Introduction:

An interrelationship between periodontal diseases of systemic health has

been implicated in the past few decades. Inflammation is the primary pathologic feature of periodontal disease and bacterial plaque is the essential etiologic factor responsible for inducing host in host inflammatory process. Individuals susceptibility to periodontitis is influenced by certain factors including systemic diseases and conditions, stress host immune response and host susceptibility. Certain systemic disorders and conditions alter host tissue and physiology which may impair host barrier integrity and host defense to periodontal infection, resulting in more destructive disease. A number of environmental, physical, psychosocial factors have the potential to alter periodontal tissues and the host immune response, resulting in more severe periodontal diseases expression. These disorders and conditions may predispose, accelerate or otherwise increase the progression of periodontitis but never initiate it.

INFLUENCE OF STRESS & PSYCHOSOMATIC DISORDER

Psychosocial stress has been implicated as one of the risk indicators for periodontal disease. Most notable example is relationship between stress and ANUG. Relationship between stress and other forms of periodontal disease (e.g., chronic periodontitis) difficult to elucidate because etiology and pathogenesis of periodontal disease are multifactorial and role of stress alone is difficult to define.

Psychosocial stress, Depression & coping

Case control studies revealed relation between chronic periodontitis, Life events and social demographs showed

Individuals with stable life style (married, employed) and minimal negative life events

Individuals with less stable lifestyle (unmarried, unemployed) and more negative life events

Less periodontal disease destruction

More periodontal destruction

Its now apparent that the effect is according to type of stress as well as the ability of individuals to cope with stress that correlate with destructive periodontal diseases

Chronic or long term types of stress and the life events which are less likely to be controllable by individual, such as

Loss of spouse Loss of family member Failed relationship Loss of employment Financial difficulties rendering the feeling of unhappiness The duration of stressful life destruction. Financial stress: Is our example of long term constant pressure that may exacerbate periodontal destruction in susceptible individuals. Individuals with high levels of financial stress of poor coping skills had twice as much periodontal disease as those with of impact of stress on periodontal health. Minimal stress and good coping skills Individuals with Problem focused (Practical) Coping skills fared better w.r.t. periodontal disease Studies showed, patient with periodontal disease were less likely to use active coping skills (i.e., situation control) and more likely to cope with stress by averting blame (emotional) than were periodontally healthy individuals. So the conclusion, that the influence of stress on periodontal disease destruction is the manner in which the individual copes with stress. Emotional coping is more common in situations that must be accepted, and by individuals who feel helpless in situation. Emotional coping methods appear to render the host more susceptible to destructive effects of periodontal disease than do practical coping methods therefore one must consider level of stress and strain that patient may experience Emotional focused (avoidance) coping skills influences on total impact of stress-induced disease

and also adequacy of their coping mechanism in assessing of impact of stress on periodontal health Stress mediates multiple changes in Endocrine System Stress and poor coping mechanism increase in salivary control Secretory IgA decrease internal colonization by pathogens IgG opsonizes bacteria so that they can be phagocytosed and killed by neutrophils

Stress- Induced Immosuppression Stress impacts the periodontal health through changes in individuals behaviors and through complex interactions among nervous, endocrine & immune system

Individuals under Stress

Have poor oral hygiene

Smoke frequently

Less likely to seek Professional care

Start or increase Clenching and grinding of their teeth

Alteration in immune system

Influence Periodontal disease destruction

Stress related immune system changes :-

1.

Production of cortisol Stress Increased ACTH released from pituitary Increased cortisol released form adrenal cortex Suppress immune response through

Suppressing Neutroplil activity All of which are critical in host Ig G production immunoinflammatory response Salivary IgA production to PD pathogen Increased Potential for destruction by periodontal pathoegens Stress Affect cellular immune response Increase release of neurotransmitters (epinephrine, norepinephrine neurokinin, substance P)

through

Which interact directly with Lymphocytes, Neutrophils, Monocytes / Macrophages via receptors. Immunosuppression Increased potential for destruction of tissues by periodontal pathogens

Note : Stress is one of the predisposing factor to destruction from periodontitis but the presence of periodontal pathogen is essential etiological factor Stress alone doesnt cause or lead to periodontitis in absence of periodontal pathogen.

Influence of Stress on Periodontal Therapy Outcomes:

Psychological situations such as stress and depression may also influence the outcome of periodontal therapy Conclusion: Stressful life events and individuals personality and coping skills are factors considered in assessing risk of periodontal disease destruction and potential for successful periodontal therapy. Depression might have a negative effect on periodontal treatment outcomes. Identify patients with emotional or defensive coping skills, care should be taken to ensure that they receive information in manner that doesnt elicit a defensive reaction.

Psychiatric influence of self inflicted injury

Self inflicting injury to Periodontium Psychosomatic disorders Development of neurotic habits (habitual trauma induced by) Grinding Injurious to periodontium and teeth Clenching teeth Nibbling on foreign objects Nail biting Excessive tobacco use

Self inflicted injuries Self inflicted Lesions are usually isolated to 1 area of mouth

Gingival injuries Like gingival recession In adult and children Not common in Psychiatric patients

TREATMENT :a. Identification of habit b. Education of patient c. Appropriate follow-up

NUTRITIONAL INFLUENCES
Research conducted upto present, doesnt support this view but the majority of opinions and research findings of the effects of nutrition on oral and periodontal tissues point to the following: 1. There are no nutritional deficiencies that by themselves can cause gingivitis or periodontitis. However, nutritional deficiencies can affect the condition of periodontium and thereby may accentuate the deleterious effects of plaque-induced inflammation in susceptible individuals. 2. There are nutritional deficiencies that produce changes in oral cavity. These changes include alterations of tissues of the lip, oral mucosa, gingiva and bone. These alterations are considered to be periodontal and oral manifestations of nutritional disease.

Vitamin Deficiency
Vit. A deficiency: Dermatologic, mucosal and degeneration of conductive tissue in gingiva,
PDL osteoporosis of alveolar bone Oral Changes : Impaired Cementum deposition Atrophy of tongue epithelium Delayed wound teealing

Protein deficiency accentuates destructive effects of bacterial plaque and occlusal trauma on periodontal tissue.

Other systemic conditions:

Hypophosphatasia: Rare familial skeletal disease Characterized by :o Rickets, poor cranial bone formation,craneostenosis. o Premature lors of deciduous or secondary teeth with no gingival inflammation. o Reduced cementum formation. Congenital Heart Disease Tetralogy of Fallot Eissenmengers syndrome. Shunting of deoxygenated blood from Right to left Cyanosis, clubbed fingers, edema of toes and fingers. Cyanosis of lip & oral mucosa. Enamel hypoplasia- Delayed eruption of primary & secondary teeth. Bluish white appearance of teeth with pulp vascular volume. Gingival disease in children.

Metal IntoxicationSystemic absorption of certain heavy metals -Pigmentation or discoloration of oral mucosa specially which is present in medicinal compound. & there industrial contact, results in oral manifestation. Bismuth intoxication: - Ulcerative gingivo-stomatitis Bluish Black pigmentation, metallic taste, burning sensation of oral mucosa sore and inflamed tongue. Bluish -Discoloration of gingival margin in areas of preexisting gingival inflammation. urticaria, exanthematous eruptions, bullous & purpuric lesions. Bismuth pigmentation assumers a linear form if marginal gingiva is inflamed. Lead Intoxication:-Gingival pigmentation is linear (Burton Ian line), steel gray and associated with local inflammation Pallor of face and lips Nausea, vomiting, lors of appetite, abdominal colic. Peripheral neuritis, psychologic disorder, encephalitis.

Mercury Intoxication:-Gingival pigmentation is linear form results from deposition of Hg 2S. The chemical also act as an irritant, which accentuates pre exiting inflammation and often leads to notable ulceration of gingival and adjacent mucosa and destruction of underlying bone, headache, insomnia, pronounced salivation metallic taste, cardiovascular symptoms. Phosphorus, chromium, Arsemic intoxication Necrosis of Alveolar Bone, loosening & exfoliation of teeth. Inflammation & ulceration of gingiva Benzene intoxication Gingival bleeding Gingival ulceration Destruction of underlying bone Metals that have been absorbed systemically are carried in blood stream & they precipitate in to tissue from blood vessels. Therefore when inflammation is present in vascular permeability increases metals are more likely to be deposited in gingival tissues

ROLE OF HAEMATOLOGIC DISORDERS

All blood cells play an essential role in maintenance of a healthy periodontium. WBCs are involved in inflammatory reaction & are responsible for cellular defense against microorganism as well as for pro inflammatory cytokine release .RBCs are responsible for gas exchange and nutrient supply to periodontal tissues & platelets & are necessary for normal homeostasis as well as recruitment of cells during inflammation & wound healing.

[A]

LEUKEMIA
It is malignant neoplasia of WBC precursors especially in bone marrow. Its characterized by i. ii. iii. Diffuse replacement of bone marrow with proliferating leukemic cells. Abnormal numbers & forms of immature WBCs in the circulating blood. Widespread infiltrates in liver, spleen, lymph nodes & other body sites.

According to lineage of WBCs involved, leukemia is classified as

Lymphoid (Lymphoblastic, Lymphocytic leukemias)

Myeloid Involving progenitor cells that gives rise to erythrocytes, granulocytes, monocytes and platelets

According to their evolution

Acute Primitive Blast cells are released into peripheral circulation.

Sub acute or chronic The abnormal cells tend to be more mature with normal morphologic characteristics & function when released into the circulation.

Leukemia results in Decreased production of RBC Decreased production of WBC Decreased production of Platelets

Leading to: Anemia Results in poor tissue oxygenation making tissue more friable & susceptible to breakdown Leucopenia Leads to increased susceptibility to infection Thrombocytopenia Leads to increased bleeding tendency especially in oral cavity

Oral Manifestations: Periodontium in leukemic patients: Leukemic infiltration Oral ulceration Bleeding Infections

a) Leukemic infiltration- into the gingiva & less frequently the alveolar bone. Gingival infiltration results in leukemic gingival enlargements. Leukemic gingival enlargement is not found in edentulous patients or in patient with chronic leukemia. Clinically: gingiva appears initially blush red & cyanotic, with a rounding & tenseness of gingival margin, then it in size, often in interdental papilla & partially covering the crowns. Leukemic gingival enlargement consists of basic infiltration of gingival corium by leukemic cells that gingival thickness & creates gingival pockets where bacterial plaque accumulates, initiating secondary inflammatory lesion that contributes to enlargement of gingival. Microscopically: Dense, diffuse infiltration of immature leucocytes in attached & marginal gingiva Mitotic figures may be seen. Leukemic cells displace normal connective tissue of gingiva Distension of blood vessels & contain predominantly leukemic cell. Reduction in number of RBCs. Epithelium may be thinned or hyperplasic. Degeneration associated with intracellular and intercellular edema and Leukocytic infiltration Microscopically, marginal gingiva differs from that of other gingival locations and it exhibits a notable inflammatory component in addition to leukemic cells Scattered foci of plasma cells & lymphocyte with edema and demarcation are present at marginal gingiva. Inner aspect of marginal gingiva is usually ulcerated and marginal necrosis with pseudomembrane formation is present PDL and alveolar bone may also be involved in acute and subacute leukemia PDL may be infiltrated with mature and immature Leukocytes

Localised area of necrosis, thrombotic blood vessels, infiltration of mature and immature leukocytes, occasionally RBCs and replacement of fatty marrow by fibrous tissue are seen in marrow of alveolar bone.

Bleeding :

Gingival hemorrhage can be early sign of leukemia o Gingival bleeding is an oral manifestation seen in acute form o It is caused by thrombocytopenia and from the inhibition of normal stem cell function by leukemic cells or their products. o Petechiae can be seen on skin and oral mucosa o A more diffuse submucosal bleeding manifests as Ecchymosis is also seen o Bleeding may also be a side effect of the chemotherapeutic agents used to treat leukemic

Oral Ulceration & Infections: Granulocytopenia (diminished WBC count) results from the displacement of normal bone marrow cells by Leukemic cells, which increase the host susceptibility to opportunistic microorganisms and leads to ulcerations and infections. Discrete, punched out ulcers penetrate deeply into submucosa and covered by firmly attached white slough, seen on oral mucosa. Lesions occur in sites of trauma such as the buccal mucosa or on the palate. Atypical large recurrent heretic ulcers are seen in patients with past history of herpes infection Exogenours Bact. Infection Or Existing Bact. Infection Gingival or periodontal Disease Cause Gingival (bacterial) infection

Clinically: - Inflamed gingiva, spongelike & friable Peculiar bluish red Bleeds persistently on slightest provocation or even spontaneously in leukemic patients Susceptible to Bacterial infection Cause Acute gingival necrosis Pseudo membrane formation

In Chronic leukemia oral manifestation (of a hematologic disturbance are) rare

Microscopic : Replacing normal fatty marrow of jaws with islands of mature lymphocytes or lymphocytic infiltration of marginal gingiva without clinical manifestation.

ANAEMIA
It is deficiency (in the quantity or quality of the blood) manifested as reduction in the number of erythrocytes & in the amount of hemoglobin. Blood loss Defective Blood formation Increased RBC destruction According to cellular morphology and teb content Results Anemia

1. Macrocytic hyperchromic Anemia (pernicious Anemia) 2. Microcytic hypochromic Anemia (iron deficiency) 3. Sickle cell Anemia 4. Normocytic Normochromic (Hemolytic or Aplastic)

Pernicious Anemia
Marked pallor in the gingiva Tongue appears red, smooth and shiny Syndrome consisting of glossits and ulceration of oral mucosa of oropharynx, inducing dysphagia (Plummer Vinson Syndrome)

Sickle Cell Anemia

Its hereditary form of chronic hemolytic anemia Occurs exclusively in blacks Characterised by pallor, jaundice, weakness, rheumatoid manifestations, leg ulcers Osteoporosis of one jaw Peculiar stepladder alignment of the trabeculae of the interdental septa Pallor and yellowish discoloration of oral mucosa

Aplastic Anemia
It results from failure of bone marrow to produce erythrocytes Etiology is usually the effect of toxic drugs on the marrow or displacement of RBCs by leukemic cells Pale discoloration of the oral mucosa and increased susceptibility to infection because of the concomitant neutropenia.

THROMBOCYTOPENIA
It describes the condition of reduced platelet count resulting from either lack of platelet production or increased loss of platelet

Purpura refers to purplish appearance of the skin or mucous membranes where bleeding has occurred as a result of decreased platelets. Thrombocytopenic purpura may be idiopathic or may occur secondary to some known etiologic factor responsible for a reduced amount of functioning marrow and resultant reduction in the number of circulating platelets. Such etiologic factors Marrow aplasia Replacement of marrow by tumor Destruction of the marrow by irradiation or radium or by drugs Characterized by Low platelet count Increase clot retraction Bleeding time Slightly prolonged clotting time Petechiae & hemorrhagic vesicles occur in oral cavity, particularly in the plate, tonsillar pillar and the buccal mucosa Gingiva are swollen, soft & friable Bleeding occurs spontaneous or on the slightest provocation.

LEUKOCYTE (NEUTROPHIL) DISORDER :

Affect production or function of Leukocytes result Severe periodontal destruction a) Neutropenia Results in low levels of neutrophils Individuals with Absolute Neutophil count (ANC) < 1500 cells / l is neutropenic Causes Genetic Drug Induced

Viral infection Neutopenia Can be i. ii. iii. iv. v. i) Cyclic Chronic Begin neutropenia of childhood Benign Familial neutropenia Secure Familial neutropenia Chronic idiopathic neutropenia

In cyclic form there is cyclic depression of PMNs in peripheral Blood a. Cyclic intervals : Between 19 & 21 days b. Clinical problem : Pyrexia, oral ulceration, inflamed gingiva, rapid periodontal breakdown, alveolar bone loss, aggressive periodontitis

ii)

Chronic benign neutropenia of childhoods onset is between 6-20 months and mostly its a self limiting condition in many patients Periodontal manifestation Bright red, hyperplastic edematous gingiva, gingival bleeding on probing, varying degree of gingival recession and pockets, area of desquamation.

iii)

Bengin Familial neutropenia is transmitted as autosomal dominant trait hypreplastic gingivitis, edematous bright red appearance, bleeding on probing, marked bone loss

iv)

Chronic idiopathic neutropenia is persistent from birth and isnt cyclical. Severe persistent gingivitis with cherry red edematous appearance.

[B] AGRANULOCYTOSIS :It is reduction in circulating granulocytes which results in Ulcerative necrotizing lesions of oral
mucosa, skin and GIT and Genitourinary tract. Cause: Drug idiosyncrasy (After administering aminopyrine, barbiturates and their derivatives , arsenical agents, sulfonamide, benzene ring derivative )or Idiopathic

SIGNS :

Fever, malaise, sore throat, general weakness

& SYMPTOMS

Ulcerations in oral cavity, oropharynx and throat is characteristic Grey and black isolated necrotic patches are on mucosa, sharply demarcated from uninvolved areas.

Striking feature:

Absence of inflammatory reaction due to lack of granulocytes Fetid odour, increase salivation, gingival hemorrhage necrosis

[C]
[D]

CHEDIAK HIGASHI SYNDROME

Affects the production of organelles found in every cell. Affects mostly : Melanocytes, platelets & phagocytes Its a genetically transmitted disease in ranch raised mink Partial albinism, mild bleeding disorders, recurrent bacterial infections Aggressive periodontitis has been described in such patients LAZY LEUKOCYTE SYNDROME Characterized by susceptibility to severe microbial infections, neutropenia, abnormal

inflammatory response, defective chemotactic response by neutrophil [E] LEUKOCYTE ADHESION DEFICIENCY (LAD) Rare genetic disease inability to produce or failure to express cell surface integrin (CD18) LAD Leukocytes cannot effectively adhere to vessel wall near site of infection Cannot migrate to infection Bacterial infection continues to destroy host tissue Respiratory tract infections, otitis media, rarely periodontal disease attributed to LAD

Oral Changes :Both primary and permanent teeth are affected, resulting in changes premature tooth loss Extremely acute inflammation and proliferation of gingiva Rapid destruction of Bone

[F]

PAPILLON LEFEVRE SYNDROME Inherited, autosomal recessive trait Parents must be the carrier of autosomal genes, to affect one offspring

Characteristics :

Hyperkeratotic skin lesion Severe destruction of periodontium Calcification of the dura Skin lesions: hyperkeratosis and ichthyosis of localized area on palm, soles, knee, elbow

Oral manifestation : Early inflammatory changes leading to bone loss and exfoliation of teeth Primary teeth are lost by 5-6 years Permanent teeth erupt normally but are lost within few years because of destructive periodontal disease. Microscopic: Marked chronic inflammation of lateral walls of pocket with predominantly plasma cell infiltrate Considerable osteoclastic activity Apparent lack of osteoblastic Thin cementum By 15 yrs patients are usually edentulous except 3rd molar Tooth extraction sites heal uneventfully

[G]

DOWNS SYNDROME o Trisomy 21 o Congenital disease caused by trisomy of chromosome no. 21 o Mental deficiency and growth retardation

Oral manifestations Malocclusions High frenum attachments Crowding of teeth Diastemata Presence of plague , calculus Deep periodontal pockets associated with plaque accumulation & moderate gingivitis Marked recession is also seen Acute necrotizing lesions High prevalence and increased severity of periodontal destruction associated with down syndrome is explained by poor PMN chemotaxis and phagocytosis