Diet and Its Relation to Endodontic Inflammation

7/30/2019 Diet and Its Relation to Endodontic Inflammation

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Introduction

‘’We are what we eat’’ is a old age adage. We all are aware of today’s ailments / diseases

which are due to improper eating habits. Most common diseases as of today are cardio

vascular diseases,brain stroke,diabetes,etc are all the ailments caused by improper that is

over eating or undereating or out timed eating habits leading to imbalance in the

equilibrium or the ratio imbalance causing ailments. Any disease for that matter is caused

by an ratio imbalance and similarly for the dental diseases. Caries is an microbiological

disease that leads to cavitation due to an loss of equilibrium between the remineralisation

and demineralization. Similarly the periodontitis due to imbalance in the bone formation

and bone resorption.

The same is true for endodontic diseases like pulpitis,periapical pathologies

that is imbalance in the ratio for disease causing pathogens to that of the body defense

cells. When the ratio of antigen to that of the antibodies in the body exceeds it manifests

itself as an disease in the form of acute or chronic inflammation depending upon the

duration of the inflammatory reaction.

Acute Inflammation:

The changes which occur

Vascular events Cellular events

Hemodynamic Changes in vascular Exudation of

Phagocytosis

changes permeability leukocytes

History

Although omega-3 fatty acids have been known as essential to normal growth and health

since the 1930s, awareness of their health benefits has dramatically increased since the

1990s.[5] New versions of ethyl esterized omega-3 fatty acids, such as E-EPA and

combinations of E-EPA and E-DHA, have drawn attention as highly purified and more

effective products than the traditional ones. In the United States and European Union,

these novel versions are often sold as prescription medications, such as Lovaza.

Elsewhere they are available as dietary supplements.

The health benefits of the long-chain omega-3 fatty acids — DHA and EPA omega-3 —

are the best-known. These benefits were discovered in the 1970s by researchers studying

the Greenland Inuit Tribe. The Greenland Inuit people consumed large amounts of fat from

meat, but displayed virtually no cardiovascular disease. The high level of omega-3 fatty



acids consumed by the Inuit reduced triglycerides, heart rate, blood pressure, and

atherosclerosis.[6]

On September 8, 2004, the U.S. Food and Drug Administration gave "qualified health

claim" status to EPA and DHA n−3 fatty acids, stating that "supportive but not conclusive

research shows that consumption of EPA and DHA [n−3] fatty acids may reduce the risk of

coronary heart disease."[7] This updated and modified their health risk advice letter of

2001 (see below). As of this writing, regulatory agencies do not accept that there is

sufficient evidence for any of the suggested benefits of DHA and EPA other than for

cardiovascular health, and further claims should be treated with caution.

The biological effects of the n−3 are largely mediated by their interactions with the n−6

fatty acids; see Essential fatty acid interactions for detail.

A 1992 article by biochemist William E.M. Lands[9] provides an overview of the research

into n−3 fatty acids, and is the basis of this section.

The 'essential' fatty acids were given their name when researchers found that they are

essential to normal growth in young children and animals. (Note that the modern definition

of 'essential' is more strict.) A small amount of n−3 in the diet (~1% of total calories)

enabled normal growth, and increasing the amount had little to no additional effect on

growth.

Likewise, researchers found that n−6 fatty acids (such as γ-linolenic acid and arachidonic

acid) play a similar role in normal growth. However, they also found that n−6 was "better"

at supporting dermal integrity, renal function, and parturition. These preliminary findings

led researchers to concentrate their studies on n−6, and it is only in recent decades thatn−3 has become of interest.

In 1964, it was discovered that enzymes found in sheep tissues convert n−6 arachidonic

acid into the inflammatory agent called prostaglandin E2,[10] which both causes the

sensation of pain and expedites healing and immune response in traumatized and infected

tissues.[citation needed] By 1979, more of what are now known as eicosanoids were

discovered: thromboxanes, prostacyclins, and the leukotrienes.[9] The eicosanoids, which

have important biological functions, typically have a short active lifetime in the body,

starting with synthesis from fatty acids and ending with metabolism by enzymes. However,

if the rate of synthesis exceeds the rate of metabolism, the excess eicosanoids may havedeleterious effects.[9] Researchers found that certain n−3 fatty acids are also converted

into eicosanoids, but at a much slower rate. Eicosanoids made from n−3 fatty acids are

often referred to as anti-inflammatory, but in fact they are just less inflammatory than those

made from n−6 fats. If both n−3 and n−6 fatty acids are present, they will "compete" to be

transformed,[9] so the ratio of long-chain n−3:n−6 fatty acids directly affects the type of

eicosanoids that are produced[citation needed].

This competition was recognized as important when it was found that thromboxane is a

factor in the clumping of platelets, which can both cause death by thrombosis and cause

death by bleeding. Likewise, the leukotrienes were found to be important in

immune/inflammatory-system response, and therefore relevant to arthritis, lupus, asthma,

and recovery from infections. These discoveries led to greater interest in finding ways to



control the synthesis of n−6 eicosanoids. The simplest way would be by consuming more

n−3 and fewer n−6 fatty acids.[9]

When administered as the ethyl ester, the omega-3 fatty acid EPA appears to form potent

anti-inflammatory molecules, called resolvins and omega-3-oxylipins,[11] which may partly

explain the positive effects of fish oil.[citation needed]

The n-3 fatty acids DHA and EPA may act as direct ligands to a cell surface G-protein

receptor, affecting anti-inflammatory and insulin sensitization in mice.[12]

Interconversion

Conversion efficiency of ALA to EPA and DHA

The short-chain n−3 fatty acids are converted to long-chain forms (EPA, DHA) with an

efficiency below 5%

[13][14] in men, and at a greater percentage in women which may be due to the

importance for meeting the demands of the fetus and neonate for DHA.[15]

These conversions occur competitively with n−6 fatty acids, which are essential closely

related chemical analogues that are derived from linoleic acid. Both the n−3 α-linolenic

acid and n−6 linoleic acid must be obtained from food. Synthesis of the longer n−3 fatty

acids from linolenic acid within the body is competitively slowed by the n−6 analogues.

Thus, accumulation of long-chain n−3 fatty acids in tissues is more effective when they are

obtained directly from food or when competing amounts of n−6 analogs do not greatly

exceed the amounts of n−3.[citation needed]

The conversion of ALA to EPA and further to DHA in humans has been reported to be

limited, but varies with individuals.[16] Women have higher ALA conversion efficiency thanmen, it is presumed due to the lower rate of use of dietary ALA for beta-oxidation. This

suggests that biological engineering of ALA conversion efficiency is possible. Goyens et al.

argue that it the absolute amount of ALA, rather than the ratio of n−3 and n−6 fatty acids,

controls the conversion efficiency.[17]

The n−6 to n−3 ratio

Main article: Essential fatty acid interactions

Some clinical studies[9][18][19] indicate that the ingested ratio of n−6 to n−3 (especiallylinoleic vs alpha-linolenic) fatty acids is important to maintaining cardiovascular health.

However, two studies published in 2005 and 2007 found that while n−3 polyunsaturated

fatty acids are extremely beneficial in preventing heart disease in humans, the levels of

n−6 polyunsaturated fatty acids (and therefore the ratios) were insignificant.

[20][21]

Both n−3 and n−6 fatty acids are essential; i.e., humans must consume them in the diets.

N−3 and n−6 eighteen-carbon polyunsaturated fatty acids compete for the same metabolic

enzymes, thus the n−6:n−3 ratio will significantly influence the ratio of the ensuingeicosanoids (hormones), (e.g., prostaglandins, leukotrienes, thromboxanes, etc.), and will

alter the body's metabolic function.[22] In general, grass-fed animals accumulate more n−3

than do grain-fed animals, which accumulate relatively more n−6.[23] Metabolites of n−6

are more inflammatory (esp. arachidonic acid) than those of n−3. This necessitates that



n−3 and n−6 be consumed in a balanced proportion; healthy ratios of n−6:n−3 range from

1:1 to 1:4 (an individual needs more n−3 than n−6.)[24][25] Studies suggest the

evolutionary human diet, rich in game animals, seafood, and other sources of n−3, may

have provided such a ratio.[26][27]

Typical Western diets provide ratios of between 10:1 and 30:1 (i.e., dramatically higher

levels of n−6 than n-3).[28] The ratios of n−6 to n−3 fatty acids in some common vegetable

oils are: canola 2:1, soybean 7:1, olive 3 –13:1, sunflower (no n−3), flax 1:3,[29] cottonseed

(almost no n−3), peanut (no n−3), grapeseed oil (almost no n−3) and corn oil 46:1 ratio of

n−6 to n−3.[30]

As a Harvard expert explains, n-6 fatty acids also reduce inflammation and protect against

heart disease, so the n-3 to n-6 ratio "is of no value in evaluating diet quality or predicting

disease".[31]

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Diet and Its Relation to Endodontic Inflammation