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CLASSIFICATION
Nutritional
Influences
Endocrine
Influences
Hematologic
Disorders
Genetic
Disorders
Effect of
systemic drug
therapy
Collagen
Vascular
Diseases
Cardiovascular
Diseases
Psychosomatic
Disorders
Other Systemic
Conditions-
Metal
Intoxication
Systemic conditions & Systemic disorders
Various systemic factors that play role in etiology of periodontal disease are as
follows:
"INFLUENCE OF SYSTEMIC DISEASES (CONDITIONS) ON PERIODONTIUM" -PART-2
INDEX
 HEMATOLOGICAL DISEASES
 Red blood cell disorders
 Platelet disorders
 White blood cell disorders
 SYSTEMIC DRUG THERAPY DISORDER
 Drug induced Gingival enlargements
 PSYCOSOMATIC DISORDER
 Stress
INDEX
 NUTRITIONAL DEFICIENCY DISEASES
 Fat soluble vitamins
 Water soluble vitamins
 Protein deficiency
 Starvation
 CARDIOVASCULAR DISEASE
 Arteriosclerosis
 Tetralogy of Fallot
 Eisenmenger’s Syndrome
INDEX
GENETIC DISORDERS
 Connective tissue alterations
 Immune alterations
 COLLAGEN VASCULAR DISEASE
 Sjogren’s syndrome
 Rheumatoid arthritis
 Lupus erythematosus
 Progressive Systemic Sclerosis and Crest Syndrome
INDEX
 METAL INTOXICATION
 Bismuth intoxication
 Lead intoxication
 Mercury intoxication
 SMOKING
HEMATOLOGIC
DISORDERS
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.
RED BLOOD CELL
DISORDERS
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
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.
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
Anemia
Classification according to cellular morphology & cellular content
i) Macrocytic hyperchromic (pernicious anemia)
ii) Microcytic hypochromic (iron deficiency anemia)
iii) Normocytic normochromic (hemolytic or aplastic anemia)
iv) Sickle cell anemia
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)
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
PLATELET
DISORDERS
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.
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
WHITE BLOOD
CELL
DISORDERS
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.
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.
Periodontium in Leukemic Patients
Oral and periodontal manifestations of leukemia consist of
 Leukemic infiltration
 Bleeding
 Oral ulcerations & infections.
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.
 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%)
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.
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.
Clinical and microscopical picture seen in leukemic patients
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.
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
Leukocyte (Neutrophil) Disorders
Secondary neutrophil impairment
i) Down syndrome
ii) Papillon-Lefevre syndrome
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.
• 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
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
• 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
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
• 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.
• 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.
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
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
• 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.
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
• 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
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)
Oral and skin lesions seen in a patient of 17 years with papillon – lefevre syndrome
 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.
Patient unable to chew food because of
inflammation, mobile teeth, multiple
abscesses and food impaction
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.
SYSTEMIC DRUG
THERAPY
DISORDERS
Drug – Induced gingival
enlargement
• Anticonvulsants
• Immunosuppressants
• Calcium channel blockers
• Idiopathic
Psychosomatic
Disorders
STRESS
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
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.
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
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
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.
•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)
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
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.
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.
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.
NUTRITIONAL
DEFICIENCY
DISEASES
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.
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.
FAT-SOLUBLE
VITAMIN
DEFICIENCY
VITAMIN A
VITAMIN D
VITAMIN E
VITAMIN A
 Essential for epithelial cell differentiation, humoral
antibody response and cell mediated immunity
 Antioxidant
 Supplement periodontal treatment
VITAMIN A DEFICIENCY
 Dermatologic, mucosal, and ocular manifestations.
 Degenerative changes occur in epithelial tissues -
keratinizing metaplasia.
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.
• 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.
• 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.
• 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
• 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.
• 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.
WATER-SOLUBLE
VITAMIN
DEFICIENCY
VITAMIN C
VITAMIN B
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.
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.
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.
"INFLUENCE OF SYSTEMIC DISEASES (CONDITIONS) ON PERIODONTIUM" -PART-2
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
- In long standing cases, tissues attain a dark blue or purple hue.
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
• 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
• 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.
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.
VITAMIN B-COMPLEX – INCLUDE
 Vitamin B1 (Thiamin)
 Vitamin B2 (Riboflavin)
 Vitamin B3 (Niacin)
 Vitamin B7 (Biotin)
 Vitamin B9 (Folic Acid)
 Vitamin B12
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
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.
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
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.
 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.
 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.
FISSURED TONGUE
 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
 Supplemental riboflavin is ineffective
to resolve cases of glossitis and
angular cheilitis that are not caused
by vitamin deficiency.
ORAL ULCERATION
ANGULAR CHEILOSIS
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
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.
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
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.
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.
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.
Fiery red tongue completely
Devoid of papilla
Folic acid deficiency
 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.
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.
VITAMIN B12 DEFICIENCY
 Deficiency symptoms develop very slowly.
 Vitamin B12 is required for RBC formation and function
• 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.
 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.
PERNICIOUS ANAEMIA
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.
 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.
PROTEIN
DEFICIENCY
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.
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.
STARVATION
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.
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.
CARDIOVASCULAR DISEASE
CARDIOVASCULAR DISEASES
Arteriosclerosis
Congenital
Heart Disease
Tetralogy of
Fallot
Eisenmenger’s
Syndrome
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.
 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.
Tetralogy of Fallot
1. Ventricular septal defect
2. Pulmonary stenosis
3. Malposition of the aorta to the right
4. Compensatory right ventricular enlargement.
 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.
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.
 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.
GENETIC DISORDERS
GENETIC DISORDERS
Connective tissue alterations:
Marfan syndrome
Ehler-Danlos syndrome.
Immune alterations
Neutrophil disorders
Hypophosphatasia
Chediak-Higiashi syndrome
Down syndrome
Papillon-Lefèvre syndrome
Chronic granulomatous disease,
Glycogen storage disease type-1b
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.
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.
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.
Marfan Syndrome
 Dental mobility has been shown to be due
to periodontitis, and is not attributable to
the primary condition of the syndrome.
 .  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
 .
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
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
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
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.
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.
Reports of oral disease in glycogen storage disease type 1b
patients are common & include:
 Oral Ulceration
 Candidiasis
 Gingivitis And Periodontitis.
COLLAGEN VASCULAR DISORDERS
COLLAGEN VASCULAR
DISEASE
 Sjogren’s syndrome
 Rheumatoid arthritis
 Lupus erythematosus
 Progressive Systemic Sclerosis and Crest
Syndrome
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)
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.
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.
 DC Calderaro et al (2016) showed association of
periodontitis and systemic lupus erythematosus
due to common genetic predisposition (shared
polymorphisms). More studies are awaited.
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 .
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.
Uniform widening of pdl space in systemic sclerosis
OTHER SYSTEMIC CONDITIONS
METAL INTOXICATION
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
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.
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.
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.
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.
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.
TREATMENT
When inflammation subsides, vascular permeability decreases and the
discoloration disappears. So treatment in these patients is only scaling
and root planing.
TOBACCO USE
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.
CONCLUSIO
N
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.

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"INFLUENCE OF SYSTEMIC DISEASES (CONDITIONS) ON PERIODONTIUM" -PART-2

  • 1. CLASSIFICATION Nutritional Influences Endocrine Influences Hematologic Disorders Genetic Disorders Effect of systemic drug therapy Collagen Vascular Diseases Cardiovascular Diseases Psychosomatic Disorders Other Systemic Conditions- Metal Intoxication Systemic conditions & Systemic disorders Various systemic factors that play role in etiology of periodontal disease are as follows:
  • 3. INDEX  HEMATOLOGICAL DISEASES  Red blood cell disorders  Platelet disorders  White blood cell disorders  SYSTEMIC DRUG THERAPY DISORDER  Drug induced Gingival enlargements  PSYCOSOMATIC DISORDER  Stress
  • 4. INDEX  NUTRITIONAL DEFICIENCY DISEASES  Fat soluble vitamins  Water soluble vitamins  Protein deficiency  Starvation  CARDIOVASCULAR DISEASE  Arteriosclerosis  Tetralogy of Fallot  Eisenmenger’s Syndrome
  • 5. INDEX GENETIC DISORDERS  Connective tissue alterations  Immune alterations  COLLAGEN VASCULAR DISEASE  Sjogren’s syndrome  Rheumatoid arthritis  Lupus erythematosus  Progressive Systemic Sclerosis and Crest Syndrome
  • 6. INDEX  METAL INTOXICATION  Bismuth intoxication  Lead intoxication  Mercury intoxication  SMOKING
  • 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
  • 13. Anemia Classification according to cellular morphology & cellular content i) Macrocytic hyperchromic (pernicious anemia) ii) Microcytic hypochromic (iron deficiency anemia) iii) Normocytic normochromic (hemolytic or aplastic anemia) iv) Sickle cell anemia
  • 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.
  • 27. Clinical and microscopical picture seen in leukemic patients
  • 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
  • 30. Leukocyte (Neutrophil) Disorders Secondary neutrophil impairment i) Down syndrome ii) Papillon-Lefevre 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.
  • 49. Drug – Induced gingival enlargement • Anticonvulsants • Immunosuppressants • Calcium channel blockers • Idiopathic
  • 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.
  • 87. VITAMIN B-COMPLEX – INCLUDE  Vitamin B1 (Thiamin)  Vitamin B2 (Riboflavin)  Vitamin B3 (Niacin)  Vitamin B7 (Biotin)  Vitamin B9 (Folic Acid)  Vitamin B12
  • 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.
  • 127. GENETIC DISORDERS Connective tissue alterations: Marfan syndrome Ehler-Danlos syndrome. Immune alterations Neutrophil disorders Hypophosphatasia Chediak-Higiashi syndrome Down syndrome Papillon-Lefèvre syndrome Chronic granulomatous disease, Glycogen storage disease type-1b
  • 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.
  • 140. COLLAGEN VASCULAR DISEASE  Sjogren’s syndrome  Rheumatoid arthritis  Lupus erythematosus  Progressive Systemic Sclerosis and Crest Syndrome
  • 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.
  • 147. Uniform widening of pdl space in systemic sclerosis
  • 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.