic leukemia (66.7%).
 Not in edentulous patients or in chronic leukemia.
 Clinically, the gingiva appears bluish red and cyanotic, with a
rounding and tenseness of the gingival margin

61. Carranza , 13th ed SA

62. Oral Bleeding
 Common and early finding in leukemic patients, even in the
absence of clinically detectable gingivitis.
 Also manifest in the skin and throughout the oral mucosa,
where petechiae are often found, with or without leukemic
infiltrates.

63. Oral Ulceration and Infection
 Discrete, punched-out ulcers
penetrating deeply into the
submucosa and covered by a firmly
attached white slough.
 Common sites - buccal mucosa &
palate.
 Patients with past history of herpes
virus infection may develop
recurrent herpetic oral ulcers.

64. Anemia
 Deficiency in the quantity or quality of the blood manifested by a
reduction in the number of erythrocytes and in the amount of
hemoglobin.
 Etiology- Blood loss, defective blood formation, or increased blood
destruction.
 Classified according to cellular morphology and hemoglobin content as
 Macrocytic hyper-chromic anemia (pernicious anemia)
 Microcytic hypochromic anemia (iron deficiency anemia)
 Sickle cell anemia
 Normocytic-normochromic anemia (hemolytic or aplastic
anemia)

65. Pernicious anemia –
 Tongue changes in 75% of cases
 Marked pallor of the gingiva
Iron deficiency anemia-
 Induces similar tongue and gingival changes.
 Plummer-Vinson syndrome-A syndrome consisting of glossitis and
ulceration of the oral mucosa and oropharynx, inducing dysphagia in
patients with Iron deficiency anemia.

66. Sickle cell anemia
 Hereditary form of chronic hemolytic anemia.
 Occurs exclusively in blacks.
 Periodontal infections may precipitate sickle cell crisis.
 Oral changes:
1. Generalized osteoporosis of the jaws.
2. Stepladder alignment of the trabeculae of the interdental septa.
3. Pallor & yellowish discoloration of the oral mucosa.

67. Thrombocytopenia
Secondary to some known etiologic factor
1. Aplasia of the marrow, as in leukemia
2. Replacement of the marrow by tumor
3. Destruction of the marrow by irradiation or by drugs such as
benzene, aminopyrine, and arsenical agents
Low platelet count
A prolonged clot retraction and bleeding time
Normal or slightly prolonged clotting time
Condition of reduced platelet count that results from either a lack of
platelet production or an increased loss of platelets.

68. Clinical Features ofThrombocytopenia
1. Spontaneous bleeding into the skin or from mucous
membranes.
2. Petechiae & hemorrhagic vesicles - palate, tonsillar pillars, &
the buccal mucosa.
3. Gingivae are swollen, soft, & friable show abnormal response
to local irritation.

69. Antibody Deficiency Disorders
Agammaglobulinemia
 Results from a deficiency in B cells.
 T-cell function remains normal.
1. Congenital (X-linked or Bruton's agammaglobulinemia)
o X –linked recessive gene (bruton’s tyrosine kinase).
o The gene is responsible for B-cell development so production of
antibodies is deficient.

70. 2. Acquired or late-onset agammaglobulinemia /common
variable immunodeficiency disease (CVID)
 Onset of recurrent bacterial infections in the 2nd & 3rd decades of life.
 Basic immunological defect is failure of B-lymphocytes
differentiation into plasma cells.
 Enlarged spleen and swollen glands or lymph nodes.
 Autoantibodies against their blood cells.
 Cause unknown.,Not genetic,
 Aggressive periodontitis is a common finding.

71. Oral manifestation:
1. Acute gingival inflammation of both primary and permanent
dentitions.
2. Gingival proliferation
3. Extremely acute inflammation
4. Rapid destruction of bone
5. Recession
6. Tooth mobility
7. Pathologic migration
8. Early tooth loss
 Cases of periodontal disease that are attributed to LAD are rare.
They begin during or immediately after the eruption of the
primary teeth.

72. Leukocyte (Neutrophil) Disorders
Neutropenia
 Caused by diseases, medications, chemicals, infections, idiopathic
conditions, or hereditary disorders.
 Chronic or cyclic
 Classification based on the Absolute Neutrophil Count (ANC)
measured in cells per micro liter of blood:
1. Mild neutropenia : 1000 to 1500 cells/ μl
2. Moderate neutropenia : 500 to 1000 cells/ μl
3. Severe neutropenia : less than 500 cells/ μl

73. Agranulocytosis
 More severe neutropenia involving neutrophil , basophils &
eosinophils (ANC <100 cells/μl).
 Characterized by reduction in number of circulating granulocytes.
 Leads to severe infection ( eg.ulcerative necrotizing lesions of the
oral mucosa, skin).
 Most common Causes- Drug idiosyncrasy ( unexplained).
 Generally acute , may be chronic or periodic with recurring
neutropenic cycles (e.g, cyclic neutropenia).

74. Clinical Features:
1. Onset: fever, malaise, general weakness, & sore throat.
2. Ulceration in the oral cavity( oropharynx), & the throat is
characteristic.
3. Absence of a notable inflammatory reaction is a striking feature.
4. Mucosa : isolated necrotic patches (black & gray) ,sharply
demarcated from the adjacent uninvolved areas.
5. Gingival hemorrhage, necrosis, increased salivation, & fetid odor.
6. With cyclic neutropenia, the gingival changes recur with
recurrent exacerbation of the disease.

75. Carranza, 11th ed
A : Clinical presentation of
periodontal condition
B: Panaromic radiograph
demonstrating severe bone loss
around all the erupted permanent
teeth.
Fig: Aggressive periodontitis in 10
year old male with cyclic neutropenia
& agammaglobulinemia

76. GENETIC DISORDERS

77. Chediak-Higashi Syndrome
 Mostly affect melanocytes, platelets, & phagocytes.
 Causes partial albinism, mild bleeding disorders, & recurrent bacterial
infections.
 Neutrophils contain abnormal, giant lysosomes.
 Oral findings : severe gingivitis, ulcerations of the tongue and buccal
mucosa.
 Early onset periodontitis leading to premature loss of both deciduous
& permanent dentitions.

78. Lazy Leukocyte Syndrome
 Neutropenia
 Defective chemotactic response by neutrophils and an abnormal
inflammatory response.
 Clinical features: Recurring infections due to both a deficiency in
neutrophil chemotaxis and a systemic neutropenia.
 Oral manifestations: Painful stomatitis, gingivitis, recurrent
ulcerations of the buccal mucosa & tongue.
 Periodontitis progressing to the point of advanced alveolar bone loss
& tooth loss has been reported.

79. LeukocyteAdhesion Deficiency (LAD)
 An inherited disorder ( autosomal recessive pattern : chromosome 21q22.3).
 Involves a deficiency in cell surface antigen CD18.
 Leukocytes cannot adhere to the vessel wall at the site of infection, cannot
migrate to the site of infection.
 Extremely acute inflammation and proliferation of the gingival tissues with rapid
destruction of the bone .
 Frequent respiratory tract infections ,sometimes otitis media.
 An early tooth loss (primary & the permanent teeth ).

80. Papillon–Lefèvre Syndrome
Occur in siblings, male and females are equally affected.
Mutations in the cathepsin C gene, on chromosome 11
Primary teeth lost by 5-6 years of age.
Permanent dentiotion erupts normally but lost within a few year .
By age of 15 years, patients are usually edentulous.
Microscopic features:
1. Marked chronic inflammation
2. Predominant plasma cell infiltrate
3. Considerable osteoclastic activity and lack of osteoblastic activity
4. Alterations in cementum

81. Hyperkeratosis of skin
Early tooth loss and severe bone loss around the remaining teeth
Carranza, 13th ed SA

82. Wiebe CB, Hakkinen L, Putnins EE et al. Successful periodontal maintenance of a case with
Papillon-Lefèvre syndrome: 12-year follow-up and review of the literature. J
Periodontol. 2001;72:824-30.
There are few case reports of successful tooth retention in
patients with Papillon–Lefèvre syndrome.
The successful retention of permanent teeth may be associated with timing
treatment (i.e, antibiotics and the extraction of erupted teeth) in
relation to the severity of syndrome symptoms.
The extraction of all primary teeth followed by a period of edentulousness may
partially explain the lack of recurrent infection. In their review of the literature,
Wiebe and colleagues reported that the symptoms of Papillon–Lefèvre
syndrome diminish with age and that teeth that erupt later may not be lost.

83. Down Syndrome
Congenital disorder due to Trisomy 0f Chromosome 21
Mental deficiency and growth retardation
Prevalence of periodontal disease is high (almost 100% of patients younger
than 30 years).
Oral hygiene is poor, the severity of periodontal destruction exceeds that
explainable by local factors alone.
Deep periodontal pockets with substantial plaque accumulation & moderate
gingivitis.
Impaired Action of immune regulatory gene ( poor PMN functions)

84. Carranza, 13th ed SA

85. STRESS AND PSCHOSOMATIC
DISORDERS

86. Stress has been implicated as a risk indicator for periodontal disease
(Genco RJ, 1996).
The most well-documented association- between stress & necrotizing
ulcerative gingivitis.
Confirming the connection between psychologic conditions & other
forms of periodontal disease has been elusive.
Monteriro da Silva et al 1996 , in a study of 80 patients
( 40 : Aggressive periodontitis & 40: Chronic periodontitis) failed to find a
relationship between psychological factors & periodontal disease.

87. Bhagat M, Tapashetti R, Fatima G. Effects of Stress over Periodontium. Galore International Journal of Health
Sciences and Research. 2020;5(1):46-57.

88. Bhagat M, Tapashetti R, Fatima G. Effects of Stress over Periodontium. Galore International Journal of Health Sciences and Research.
2020;5(1):46-57.

90. Acc to Sabbah et al (2018) Psychological stressors have been
repeatedly shown to play an important role in periodontitis
because they are able to influence the behavioral risk factors for
periodontitis and/or affect periodontal tissues directly.
Studies have shown that individuals under stresses are more
likely to smoke, less likely to brush their teeth, & less likely to
visit a dentist all-important behavioral determinants of
periodontal diseases.
On the other hand, stressors have been shown to have an
impact on the body, increasing susceptibility to
inflammation and affecting the host immune response
and endocrine systems
* Sabbah W,Gomaa N, Gireesh A .Stress, allostatic load, and periodontal diseases . Periodontology 2000. 2018;78:154–61.

91. Influence of Stress on Periodontal Therapy
Outcomes
Axtelius et al ,1998 compared psychologic characteristics of 11 individuals who
were responsive to periodontal treatment compared with 11 individuals who were not
responsive. The responsive group had a more rigid personality, whereas the
nonresponsive group had a more passive, dependent personality and reported more
stressful life events in their past.

92. Bhagat M,
Tapashetti R,
Fatima G.
Effects of
Stress over
Periodontium.
Galore
International
Journal of
Health
Sciences and
Research.
2020;5(1):46-
57.

93. Psychiatric Influence of Self Inflicted Injury
 Psychosomatic disorders induced
neurotic habits
1. Grinding or clenching the teeth
2. Nibbling on foreign objects (e.g,
Pencils, pipes)
3. Nail biting
4. Excessive use of tobacco
Severe gingival recession
localized to the labial surface of
all mandibular incisors.
Carranza, 11th ed

94. Effect Of Nutrition On Periodontal Health

95.  There are no nutritional deficiencies that by themselves can
cause gingivitis or periodontitis.
 Nutritional deficiencies can affect the condition of the
periodontium , thereby may accentuate the deleterious effects of
plaque-induced inflammation in susceptible individuals.
 Nutritional deficiencies that produce changes in the oral cavity
are considered to be the periodontal and oral manifestations of
nutritional disease.
 The role of nutrition in periodontal disease may be related to
the effect of nutrition on inflammation.

96.  High carbohydrate intake has been
implicated in periodontal disease and dental
caries.
 Polyunsaturated fats (such as omega-3s) have
been observed to have a positive effect on
periodontal health.

97. Carbohydrates and Periodontal Health
 Sugar intake has long been established as the major
contributing factor in plaque formation.
 Sugars contribute to dental caries and periodontal disease
because bacteria ferment them and produce acid, leading to the
demineralization of the tooth structure.
 Lactose (milk sugar) is less cariogenic than other sugars.
 A reduction of sugar intake, coupled with scaling, root planing,
& the use of xylitol- and maltitol-containing gums have the
potential to improve the periodontal health.

98. VitaminADeficiency
 Maintains the health of epithelial cells of the skin and mucous membranes.
 Deficiency results in dermatologic, mucosal, and ocular manifestations,
keratinizing metaplasia.
 In experimental animals, vitamin A deficiency results in hyperkeratosis and
hyperplasia of the gingiva with a tendency for increased periodontal pocket
formation and retardation of gingival wound healing proliferation of the
junctional epithelium.*
*Frandsen AM. Periodontal tissue changes in vitamin A deficient young rats. Acta Odontol Scand.
1963;21:19–34

99. Vitamin D Deficiency
 Vitamin D or calciferol is essential for the absorption of
calcium from the gastrointestinal tract & for the maintenance of
the calcium– phosphorus balance.
 A deficiency of vitamin D & 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.

100.  Calcitriol- regulates the plasma levels of calcium & phosphate
 Acts at 3 different levels- Intestine, Bone, Kidney
CALCITRIOL
Bone calcium
mobilization
increases
Intestinal calcium
absorption increases
Renal calcium
absorption increases
PTH increases
Plasma calcium decreases

101. Vitamin E Deficiency
 Antioxidant , limit free-radical reactions and protect cells from
lipid peroxidation.
 Cell membranes, which are high in polyunsaturated lipids, are the
major site of damage
 No relationship has been demonstrated between deficiencies in
vitamin E and oral disease
 But in the rat, systemic vitamin E appears to accelerate gingival
wound healing.

102. B-Complex Deficiency
 The vitamin B complex family consists of
 B1 (thiamine)
 B2 (riboflavin)
 B3 (niacin)
 B5 (pantothenic acid)
 B6 (pyridoxine, pyridoxal, pyridoxamine)
 B7 (biotin), B9 (folic acid)
 B12 (cobalamins)
 Vitamin B play a vital role in cell metabolism, repair, & proliferation.

103. Thiamin Deficiency
 Beriberi, is characterized by
 Paralysis; cardiovascular symptoms, including edema;
and loss of appetite.
 Oral disturbances –
1. Hypersensitivity of the oral mucosa
2. Minute vesicles (simulating herpes) on the buccal mucosa,
under the tongue, or on the palate
3. Erosion of the oral mucosa.

104. Riboflavin Deficiency
 Ariboflavinosis includes
1. Glossitis (magenta discoloration and atrophy of the papillae).
2. Angular cheilitis
3. Seborrheic dermatitis
4. Superficial vascularizing keratitis.
 In mild to moderate cases- dorsum exhibits a patchy atrophy of the
lingual papillae & engorged fungiform papillae, which project as
pebble-like elevations.
 In severe deficiency, the entire dorsum is flat, with a dry & often
fissured surface.

105. Niacin Deficiency
1. The most common finding is necrotizing ulcerative
gingivitis.
2. Black tongue
3. Gingival inflammation with destruction of the gingiva,
periodontal ligament, and alveolar bone.
4. Leukopenia

106.  Pellagra is characterized by
1. Dermatitis
2. Diarrhea
3. Dementia
 Glossitis, gingivitis, & generalized stomatitis are also
present
 Glossitis and stomatitis may be the earliest clinical signs

107. FolicAcid Deficiency
 Most common vitamin deficiency in humans.
 Deficiency causes Megaloblastic anemia.
 Folic acid deficient animals demonstrate:
1. Necrosis of the gingiva, periodontal ligament, alveolar bone
2. Angular cheilosis
3. Gingivitis

108. Hemorrhagic lesions
into muscles, joints,
nail beds; petechial
hemorrhages, often
around hair follicles;
Increased
susceptibility to
infections; and
impaired wound
healing,Bleeding,
swollen gingiva and
loosened teeth
Characterized by
increased capillary
permeability,
hyporeactivity of the
contractile elements
of the peripheral
blood vessels, and
sluggishness of blood
flow.
Vitamin C (Ascorbic Acid) Deficiency
Results in scurvy, characterized by hemorrhagic diathesis and
retardation of wound healing.

109. Possible Etiologic Relationships betweenAscorbicAcid and
Periodontal Disease
 Deficiency-
1. Influence the metabolism of collagen within the
periodontium
2. Interferes with bone formation, leading to loss of periodontal
bone.
3. Changes that occur in alveolar bone & other bones as a result
of failure of the osteoblasts to form osteoid take place very
late in the deficiency state.

110. 4. Deficiency increases the permeability of oral mucosa to tritiated
endotoxin & tritiated inulin & of normal human crevicular
epithelium to tritiated dextran.
5. Increasing levels enhance the chemotactic & migratory action of
leukocytes without influencing their phagocytois.
6.Maintain periodontal microvasculature integrity, & vascular
response to bacterial irritation and wound healing.
7. Depletion interfere with the ecologic equilibrium of bacteria in
plaque & pathogenicity.

111. Gingivitis
 Gingivitis with enlarged, hemorrhagic,
bluish-red gingiva is classic sign.
 Vitamin C deficiency may aggravate
the gingival response to plaque ,
worsen the edema, enlargement, &
bleeding.

112. Periodontitis
 Results in edema and hemorrhage in the periodontal ligament
 Osteoporosis of the alveolar bone
 Tooth mobility
 The exaggerated destruction results from inability of defensive
connective tissue barrier function & partly from destructive tendencies
caused by the deficiency itself, including
1. Inhibition of fibroblast formation and Differentiation to osteoblasts.
2. Impaired formation of collagen and mucopolysaccharide ground
substance.

113. Third National Health and Nutrition Examination Survey (NHANES III),
Nishida et al,2000 found weak but statistically significant dose-response
relationship between the levels of dietary vitamin C intake and
periodontal disease in current and former smokers as measured by
clinical attachment.
Nishida M, Grossi SG, Dunford RG et al. Dietary vitamin C and the risk for periodontal disease. J
Periodontol.2000;71:1215-23.

114. Protein Deficiency
Hypoproteinemia causes
1. Muscular atrophy
2. Weakness
3. Weight loss
4. Anemia
5. Leukopenia
6. Edema
7. Impaired lactation
8. Decreased resistance to
infection
9. Slow wound healing
10. Lymphoid depletion
In experimental animals
1. Degeneration of the connective
tissue of the gingiva and PDL
2. Osteoporosis of alveolar bone
3. Retardation in the deposition of
cementum
4. Delayed wound healing
5. Atrophy of the tongue epithelium.

115. Bisphosphonates
 First synthesized in the 1950s as a substitute for pyrophosphate
 Primarily used to treat cancer (i.v.) and osteoporosis (oral).
 Act by inhibiting osteoclastic activity, which leads to less bone
resorption, less bone remodeling, and less bone turnover.
 In the treatment of osteoporosis, it prevent bone loss and increase
bone mass by creating an advantage for osteoblastic activity.

116. Osteoclast inhibition-By two mechanisms that depend on whether the R2
side chain contains nitrogen.
NONAMINOBISPHOSPHONATES: Metabolized by osteoclasts to form
an adenosine triphosphate analog that interferes with energy production and
causes osteoclast apoptosis
AMINOBISPHOSPHONATES ( zoledronate alendronate) are more potent
& cause
(1) Inactivation of adenosine triphosphate
(2) Osteoclast cytoskeletal disruption
(3) Impairment of osteoclast recruitment
(4) Induction of osteoblasts to produce osteoclast-inhibiting factor

117. BRONJ
Definition- as exposure/necrosis of portions of the jaw bone in patients
exposed to bisphosphonates that has persisted more than 8 weeks with
no past history of radiation therapy to the jaws.
 First reported in 2003 by Marx
 Various terms - avascular necrosis, bisphosphonate-related or -
associated ONJ (BRONJ), and bisphosphonate-induced ONJ
(BIONJ).
 Have a high affinity for hydroxyapatite & rapidly absorbed in
bone, Especially in areas of high activity(jaw)

118.  The bisphosphonate molecule gets incorporated into bone
without being metabolized or modified.
 During osteoclastic resorption of bone, the trapped bisphosphonate
is released and able to affect osteoclasts again.
 Half life of bisphosphonates in the bone is 10 years or more.
Multiple etiopathogenic factors of ONJ-
1. Systemic medications
2. Radiation
3. infection
4. Trauma
5. Direct chemical toxicity
6. Idiopathic mechanisms

119. Clinical signs- painful sites with surrounding soft tissue induration and
inflammation, drainage may be present.
Radiographically, lesions appear radiolucent with sclerosis of lamina dura,
loss of lamina dura, or widening of periodontal ligament.
Histologically, bone appears necrotic with empty lacunae. In advanced
cases, pathologic fracture may be present
The high potency of IV bisphosphonate for cancer treatment explain the
high incidence of BIONJ
The incidence is 2.5% to 5.4%(in cancer treated patients) and 0.007% to
0.04% Patient taking oral bisphosphonate

120. Potential risk factors that may contribute to BIONJ include
1. Systemic Corticosteroid Therapy
2. Smoking
3. Alcohol
4. Poor Oral Hygiene
5. Chemotherapy
6. Radiotherapy
7. Diabetes
8. Hematologic Disease
The precipitating factors or events leading to BIONJ include
1. Extractions
2. Root Canal Treatment
3. Periodontal Infections
4. Periodontal Surgery
5. Dental Implant Surgery

121.  Estilo et al 2007, found that
 Type of cancer, duration of bisphosphonate therapy, sequential IV
bisphosphonate treatment with pamidronate followed by
zoledronate, comorbid osteoarthritis, rheumatoid arthritis, and benign
hematologic conditions were significantly associated with an
increased likelihood of ONJ.
 In their study, systemic administration of corticosteroids was not
found to be associated with an increased risk BRONJ.
 The use of bisphosphonates in bone regeneration has
been proposed as well.

122. Corticosteroids
In humans, systemic
administration of cortisone
found unrelated to severity
of gingival and periodontal
disease.
But renal transplant patients
receiving
immunosuppressive therapy
have significantly less
gingival inflammation than
control subjects with similar
amounts of plaque.
Stress increases circulating
endogenous cortisol levels
through stimulation of the
adrenal glands .
It adversely affect
periodontium by
diminishing the immune
response to periodontal
bacteria.

123. OSTEOPOROSIS
 Definition- It is a systemic skeletal disease characterized by low
bone mass and microarchitectural deterioration with a consequent
increase in bone fragility and susceptibility to fracture.
 Incidence increases with age for both men and women, with
women affected earlier than men.
 It is greatest for women during the peri-menopausal years.

124.  Bone mass can be measured with accuracy and precision with
dual x- ray absorptiometry (DEXA).
 One of the difficulties is the fact that both osteoporosis and
periodontitis are chronic, multifactorial diseases that result in
bone loss, and bone loss in each condition is exacerbated by local
and systemic factors.

125. Definitions of Osteoporosis & Osteopenia Indicated by T- scores
Ranges of T- Scores are based on Standard deviation outside of normal, which is based
on BMD of a healthy 30- year- old adult. ( Carranza , 13th ed SA)

126. Martínez-Maestre MÁ, González-Cejudo C, Machuca G, Torrejón R, Castelo-Branco C.
Periodontitis and osteoporosis: a systematic review. Climacteric. 2010 ;13(6):523-9.

127. Out of 35 studies
10 studies (diagnosis
of osteoporosis -
existence of non-
traumatic fracture)
9 studies
(radiographs for
diagnosis) - 6 studies
were found to have a
positive correlation
Martínez-Maestre MÁ, González-Cejudo C, Machuca G, Torrejón R, Castelo-Branco C.
Periodontitis and osteoporosis: a systematic review. Climacteric. 2010 ;13(6):523-9.

128. CARDIOVASCULAR DISEASES
Arteriosclerosis
 In aged individuals, arteriosclerosic changes are common in
vessels throughout the jaws, as well as in areas of periodontal
inflammation
 Circulatory impairment induced by vascular changes may increase
the patient's susceptibility to periodontal disease.
 But, recent evidence to suggest that individuals with periodontal
disease may be at greater risk for heart disease.

129. Congenital Heart Disease
 About 1% in live births & fatal.
 Cardiac defect involves the heart the adjacent vessels or a
combination of both.
 Risk of the development of infective endocarditis.
Clinical features include
1. Cyanosis of the lips and oral mucosa
2. Delayed eruption of both deciduous and permanent dentition
3. Increase positional abnormalities and enamel hypoplasia.
4. The teeth have a bluish white appearance
5. Severe caries and periodontal disease

130. Tetralogy of Fallot
 Characteristic of four cardiac defects
1. Ventricular septal defect
2. Pulmonary stenosis
3. Malposition of the aorta to the right
4. Compensatory right ventricular enlargement.
 Clinical features- cyanosis, audible heart murmurs & breathlessness.
 Oral changes- purplish red discoloration of the lips & gingiva
 Sometimes severe marginal gingivitis and periodontal destruction.
 The tongue appears coated, fissured, and edematous.
 Extreme reddening of the fungiform and filiform papillae.

131. Eisenmenger’s Syndrome
Pulmonary insufficiency through the septal defect
Increase of pulmonary blood flow
Progressive pulmonary fibrosis, small vessel occlusion, high pulmonary vascular
resistance, diastolic murmur
 Increase in cyanosis over many years can lead to cardiac failure.
 The lips, cheeks, and buccal mucous membranes are cyanotic.
 Severe generalized marginal gingivitis may be found.
 In coarctation of the aorta, show marked inflammation of the gingiva in the
anterior part of the mouth.

132. Lead Intoxication
 Slowly absorbed, and toxic symptoms are
not particularly definitive.
 Pallor of the face and lips
 Nausea, vomiting, loss of appetite, and
abdominal colic.
 Peripheral neuritis, psychologic disorders,
and encephalitis also reported.
 Oral signs are salivation, coated tongue, a
peculiar sweetish taste, gingival
pigmentation, and ulceration.
 Gingival pigentation is linear (burtonian
line), steel gray, and associated with local
irritation.

133. Mercury Intoxication
 Headache, insomnia, cardiovascular symptoms, pronounced salivation
(ptyalism), & a metallic taste.
 Gingival pigmentation in linear form results from the deposition of
mercuric sulfide.
 Accentuates the preexistent inflammation & ulceration of the gingiva.

134. Other Chemicals
 Phosphorus, arsenic, and chromium, may cause necrosis of the
alveolar bone with loosening and exfoliation of the teeth.
 Benzene intoxication is accompanied by gingival bleeding and
ulceration with destruction of the underlying bone

135. Today, we have a better appreciation for the complexity and
significance of interrelationships between periodontal
infections and host defense. 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. It is important to recognize
that the systemic diseases, disorders, or conditions themselves
do not cause periodontitis; rather, they may predispose,
accelerate, or otherwise
increase disease progression.
CONCLUSION

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140. Thank
You