This document discusses various systemic conditions and disorders that can influence periodontal disease, including:
1. Hematologic disorders like red blood cell disorders (such as sickle cell anemia), platelet disorders, and white blood cell disorders (such as leukemia) which can cause bleeding, infection, and gingival enlargement.
2. Systemic drug therapy that can cause gingival enlargement as a side effect, such as from anticonvulsants, immunosuppressants, and calcium channel blockers.
3. Psychosomatic disorders like stress, which may exacerbate periodontal disease through its effects on the immune system and increased production of pro-inflammatory mediators.
8. Haematological disorders
• Red blood cell disorders
• White blood cell disorders
• Platelet disorders
The white blood cell or leucocyte disorders constitute the major
proportion of hematological disorders affecting the periodontium.
10. Red blood cell disorders
Erythrocyte disorders do not profoundly affect the periodontium. Conditions that has been
associated with severe periodontal destruction are:
• Acatalasia
• Aplastic anemia
Generalized pancytopenia
• Pure red cell aplasia
• Sickling disorders
11. Acatalasia
Rare, inherited (autosomal recessive) disorder caused by the
lack of catalase in cells, especially red and white blood cells.
• Catalase protects these cells from harmful oxidizing agents
which could denature hemoglobin and produce local hypoxia
and necrosis.
• Severe periodontal destruction and gingival necrosis seen
• 25–50% suffer an oral condition called Takahara’s disease,
characterized by painful ulcerations of the gingiva and tonsillar
lacunae.
12. Anemia
Deficiency in quality or quantity of blood, manifested by
↓ in no. of erythrocytes & hemoglobin
Cause:
i) Blood loss
ii) Defective blood formation
iii) Increased RBC destruction
14. Pernicious anemia
i) Tongue changes (75%) – red, smooth & shiny because of atrophy of tongue
ii) Gingiva – marked pallor
Iron deficiency anemia
i) Similar tongue & oral changes
ii) Plummer Vinson syndrome (glossitis, ulceration of oral mucosa & oropharynx, dysphagia)
15. Sickle cell anemia
i) Hereditary form of chronic hemolytic anemia
ii) Pallor, jaundice, weakness, rheumatoid manifestations, leg ulcers
iii)Oral changes – generalized osteoporosis of jaws with peculiar STEP LADDER pattern of trabeculae of
interdental septa, pale and yellowish discoloration of oral mucosa
Aplastic anemia
i) Failure of bone marrow to produce erythrocytes
ii) Oral changes – pale discoloration, susceptibility to infection because of concomitant neutropenia
17. Thrombocytopenia
• Reduced platelet count resulting from either lack of platelet production or increased loss
of platelets.
• Purpura - purplish appearance of skin or mucous membrane where bleeding has
occurred as a result of decreased platelets
• Thrombocytopenic purpura may be idiopathic or may occur secondary to some etiologic
factors responsible for ↓ functioning of bone marrow causing resultant ↓ in no. of
circulating platelets.
18. Clinical features
i) ↓ platelet count
ii) Prolonged clot retraction
iii) Prolonged bleeding time (BT)
iv) Normal or slightly prolonged clotting time (CT)
v) Spontaneous bleeding from skin or mucous membrane
vi) Petechial & hemorrhagic vesicles seen in oral cavity (palate, tonsillar
pillars, buccal mucosa)
vii) Gingiva – soft, swollen & friable, bleeding spontaneously or on slightest
provocation & is difficult to control
x) Abnormal response to local irritation
20. Leukemia
Malignant neoplasm of WBC precursors characterized by
i) Diffuse replacement of bone marrow with proliferating leukemic cells.
ii) Abnormal number and forms of immature WBC’s in circulating blood
iii) Widespread infiltrates in liver, spleen, lymph nodes and other body
sites.
21. Leukemia
Acc. to lineage of WBC involved, leukemia can be lymphocytic or myelocytic.
Acc. to their evolution, it can be acute, sub acute or chronic. Out of these
acute is extremely fatal and gingival changes are more common in acute
leukemia.
In all leukemias, the normal marrow function is impaired and thus anemia,
infections and thrombocytopenia are common.
Several factors are implicated in the etiology of leukemia – radiation,
chemical injury, genetic factors, immune deficiency and viral infections.
22. Periodontium in Leukemic Patients
Oral and periodontal manifestations of leukemia consist of
Leukemic infiltration
Bleeding
Oral ulcerations & infections.
23. 1. Leukemic Infiltration of Periodontium
(Gingival enlargement)
Leukemic cells can infiltrate the gingiva and, less frequently, the alveolar bone.
It causes gingival enlargement.
Leukemic gingival enlargement consists of a basic infiltration of the gingival corium by
leukemic cells. It creates gingival pockets where bacterial plaque accumulates, initiating a
secondary inflammatory lesion that contributes also to the enlargement of the gingiva.
Gingiva appears initially bluish red and cyanotic, with a rounding and tenseness of the
gingival margin; then it increases in size, most often in the interdental papilla and partially
covering the crowns of the teeth.
24. Mainly seen in acute myelogenous leukemia (AML);not in chronic
leukemia. AML has 8 subtypes (M0-M7).
Incidence of gingival enlargement: acute monocytic leukemia
(Subtypes M5) (66.7%), acute myelomonocytic leukemia (M4)
(18.5%), acute myelocytic leukemia (M1,M2) (3.7%)
25. 2. Bleeding
• Bleeding in oral mucosa and skin is early sign of leukemia.
• Due to the thrombocytopenia that results from replacement of the
bone marrow cells by leukemic cells and also by inhibition of normal
stem cell function by leukemic cells or their products.
• Oral bleeding has been reported as a presenting sign in 17.7% of
patients with acute leukemia and in 4.4% of patients with chronic
leukemia.
26. Oral Ulceration and Infection
Granulocytopenia resulting from the replacement of bone marrow cells by leukemic cells reduces
the tissue resistance to opportunistic microorganisms and leads to ulcerations and infections.
These lesions occur in sites of trauma such as the buccal mucosa in relation to the line of occlusion
or the palate. Acute gingivitis and lesions of necrotizing ulcerative gingivitis are more frequent and
severe.
The inflamed gingiva differs clinically from inflamed gingiva in non leukemic individuals. It is a
peculiar bluish red, is markedly sponge like and friable, and bleeds persistently on the slightest
provocation or even spontaneously.
Patients with past history of herpes infection may develop recurrent herpetic oral ulcers, commonly
after chemotherapy.
28. Treatment of leukemic gingival
enlargement
BT, CT and platelet count of the patient should be checked and the
hematologist consulted before starting periodontal treatment
Gently removing the local irritating factors with cotton pellets, performing
superficial scaling to control the inflammatory component of the
enlargement.
Instructing the patient in oral hygiene for plaque control including daily use
of chlorhexidine mouthwash.
29. Leukocyte (Neutrophil) Disorders
• It could be primary or secondary
Primary neutrophil impairment
i) Neutropenia
ii) Agranulocytosis
iii) Chediak – Higashi syndrome
iv) Lazy leukocyte syndrome
v) Leukocyte adhesion syndrome
31. i) Neutropenia
• Low levels of circulating neutrophils characterized by cyclical depletion of PMN
numbers, typically in three-week cycles, although this can be between 2-5
weeks.
• The episode of neutropenia is usually short but the patient’s PMN count never
returns to normal levels and the differential blood cell count for PMNs is at
least 40 percent less than normal levels.
32. • The cyclical depression of PMN numbers is thought to be due to a disorder
of hematopoietic control.
• Absolute neutrophil count (ANC) is less than 1500 cells/µl
• Can be genetic or drug induced or may be induced from viral infection
• May be chronic or cyclic, severe or benign
• Serious condition, could be life threatening if ANC is <500 cells/µl
33. ii) Agranulocytosis
• It is reduction in no. of circulating granulocytes and results in severe
infections, including ulcerative necrotizing lesions of oral mucosa, skin, GIT
and genitourinary tracts
• Common cause – drug idiosyncrasy – seen with drugs like aminopyrine,
barbiturates, benzene ring derivatives, sulfonamides, gold salts, or arsenical
agents
34. • Clinical onset – fever, malaise, general weakness, and sore throat.
i) Ulceration in oral cavity, oropharynx and throat
ii) Isolated necrotic patches that are black and gray and are
sharply demarcated from the adjacent uninvolved areas.
iii) Absence of notable inflammatory reaction caused by lack
of granulocytes is a striking feature
iv) Gingival hemorrhage, necrosis, increased salivation and
fetid odor
35. iii) Chediak – Higashi Syndrome
• Rare disease, that affects the organelles found in almost every cell, described as a genetically
transmitted disease
• Site – melanocytes, platelets and phagocytes
• Clinical features
i) Partial albinism
ii) Mild bleeding disorders
iii) Recurrent bacterial infections
iv) Delayed killing of the ingested microorganisms, due to inability of phagocytes to release their
contents
36. • Oral findings include
1. Gingivitis
2. Ulcerations of both tongue and buccal mucosa
3. Early onset periodontitis leading to loss of both the dentitions.
This syndrome was first described by Beguecesar in 1943, but acquired its
name 10years later from separate reports by Chediak in 1952 and Higashi in
1954.
Average life span of children with this syndrome is only 6years. Treatment
includes bone marrow transplantation for correcting neutrophil abnormalities.
37. • Hallmark of this syndrome is presence of large Azurophilic granules in the
cytoplasm of the neutrophils. These large inclusions impair neutrophil migration,
possibly by inhibiting cell deformability, that renders neutrophils unable to
phagocytose microbes. The patients of this syndrome are more prone for
recurrent infections in early childhood.
• Lab diagnosis is made by presence of Azurophilic granules within the neutrophils.
38. iv) Lazy leukocyte syndrome
Caused by abnormal neutrophil motility
Characteristics
i) Susceptibility to severe microbial infections
ii) Neutropenia
iii) Defective chemotactic response by neutrophils
iv) Abnormal inflammatory response
v) Susceptibility to aggressive periodontitis
39. v) Leukocyte adhesion
syndrome
• Rare genetic disorder, often diagnosed at birth. Many children do
not survive.
• Cause – inability to produce or express normally CD18 – an
important cell surface integrin necessary for leukocytes to adhere to
the vessel wall at the site of infection.
• Due to this, leukocytes cannot migrate to site of infection, and
bacterial destruction goes unimpeded by the normal host immune
response
40. • Periodontal disease, usually start during or immediately after
eruption of primary teeth. Extremely acute inflammation and
proliferation of gingival tissues with rapid destruction of bone is
seen
• Respiratory infections and sometimes otitis media could be noted.
• Both primary and permanent tooth are affected, resulting in early
tooth loss.
41. i) Down syndrome
• Periodontal disease in Down syndrome is characterized by a generalized early periodontitis,
which commences in the deciduous dentition and continues into the adult dentition.
• Mongolism, Trisomy 21
• Chromosomal abnormality --- resulting in mental deficiency and growth reduction
• Even though oral hygiene of these patients is poor, the periodontal destruction in
these patients exceeds that explainable by local factors alone.
• Periodontal disease is characterized by deep periodontal pockets.
• Commonly seen in lower anterior region
42. • Marked recession associated with high frenal
attachment. The disease progresses rapidly.
• Acute necrotizing lesion is a frequent finding
• The high prevalence of periodontitis in down
syndrome patients is explained by
(a) Reduced resistance due to poor circulation
especially in those area of terminal
vascularization such as gingival tissue and
defect in T cell maturation and PMN
chemotaxis.
(b) Increase in number of P. intermedia in mouths
of children with down syndrome
43. ii) Papillon – Lefevre Syndrome
• Inherited as an autosomal recessive pattern.
• Parents are not affected, but both carry the autosomal genes for syndrome to
appear in the offspring.
• Characteristics
i) Hyperkeratotic skin lesions (palms, soles, knees and elbows)
ii) Severe destruction of periodontium
iii) Calcification of dura (occasionally)
44. Oral and skin lesions seen in a patient of 17 years with papillon – lefevre syndrome
45. Early inflammatory changes that lead to bone loss and
exfoliation of teeth.
Primary teeth are lost by 5-6 years of age. Permanent dentition
erupts normally, but are lost in few years due to periodontal
destruction
↓
By age of 15 years, patient is usually edentulous, except for 3rd
molars, which are also lost few years after eruption.
46. Patient unable to chew food because of
inflammation, mobile teeth, multiple
abscesses and food impaction
47. Microscopically, there is marked chronic inflammation of lateral wall
of pocket, with predominantly plasma cell infiltrate, considerable
osteoclastic activity and reduced osteoblastic activity, and
extremely thin cementum
↓
Bacterial flora is similar to that of chronic periodontitis, with
spirochete rich zones in apical portion of pocket.
52. Stress & Periodontal Disease
• It is the type of stress and the ability of the individual to cope
with stress that determine the extent of destructive periodontal
disease.
• Cause of stress
i) Loss of spouse or family member
ii) A failed relationship
iii) Loss of employment and financial difficulties
53. MECHANISM OF ACTION
2 ways in which psychosomatic disorders may be induced in the
oral cavity are:
# through the
development of habits
that are injurious to the
periodontium.
# by the direct effect of
the autonomic nervous
system on the
physiologic tissue
balance.
54. 1. Habits related to stress
i) Poor oral hygiene
ii) Start or increase clenching and grinding of their teeth
iii) May start smoking or use of other forms of tobacco
iv) Less likely to seek professional care
v) Nibbling of foreign objects (pencils, pipes)
vi) Nail biting
55. 2 (a). Stress induced immunosuppression
ACTH (adrenocorticotrophic hormone) secretion from pituitary gland
↓
Increased cortisol production from adrenal cortex
↓
Affects immune system by suppression of
i) Neutrophil activity
ii) IgG activity
iii) Salivary IgA secretion
↓
Increased potential of destruction by periodontal pathogens
56. 2(b). Stress also effect cellular immune responses by direct effects on
neurotransmitters including epinephrine, norepinephrine, neurokinin and
substance P.
These neurotransmitters interact directly with lymphocytes, neutrophils,
and lymphocytes via receptors causing an increase in tissue destruction.
57. •Psychosomatic disturbances and
effects on oral mucosa
1. Oral psychosomatic disease
Lichen planus
Apthous stomatitis
Glossitis and stomatitis
2. Oral disease in which psychosomatic factor may play etiological role
Erythema multiforme
Mucous membrane pemphigoid
Chronic periodontal disease
3. Oral infections in which psychosocial factors plays an etiological role
Recurrent herpes labialis
Necrotizing ulcerative gingivitis (NUG)
58. 4. Oral disease included by necrotic habits
Leukoplakia
Biting of oral mucosa
Mechanical / physical irritation with foreign objects
Dental and periodontal disease caused by bruxism
Poor oral hygiene (Gingivitis)
5. Neurotic oral symptoms
Glossodynia
Altered taste perception
Mucosal pain
59. GINGIVITIS
Stress diminishes
saliva flow and
increases dental
plaque formation.
Deinzer R et al. (2002)-
examined the impact of
academic stress by
students at university
during their examination
period on periodontal
health. Academic stress
was shown to be a risk
factor for gingival
inflammation with
increasing crevicular
interleukin-1β levels and a
diminution of the quality of
the oral hygiene.
In a pilot study in
1998, Axtelius
showed the
presence of
cortisol in gingival
crevicular fluid for
first time.
A study by
Johanssen (2006)
confirmed the fact
that the
concentration of
cortisol in the
gingival crevicular
fluid is higher in
persons showing
depression signs.
60. NECROTIZING PERIODONTAL DISEASES
The first reports were written about mouth pain among the
soldiers of Alexander the Great.
• The first studies showing this influence were made by
Pindborg (1951) (higher number of necrotic periodontitis
during military service) and in 1963–1964 by Giddon (more
necrotic periodontitis in college during examination period).
• The main risk factors for necrotic periodontitis are: past
episode of necrotic periodontitis, bad oral hygiene, bad
sleep, unusual emotional stress, tobacco, alcohol, bad
alimentation and recent illness.
61. CHRONIC
PERIODONTITIS
• Linden et al (1996), Vettore et al (2003) found positive
association between anxiety and occupational stress with
progression of chronic periodontitis.
• More research needs to be done.
63. NUTRITIONAL DISEASES
Nutritional deficiencies produce changes like
alterations of the lips, oral mucosa, bone as well as
other periodontal tissues. These changes are
considered to be periodontal or oral manifestations
of nutritional disease.
64. NUTRITIONAL DISEASES
There are no nutritional deficiencies that by
themselves can cause gingivitis or periodontal
pockets. Plaque is always the initiating factors.
Nutritional deficiencies only aggravate the
inflammatory changes.
67. VITAMIN A
Essential for epithelial cell differentiation, humoral
antibody response and cell mediated immunity
Antioxidant
Supplement periodontal treatment
68. VITAMIN A DEFICIENCY
Dermatologic, mucosal, and ocular manifestations.
Degenerative changes occur in epithelial tissues -
keratinizing metaplasia.
69. VITAMIN A DEFICIENCY
Periodontal changes
Animal studies: Hyperplasia and hyper keratinization of the
gingival epithelium with proliferation of the junctional
epithelium and retardation of gingival wound healing. In the
presence of local factors, vitamin A-deficient rats develop deep
periodontal pockets.
Humans: No relation between this vitamin deficiency and
periodontal disease. More studies are awaited.
70. • VITAMIN D
Required for absorption of calcium, magnesium, iron,
phosphate, zinc from intestines.
Inhibit pro inflammatory cytokines and T cell proliferation.
Maintain calcium and phosphorus levels by affecting bone
development and metabolism.
Required for cell maturation, neuromuscular functioning
Plays vital role in innate immunity as monocytes and
macrophages have VDR (vitamin D receptor) on their
surfaces.
71. • VITAMIN D DEFICIENCY
Animal studies (young dogs):
• osteoporosis of alveolar bone
• osteoid that forms at a normal rate but remains uncalcified
• failure of osteoid to resorb
• reduction in the width of the periodontal ligament space
• a normal rate of cementum formation, but defective calcification
• Distortion of the growth pattern of alveolar bone.
72. • VITAMIN D DEFICIENCY
• Osteomalacic animals: Rapid, generalized, severe osteoclastic
resorption of alveolar bone, proliferation of fibroblasts that replace bone
and marrow, and new bone formation around the remnants of
unresorbed bony trabeculae.
• Radiographically: generalized partial to complete disappearance of the
lamina dura, loss of trabeculae, increased radiolucency of the
trabecular interstices, and increased prominence of the remaining
trabeculae
73. • VITAMIN D SUPPLEMENTATION
Reduce susceptibility of gingival inflammation through anti-
inflammatory effects.
• Local effects of vitamin D supplementation seems to be more useful
than systemic. Vitamin D coated dental implants may enhance
Osseointegration with bone (Javed F et al, 2016).
• More studies are awaited to seek the results of its supplementation
on periodontal bone formation during periodontal surgery.
74. • VITAMIN E
α-tocopherol is the most active biological form of Vitamin E.
Potent antioxidant, protects membrane lipids from oxidative
damage, reduce prostaglandin E2.
Its level is found to be decreased in patients with periodontitis than
healthy patients (Asman B et al,1994), its overall effect on
periodontal health is not yet clear.
77. VITAMIN C – PERIODONTAL
MANIFESTATIONS
•Vitamin C (Ascorbic acid) deficiency in
humans result in scurvy, a disease
characterized by hemorrhagic diathesis
and retardation of wound healing.
78. MECHANISM OF VITAMIN C DEFICIENCY
Low levels of ascorbic acid influences the metabolism of collagen
within the periodontium, thereby affecting the ability of the tissue to
regenerate & repair by itself.
It affects fibroblasts, osteoblasts and odontoblasts. The cells fail to
produce normal collagen, osteoid, dentin; and ability of cells to form
epithelial and vascular basement membranes is also restricted
Optimal levels of ascorbic acid is required to maintain the integrity
of the periodontal microvasculature and wound healing. Deficiency
make blood vessels fragile and susceptible to rupture.
79. GINGIVITIS IN VIT.C DEFICIENCY
Enlarged, hemorrhagic, bluish red gingiva
In severe cases, the gingiva becomes brilliant red, tender
and grossly swollen.
The spongy tissues are extremely hyperemic and bleed
spontaneously.
81. PERIODONTITIS IN VIT.C DEFICIENCY
Acute vitamin C deficiency results in edema and hemorrhage in the
periodontal ligament,
osteoporosis of the alveolar bone,
tooth mobility,
hemorrhage,
edema and degeneration of collagen fibers in gingiva
impaired gingival healing.
The periodontal ligament is widened due to resorption of surrounding
bone and breakdown of collagen fibers in periodontium
82. - In long standing cases, tissues attain a dark blue or purple hue.
83. VITAMIN C – PERIODONTAL
MANIFESTATIONS
• Clinical manifestations
• Increased susceptibility of infections
• Impaired wound healing
• Bleeding and swollen gums
• Mobile teeth
• Hemorrhagic lesions into the muscles of extremities,
joints and sometimes nail beds
• Petechial hemorrhages often around hair follicles
84. • Histopathological features
• Defective formation and maintenance of collagen
• Retardation or cessation of osteoid formation & impaired
osteoblastic function
• Increased capillary permeability
• Susceptibility to traumatic hemorrhages
• Hyporeactivity of contractile elements of the peripheral blood vessels
• Sluggishness of blood flow
85. • TREATMENT:
Dietary intake of 10mg/day of vitamin C is necessary to prevent
scurvy.
Gingivitis/Periodontitis is not caused by vitamin C deficiency
alone. Its deficiency may aggravate the gingival response to
plaque and worsen the edema, enlargement and bleeding.
So, we can say that vitamin C deficiency has its greatest impact
on periodontal disease when preexisting disease and other co-
destructive factors are present. Scaling and root planing should
be done to remove local factors.
86. VITAMIN B-COMPLEX – PERIODONTAL
MANIFESTATIONS
Oral disease is rarely due to deficiency in just
one component of the B-complex group. It
generally occurs in combination to various
deficiencies in B-complex group.
88. VITAMIN B-COMPLEX – PERIODONTAL
MANIFESTATIONS
Oral changes generally seen in vitamin B-complex
deficiencies are:
• Gingivitis
• Glossitis
• Glossodynia
• Angular cheilitis
• Inflammation of the entire oral mucosa
89. VITAMIN B1 DEFICIENCY-
MANIFESTATIONS
Affects both central and peripheral nervous system. Deficiency cause
typical neuralgia, hyperesthesia.
Leads to reduced capacity of cells to generate energy as it is required for
carbohydrate metabolism. So it is helpful in postsurgical healing.
90. VITAMIN B1 - PERIODONTAL
MANIFESTATIONS
Oral disturbances attributed to thiamine deficiency are:
Hypersensitivity, satiny appearance of the oral mucosa
Minute vesicles (simulating herpes) on the buccal mucosa,
under the tongue, or on the palate.
Erosion of the oral mucosa
91. VITAMIN B2 – RIBOFLAVIN
DEFICIENCY
Oral changes include glossitis; angular cheilitis;
seborrheic dermatitis; and superficial vascular
keratitis.
Tongue, oral mucosa and marginal gingiva show
purplish magenta discoloration and swelling.
92. In mild to moderate cases, dorsum exhibits a
patchy atrophy of the lingual papilla and
engorged fungiform papilla, which project as
pebble like elevations.
In severe deficiency, the entire dorsum is flat,
with a dry and often fissured surface.
93. Itching burning sensation of oral mucosa;
dryness, ulceration of marginal gingiva and
interdental papillae; marginal gingivitis,
periodontitis.
Its deficiency is often seen in chronic alcoholics
Primarily needed for breakdown of fat,
carbohydrate, proteins. So supplementation is
helpful in postsurgical healing.
95. Angular cheilitis, begins as an
inflammation of the commissure of the
lips, followed by erosion, ulceration and
fissuring.
Riboflavin deficiency is not the only
cause of angular cheilitis. Loss of vertical
dimension, together with drooling of
saliva into the angle of the lips, may
produce a condition similar to angular
cheilitis.
Candidiasis may develop in the
commissures of the debilitated persons,
lesion been termed as PERLECHE.
ORAL ULCERATION
ANGULAR CHEILOSIS
96. Supplemental riboflavin is ineffective
to resolve cases of glossitis and
angular cheilitis that are not caused
by vitamin deficiency.
ORAL ULCERATION
ANGULAR CHEILOSIS
97. VITAMIN B3 – NIACIN
DEFICIENCY
Niacin deficiency usually results in Pellagra
characterized by diarrhea, dermatitis and dementia. Also,
it results in glossitis, gingivitis and generalized stomatitis.
Fiery red lesions of oral mucosa and tongue with intense
burning
98. Oral manifestations of niacin deficiency
in experimental animals include:
• Black tongue
• Gingival inflammation with destruction of gingival, periodontal
ligament and alveolar bone.
• Gingivitis is extremely painful with wedge shaped punched out
ulcers involving interdental papillae and marginal gingiva.
• Lesions are necrotic, exudative and foul smelling.
• NUG (Necrotizing Ulcerative Gingivitis) and leucopenia are the
terminal features of niacin deficiency.
99. VITAMIN B7 (BIOTIN)
• Synthesized by bacteria in intestine, so deficiency is
rare.
• Deficiency seen after prolonged antibiotic therapy that
deplete intestinal flora
• It assist in utilization of other B complex vitamins and
promote proper carbohydrate metabolism
100. Biotin deficiency
Oral signs of biotin deficiency are
pallor of the tongue, and
patchy atrophy of the lingual papilla.
Although the pattern resembles geographic tongue, it is
confined to the lateral margins or is generalized to the
entire dorsum.
101. VITAMIN B9 (FOLIC ACID) DEFICIENCY –
MANIFESTATIONS
• Folic acid is required for DNA synthesis, so its deficiency leads
to macrocytic anemia with megaloblastic erythropoiesis,
accompanied by oral changes and gastrointestinal changes
(diarrhea and intestinal malabsorption).
• Folic acid deficient animals demonstrate necrosis of gingiva,
periodontal ligament and alveolar bone without inflammation.
The absence of inflammation is due to deficiency induced
granulocytopenia.
102. FOLIC ACID DEFICIENCY –
PERIODONTAL MANIFESTATIONS
Generalized stomatitis occur, accompanied by glossitis and cheilitis.
Ulcerative stomatitis is an early indication of the toxic effect of folic
acid antagonists (eg .Methotrexate) used in the treatment of
leukemia.
Gingival changes associated with pregnancy and oral
contraceptives may be partly related to suboptimal levels of folic
acid in the gingiva.
103. Fiery red tongue completely
Devoid of papilla
Folic acid deficiency
104. In a clinical study of pregnant women, a reduction in gingival
inflammation occurred with use of topical folate mouth rinses, but
no change was found with systemic folic acid.
Folate is reported to reduce gingival inflammation by binding to
endotoxins from bacterial plaque preventing irritation of gingiva.
Folic acid supplementation in patients taking phenytoin shows
reduction of phenytoin induced gingival enlargements; as
phenytoin reduces systemic absorption of folic acid.
105. VITAMIN B12 DEFICIENCY
A deficiency of vitamin B12 is rarely caused by insufficient dietary
sources unless strict vegan diets are followed.
Lack of intrinsic factor is the primary cause of deficiency. Intrinsic
factor helps in absorption of Vitamin B12
Pernicious anemia (a megaloblastic anemia) is one of the cause of
vitamin B12 deficiency. It occurs frequently in the elderly relative to
achlorhydria (decreased production of hydrochloric acid in the
stomach) and decreased synthesis of intrinsic factor by the parietal
cells.
106. VITAMIN B12 DEFICIENCY
Deficiency symptoms develop very slowly.
Vitamin B12 is required for RBC formation and function
107. • Symptoms:
• Glossopyrosis (unexplained pain of the tongue), followed
by swelling and pallor with eventual disappearance of the
filiform and fungiform papilla. The tongue may be
completely smooth, shiny and deeply reddened with loss
or distortion of taste.
Bright red, diffuse, excruciating painful lesions may
occur in the buccal, pharyngeal mucosa and
undersurface of the tongue.
108. Oral examination may reveal stomatitis or a pale or yellowish
mucosa, xerostomia, cheilosis, hemorrhagic gingival and bone loss.
Neurological symptoms like numbness or tingling, occur as a
consequence of demyelination of nerves. Deficiency symptoms are
relatively corrected with vitamin B12 injections.
In a totally vegan community, children with vitamin B12 deficiency
may have stunted growth. Other symptoms include anorexia (loss of
appetite), altered taste sensation, abdominal pain, and general
weakness.
110. CONCLUSION
Vitamin B1, B2, B3 help in energy production;
Vitamin B6 essential for amino acid
metabolism; Vitamin B12 and Folic acid
required for cellular division.
Dietary intake of Vitamin B complex increases
resistance to infection secondary to antibody
formation and proper functioning of WBC.
111. Studies have shown that its supplementation for 30 days
after flap surgery resulted in more clinical attachment
gain as compared to control group (Neiva RF; 2003). So
it restores periodontal health in post operative surgical
healing period.
113. Protein deficiency
• Protein depletion results in Hypoproteinemia with many
pathologic changes including muscular atrophy, weakness,
weight loss, anemia, leucopenia, edema, impaired lactation,
decreased resistance to infection, slow wound healing, lymphoid
depletion and reduced ability to form certain hormones and
enzyme systems.
114. Protein deficiency
Changes in periodontium
Protein deprivation causes the following changes in the
periodontium of experimental animals. Degeneration of the
connective tissue of the gingiva and periodontal ligament,
osteoporosis of alveolar bone, retardation in the deposition of
cementum, delayed wound healing.
116. Starvation
• In a study of controlled semi-starvation in young
adults there were no changes in the oral cavity or
skeletal system despite a 24% loss of body weight.
Another study showed a reduction in plaque index
scores and a considerable increase in gingival
index scores as the fasting period lengthened.
117. Starvation
In experimental animals, acute starvation results
in osteoporosis of alveolar bone and other bones,
reduction in the height of alveolar bone and
accentuated bone loss associated with gingival
inflammation.
120. ARTERIOSCLEROSIS
Both periodontal disease and arteriosclerosis increase with age.
Circulatory impairment induced by vascular changes may increase the
patient's susceptibility to periodontal disease.
Conversely, there is recent evidence to suggest that individuals with
periodontal disease may be at greater risk for heart disease as a result of
chronic periodontal infection and inflammation.
121. In experimental animals, partial ischemia of more than 10 hours' duration
created by arteriolar occlusion produces changes in the oxidative enzymes
and acid phosphatase activity and in the glycogen and lipid content of the
gingival epithelium. Focal necrosis followed by ulceration occurs in the
epithelium, with the junctional epithelium least affected.
Changes typical of periodontal disease do not occur. Ischemia is followed by
hyperemia, which is accompanied by metabolic changes and increased DNA
synthesis in the epithelium. The gingival response to arteriolar occlusion is
epithelial proliferation and thickening.
122. Tetralogy of Fallot
1. Ventricular septal defect
2. Pulmonary stenosis
3. Malposition of the aorta to the right
4. Compensatory right ventricular enlargement.
123. The oral changes include a purplish red discoloration of the lips and
gingiva; and sometimes severe marginal gingivitis with periodontal
destruction.
The discoloration of the lips and gingiva corresponds to the general
degree of cyanosis and returns to normal after corrective heart
surgery.
124. Eisenmenger’s Syndrome
Among patients with ventricular septal defects, about half
with large defects (>1.5 cm in diameter) develop
Eisenmenger syndrome. This syndrome is distinguished
by a greater blood flow from stronger left ventricle to the
right ventricle (backward flow) through the septal defect
causing increased pulmonary blood flow, which in turn
leads to progressive pulmonary fibrosis, small vessel
occlusion, and high pulmonary vascular resistance.
125. The natural history of a patient with untreated Eisenmenger’s
syndrome is a gradual increase in cyanosis over many years,
eventually leading to cardiac failure.
In cases of Eisenmenger syndrome, the lips, cheeks, and buccal
mucous membranes are cyanotic, but markedly less so than in
tetralogy of Fallot. Severe generalized marginal gingivitis may be
found.
128. CONNECTIVE TISSUE ALTERATIONS
Ehlers-Danlos Syndrome (EDS)
Covers a group of connective tissue disorders that
are characterized by defective collagen synthesis.
Autosomal dominant
Mainly affect the joints and skin.
Types IV and VIII have an increased susceptibility
to periodontitis.
129. CONNECTIVE TISSUE ALTERATIONS
Ehlers-Danlos Syndrome (EDS)
EDS Type VIII- in particular is associated with fragile
oral mucosa and blood vessels and severe generalized
periodontitis with the clinical appearance of generalized
early-onset periodontitis.
In EDS Type VIII - there is considerable interfamilial
variability but the distinguishing finding is periodontitis,
resembling clinically the early-onset form, leading to
premature loss of permanent teeth.
130. Marfan Syndrome
Generalized disorder of connective tissue with skeletal, ocular and
cardiovascular malformations. Characteristically, these patients
are tall and thin with arachnodactyly and joint hypermobility.
In the case of Marfan syndrome, periodontitis manifests in a
chronic and severe form with patterns of both horizontal and
vertical bone resorption, and in accordance to the presence of
bacterial plaque.
131. Marfan Syndrome
Dental mobility has been shown to be due
to periodontitis, and is not attributable to
the primary condition of the syndrome.
132. . Genetic disorder caused by defective
mineralization, in which bones and teeth could
not take up calcium and phosphorus.
Bones remain soft and fracture easily.
Caused by mutation in alkaline phosphatase
(ALPL) gene leading to low activity of tissue
nonspecific alkaline phosphatase enzyme.
Alkaline phosphatase is required for
mineralization of bones and teeth.
Hypophosphatasia
133. .
Severe loss of alveolar bone and premature loss of
the deciduous teeth, particularly anterior teeth.
Microscopically, the teeth show either complete loss
of cementum or isolated areas of cementum
resorption
Hypophosphatasia
134. Chronic Granulomatous Disease
Hereditary disease in which certain immune cells have
difficulty forming reactive oxygen compounds mainly
superoxide radical used to kill ingested pathogens. This
leads to formation of granulomas in many organs.
Inability of Neutrophils and macrophages to mount
respiratory burst and kill invading bacteria and fungi
135. Chronic Granulomatous Disease
Oral findings (Najla S Dar-Odeh et al,2010)
Oral ulcers, gingivitis, periodontitis, mucositis on upper lip,
oral candidiasis, geographic tongue, caries; if oral hygiene
is not maintained
136. Chronic Granulomatous Disease
Hereditary disease in which certain immune cells have
difficulty forming reactive oxygen compounds mainly
superoxide radical used to kill ingested pathogens. This
leads to formation of granulomas in many organs.
137. Glycogen storage disease type 1b
Autosomal recessive disorder caused by a defect in the glucose-6-phosphate
transporter protein.
Clinical features :‘‘doll like’’ facial appearance, stunted growth, hypoglycemia,
ketosis, lactic acidosis, hyperlipidemia, gout, and bleeding episodes brought on by
impaired platelet function secondary to metabolic disorders.
Additional distinguishing features of glycogen storage disease type 1b are
neutropenia, neutrophil dysfunction, and an increased susceptibility to infection.
Defects in both random and directed PMN migration.
138. Reports of oral disease in glycogen storage disease type 1b
patients are common & include:
Oral Ulceration
Candidiasis
Gingivitis And Periodontitis.
141. SJOGREN’S SYNDROME
• dryness of the eyes and mouth.
Primary -sicca
syndrome
• triad of dry eyes with keratoconjunctivitis sicca,
xerostomia and an associated autoimmune
disease, usually rheumatoid arthritis
Secondary form
• 2.2 higher risk of having adult periodontitis.
Study by
Najera et al
(1997)
142. RHEUMATOID ARTHRITIS
Occurrence of Sjogren’s syndrome in approx. 15% of such patients.
More than 50% of Sjogren’s patients are affected by rheumatoid
arthritis.
deterioration of TMJ
loss of vertical dimension of the condyle anterior open bite.
excessive occlusal forces in the molar regions
lost bone support from extrusion of the anterior teeth.
143. LUPUS ERYTHEMATOSUS
• chronic autoimmune disease that affects the connective tissue and multiple
organ systems.
An increased incidence of infection in systemic lupus erythematosus patients is
an often-reported finding. It is estimated that at least 50% of systemic lupus
erythematosus patients suffer an infection during the course of the disease.
Hematologic disorders that may explain this increased incidence of infection
are a tendency to neutropenia and various neutrophil abnormalities.
Oral manifestation - formation of multiple white plaques with dark, reddish or
purple margins with a tendency to form telangiectasia and ulceration.
144. DC Calderaro et al (2016) showed association of
periodontitis and systemic lupus erythematosus
due to common genetic predisposition (shared
polymorphisms). More studies are awaited.
145. PROGRESSIVE SYSTEMIC
SCLEROSIS AND CREST
SYNDROME
Most conspicuous oral manifestation - fibrosis of the facial skin to affect
35% of Sjogren’s syndrome patients. 39% of patients complained of
dysphagia and 28% reported limited mouth opening as a consequence
of the sclerosis.
The advanced progression of facial tissue fibrosis has been described as
the cause for resorption of the mandibular bone in the area of the
mandibular angles .
146. PROGRESSIVE SYSTEMIC
SCLEROSIS AND CREST
SYNDROME
A relatively characteristic oral manifestation of progressive
systemic sclerosis is the radiographic demonstration of apparent
widening of the periodontal ligament space. This typically affects
posterior teeth and the periodontal ligament space may be
increased as much as 3-4 times the normal thickness.
149. Metallic Pigmentation
Occurs in patients working in metal industry as they
contain metal in their blood. (It is not toxicity and normal
condition)
Occurs only in inflamed gingiva and disappears after
scaling and root planing.
In inflammation due to increase in vascular permeability,
plasma comes out along with metal in it. These metals
form metallic sulphides in perivascular areas giving color
to gingiva
150. Bismuth pigmentation in the oral cavity
narrow, bluish-black discoloration of the
gingival margin in areas of preexistent
gingival inflammation.
Such pigmentation results from the
precipitation of particles of bismuth
sulfide associated with vascular changes
in inflammation.
151. Bismuth pigmentation in the oral cavity
It is not evidence of intoxication but
simply indicates the presence of bismuth
in the bloodstream.
Bismuth pigmentation in the oral cavity
also occurs in cases of intoxication. It
assumes a linear form if the marginal
gingiva is inflamed.
152. Lead Intoxication.
Pallor of the face and lips and gastrointestinal symptoms
consisting of nausea, vomiting, loss of appetite, and
abdominal colic.
Peripheral neuritis, psychologic disorders, and
encephalitis have been reported.
153. Lead Intoxication
Oral signs- salivation, coated tongue, a peculiar sweetish
taste, gingival pigmentation, and ulceration.
The pigmentation of the gingiva is linear (burtonian line),
steel gray and associated with local irritation. Oral signs
may occur without toxic symptoms.
154. Mercury Intoxication
Headache, insomnia, cardiovascular symptoms, pronounced salivation (ptyalism),
and a metallic taste.
Gingival pigmentation in linear form results from the deposition of mercuric sulfide.
The chemical also acts as an irritant, which accentuates the preexistent
inflammation and commonly leads to notable ulceration of the gingiva and adjacent
mucosa and destruction of the underlying bone.
Mercurial pigmentation of the gingiva also occurs in areas of local irritation in
patients without symptoms of intoxication.
155. TREATMENT
When inflammation subsides, vascular permeability decreases and the
discoloration disappears. So treatment in these patients is only scaling
and root planing.
157. Vascular
constriction
of the blood
vessels of
the gingiva
Immune
deleterious
effects on
leukocyte
function.
suppress serum
antibody levels to
certain periodontal
bacteria.
suppresses
production of the
IgG2 both in
patients with
periodontitis and
in those with
normal
periodontium.
Direct
effects on
tissues
cytotoxic
substances
can
penetrate
the
epithelium
and may
exert
deleterious
effects on
fibroblasts.
Bone
decreases
intestinal
absorption of
calcium and
may thereby
affect
osteoblast
function and
increase
bone loss in
otherwise
healthy
postmenopau
sal women.
Healing
Postsurgical
healing may
be interfered
with by
absorption
of the toxic
substances
in tobacco
smoke by
the root
surfaces.
159. Progression of periodontitis is influenced by variety of risk
factors. In general, these factors do not initiate chronic
destructive periodontitis, but they may predispose,
accelerate, or otherwise increase its progression toward
periodontal tissue destruction. With the large array of
factors that influence the development and progression of
periodontitis, understanding what the relationships of these
factors and determinants are to the initiation and
progression of periodontal disease is very important to
prevent and treat periodontal disease.