Role of neutrophils in host-microbial interactions

Neutrophilic polymorphonuclear leukocytes or polymorphonuclear neutrophils (PMNs) play a crucial role in host defense, by phagocytosing and killing the invading microorganisms, and in the pathogenesis of inflammatory diseases 1, 2. Neutrophils accumulate at the site of inflammation and can promote vascular injury through the secretion of granule constituents, reactive oxygen metabolites, and phospholipase products, resulting in local edema, thrombosis or hemorrhage. Neutrophils have intracellular vesicles or granules that secrete proteins by a process referred to as exocytosis or degranulation, which is of particular significance with respect to tissue damage in inflammatory diseases. The cytoplasmic granules of neutrophils are involved in a wide spectrum of functions including, engulfment and killing of foreign particles and pathogens, cell-cell interaction and adhesion, cell signaling, modulation of the surrounding environment, and transendothelial migration. As high amounts of deleterious constituents are stored inside the neutrophilic cytoplasmic granules and their release must be perfectly controlled in order to avoid tissue injury. Exocytosis involves the fusion of granules with the plasma membrane, leading to the release of granule contents and exposure of granule membrane proteins at the cell surface.

Neutrophil structure

 Neutrophils are the most abundant type of granulocytes. They constitute about 70% of the white blood cells. Their diameter ranges from 12-15 µm. Neutrophils are named so because of their neutral staining with Wright stain. They have nucleus divided into 2-5 lobes (Figure 8.1). The multilobed nucleus contributes to the extreme elasticity of the cell, which is important for the cell to make the rapid transit from the blood through tight gaps between the endothelial cells during transendothelial migration. In the cytoplasm the Golgi apparatus is small, mitochondria and ribosomes are sparse and rough endoplasmic reticulum is absent. Cytoplasm contains abundant secretory vesicles.

Figure 8.1 Structure of a neutrophil

Structure of a neutrophil

Secretory vesicles:

They are the most important components of the neutrophil structure. Secretory vesicles have an endocytotic origin 3 and they represent a pool of membrane-associated receptors, that get incorporated into the plasma membrane after the release of the vesicles 4. The most abundant receptors within the secretory vesicle membrane are β2-integrins, CR1, formyl peptide receptors (fpr), CD14, and CD16. When secretory vesicles mobilize to the cell membrane, the phenotype of PMN is completely changed. Now, the relatively inactive PMN is transformed into a cell that is capable of interacting with the endothelium, monocytes, and dendritic cells and can receive inflammatory signals from the environment. Besides plasma proteins like albumin, only one additional protein is described to be stored in the secretory vesicles: heparin binding protein (HBP, also known as CAP 37 and azurocidin) 5. HBP is released at the initial stage of PMN transendothelial migration. It is thought to be of essential importance in the PMN-induced increase in vascular permeability 6 and adhesion of monocytes to the endothelial cells 7.

Neutrophils contain releasable membrane-bound secretory vesicles or phosphasomes.  There are three major functional types of granules in the neutrophils, namely: azurophilic or primary granules, specific or secondary granules, and gelatinase-containing tertiary granules 8-12 (Table 8.1). Some proteins have been localized in additional cytoplasmic organelles that do not perfectly fit with the above mentioned major cytoplasmic granule populations, including organelles containing transforming growth factor-α 13, and vesicles containing tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) 14. A brief description of the primary, secondary and the tertiary granules of neutrophils is as follows,

  1. Primary or azurophil granules: Azurophilic granules are characterized by their content of myeloperoxidase and β-glucoronidase. Azurophil granule degranulation is confined primarily to internalized phagocytic vacuoles during phagocytosis 15, indicating that this granule is mainly involved in phagocytosis.
  2. Secondary or specific granules: Markers from specific granules have lactoferrin and vit-B12 binding proteins. Because specific granules contain four types of extracellular matrix receptors (laminin, fibronectin, vitronectin receptors, as well as the receptor for C3bi/fibrinogen CD11b/CD18) they have been named as “adhesomes” 16.
  3. Tertiary or secretory granules: Tertiary granules contain adhesion proteins (e.g. CD11b/CD18) 17, 18 as well as heparanase and gelatinase, two major extracellular matrix degradative enzymes involved in extravasation processes 19. Tertiary granules are most rapidly released.

Table 8.1 Contents of neutrophilic granules

1°  or azurophilic granules 2° or specific granules 3° or secretory granules
Matrix Components:

  • Cellular myeloperoxidase
  • Lysozyme
  • Heparin-binding
  • Low molecular weight cationic proteins
  • Defensins
  • Acid hydrolase
  • β-glucuronidase
  • Acid phosphatase
  • α-mannosidase
  • Neutral protease
  • Elastase
  • CathepsinB/D/G

Membrane Components:

  • CD 63
  • CD 68
Matrix Components:

  • Lysozyme
  • Alkaline phosphatase
  • Collagenase
  • Vitb12 binding protein
  • Lactoferrin
  • LL-37
  • MMP-8

Membrane Components:

  • CR3
  • CR4
  • FMLP receptors
  • Laminin receptors
  • TNF-r
  • Formyl peptide receptors (fpr)
Matrix Components:

  • Gelatinase
  • Cathepsin B
  • Cathepsin D
  • β-d-glucuronidase.
  • α-mannosidase
  • Plasminogen activator
  • MMP-9

Membrane Components:

  • Formyl peptide receptors (fpr)
  • CD 11b

Neutrophil homeostasis

Neutrophils are the primary leukocytes recruited in the gingival crevice in response to the bacterial biofilm 20, 21. They make the primary line of defense against microorganisms present in the dental plaque. Their absence or excess, both result in damage to the host tissue, thus the number of neutrophil and their distribution are very important for the maintenance of periodontal health. Let us try to understand the biology of the production of neutrophils, their trafficking, and their clearance.

Neutrophils are produced in the bone marrow from where they are released into the circulation. The granulocyte colony-stimulating factor (G-CSF) plays a primary role in ………………….

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After neutrophils enter the circulation, they quickly mobilize to the site of inflammation where they transmigrate from the blood vessels through the process of transendothelial migration. The mechanism of transendothelial migration has been discussed in detail in “Basic concepts in immunity and inflammation”. The migration of neutrophils from blood vessels into the connective tissue can be regulated by tissue-derived cytokines and chemokines, which control the expression of endothelial adhesion molecules and induce conformational changes in them 27.

The clearance of neutrophils takes place by their phagocytosis by the phagocytes, such as macrophages and dendritic cells in the tissue. This process not only removes the old cells, but also regulates the production of new neutrophils. Phagocytosis of an apoptotic neutrophil triggers an anti-inflammatory response which is mediated by the reduced production of IL-23 by macrophages. As IL-23 induces the production of IL-17 by many cells of the immune system, its reduced production down-regulates IL-17 production. The reduced IL-17 levels lead to less G-CSF production and as a consequence, there is less neutrophil production 28. This mechanism of feedback control over neutrophil production is referred to as “neutrostat” (neutrophil rheostat) which maintains steady-state neutrophil levels in the circulation. The senescent neutrophils return to the bone marrow for clearance after they have an increased expression of CXCR4.

 Figure 8.2 The regulation of neutrophil production and distribution

Regulation of neutrophil function and distribution

Neutrophil function during periodontal inflammation

As discussed earlier in “Host-microbial interactions in periodontal diseases”, PMN’s are one of the first-responders of inflammatory cells to migrate toward the site of periodontal inflammation. This migration of cells is mediated by chemoattractants such as IL-8 secreted by oral epithelial cells, connective fibroblast and immune cells 29. There are multiple mechanisms by which neutrophils exert their antibacterial activity, including phagocytosis, the release of antimicrobial substances, and the formation of neutrophil extracellular traps (NETs) 30. Neutrophils produce various proteinases which cause damage to the host tissues and produce various chemical mediators which influence the inflammatory as well as the immune response 31. Following is a brief description of neutrophil functions,

Adherence:

The surface of neutrophils is coated with surface adhesion molecules. These adhesion molecules interact with intracellular adhesion molecule (ICAM)-1 and 2 on endothelial cells. ICAM-1 and ICAM-2 belong to the immunoglobulin superfamily. The expression of ICAM-1 is induced by tumor necrosis factor (TNF), interlukin-1 (IL-1) and interferon- γ (IFN-γ). Adhesins on the surface of PMN’s are composed of a group of glycoproteins referred to as α and β subunits. β subunit is known as CD18 and α subunit is known as CD11. The α subunit is found in 4 forms viz. a,b,c and d. So, based on α subunit variability glycoproteins are classified as CD11a/CD18, CD11b/CD18, CD11c/CD18, CD11d/CD18 (see “Basic concepts in immunity and inflammation” for more detail).

Chemotaxis: 

The invading organisms are coated with plasma proteins like, IgG or C3B. This process is called as opsonization. Opsonization done by IgG and IgM is heat stable, whereas opsonization done by C3b and ic3b i.e. compliment is heat labile.

Receptor for IgG on neutrophil: Fcγ

Receptor for C3b on neutrophil: Cr1

The mechanism of neutrophil chemotaxis has been described in detail  “Host-microbial interactions in periodontal diseases”.

Microbial killing by phagocytosis:

It involves the fusion of phagosome with the neutrophilic granules, leading to the discharge of granule contents into phagosome, resulting in the intracellular killing of bacteria. The important step in this process is the recognition of the particle as foreign by the neutrophil. The interactions between opsonins IgG and C3b and their receptors on the surface of the neutrophil are involved in this step 32. These interactions result in the submembranous activation of contractile elements (microfilaments), which leads to pseudopod formation and engulfment of the bacteria 33, 34. After the formation of the phagolysosome, the bactericidal agents present in the neutrophil granules are released into it and the ingested microorganism is killed and digested. The neutrophil may perform bacterial killing by oxygen-dependent or -independent mechanisms 35-39.

Respiratory burst:

The formation of H2O2 and superoxide anion constitutes the phenomenon of the respiratory burst. Neutrophil stimulation results in a sharp increase in the oxygen consumption by the cell. Cell activation leads to the release of an enzyme, NADPH oxidase from the cytosolic side of the plasma membrane. NADPH is oxidized to NADP on the outer surface of PMN. This leads to the production of superoxide anion (O2-) on the cell surface. Superoxide is converted into H2O2 by the action of the enzyme superoxide dismutase. H2O2 in itself is not damaging to the tissues, but when it combines with myeloperoxidase (azurophilic granule enzyme) and halide ions from the plasma membrane, the result is the formation of hypochlorous acid, which is a potent oxidant and very toxic 40, 41. The myeloperoxidase system is effective in killing bacteria, fungi, viruses, and mycoplasma. It is also capable of destroying the tissues.

Neutrophil extracellular traps (NETs):

This mechanism of microbial killing by neutrophils has been recently explained 27, 42, 43. In this mechanism, the nuclear and mitochondrial DNA is released into the ……………………

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Action of neutrophils on biofilm

Earlier, it was believed that neutrophils cannot affect the microorganisms in the biofilm. However, recent investigations have shown that neutrophils do exert their antimicrobial activity on microorganisms in a protected environment of biofilm. As already discussed in the previous chapter, neutrophils are attracted towards the site of infection by various host and bacterial derived chemoattractants. The epithelial cells, other immune cells or neutrophils themselves secrete molecules that act as chemoattractants, facilitating neutrophil migration 45, 46. Small QS (quorum sensing) molecules of the N-acyl homoserine lactone (AHL) family as well as bacteria-derived formyl-Met–Leu–Phe act as potent chemoattractants for neutrophils 47, 48. Neutrophils identify biofilm by their receptors for lipopolysaccharides, peptidoglycans, microbial DNA, and other pathogen-associated molecular patterns (PAMPs) 49, 50. Various in vitro and in vivo studies have demonstrated the accumulation of neutrophils around or within the biofilm, demonstrating neutrophil activity against microorganisms in the biofilm 51-58. Neutrophils exert their antimicrobial activity on or within biofilm by various mechanisms, including phagocytosis, degranulation, NETosis and respiratory burst.

Protective mechanism of biofilm against neutrophils

The biofilm has its own defense mechanisms against neutrophils. These mechanisms can either directly counter the neutrophils or may camouflage the biofilm. Quorum sensing plays an important role in these protective mechanisms. It has been demonstrated that quorum sensing molecules promote the production of bacterial surfactants (rhamnolipids) by P. aeruginosa biofilms and result in a rapid rate of neutrophil death 59. Furthermore, toxins produced by the planktonic cultures of S. aureus and Aggregatibacter actinomycetemcomitans have been shown to induce lysis and degranulation of neutrophils 60-62. Along with this, bacteria in a biofilm can render themselves resistant to neutrophil-mediated killing by making them non-recognizable by neutrophils. It has been shown that expression of certain lipooligosaccharide glycoforms shield PAMPs of bacteria, thus inhibiting their recognition and opsonization 63-65. Biofilms have also demonstrated the mechanism of protection against reactive oxygen species (ROS) produced by neutrophils during respiratory burst. The P. aeruginosa biofilms have demonstrated mutations in the mucA gene upon stimulation with neutrophils and ROS. This mutation results in the enhanced formation of mucus, which provides protection to the bacteria from ROS 66.

  

Know more………..

Do neutrophils promote or retard biofilm formation?

It is well known that biofilm cannot be completely eliminated from the periodontal arena. As a result of which, neutrophils are always present at the site of biofilm formation. These neutrophils release their granular products to kill the microorganisms in the biofilm, but since the oral cavity is an open cavity and the colonization of these microorganisms in a biofilm is a continuous process, neutrophils may themselves …………………

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Neutrophil disorders

Neutropenia and Agranulocytosis:

Neutropenia may be defined as a neutrophil granulocyte count of less than 1,500/ mm 75. There are three general guidelines used to classify the severity of neutropenia based on the absolute neutrophil count, measured in cells per microliter of the blood,

  • Mild neutropenia, where the absolute neutrophil count is ≥ 1000 and < 1500- Patient has minimal risk of infection
  • Moderate neutropenia, where the absolute neutrophil count is ≥ 500 and < 1000- Patient has moderate risk of infection
  • Severe neutropenia, where the absolute neutrophil count is < 500- Patient has a severe risk of infection. Neutrophil count of less than 500/mm3 is also referred to as agranulocytosis.

Three lines of evidence support that neutrophils protect the periodontium against infections. Firstly, primary neutrophil or myeloid abnormalities have been associated with severe periodontal destruction; secondly, otherwise healthy individuals with severe periodontal problems have a defective neutrophil function, and thirdly, experimental neutropenia in animals results in a rapid periodontal infection. Neutropenia may be primary or secondary in its etiology.

Primary:              

  • Genetic defect in elastase gene.
  • Morbus kostmann’s syndrome (MKS).

 Secondary:

  • Myelosuppression.
  • Drugs (idiosyncratic reactions).
  • Autoimmune disorders.

The neutropenic phase in any of the above conditions may clinically manifest as recurrent fever, malaise, headaches, anorexia, pharyngitis, bacterial infections, ulcers of the oral membrane, and periodontal disease. Because of the absence of normal neutrophil function, a rapid periodontal destruction may occur, especially in the absence of adequate oral hygiene. Following is the description of some diseases/conditions associated with neutrophilic defects which usually present with periodontal manifestations,

Chediak-Higashi syndrome (CHS):

It has an autosomal recessive mode of inheritance, localized to chromosome 1q43. In this disease, azurophilic granules and specific granules fuse to form giant granules called megabodies. Neutropenia, depressed inflammation and relative lack of neutral serine proteases occur in CHS. Formation of reduced oxygen metabolites is greatly exaggerated. Oral manifestation of this disease includes severe periodontitis and oral mucosal ulcerations. Patients usually experience gingival hemorrhage and early dental loss 76, 77. The increased number of putative periodontal pathogens, including Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia have been found in the periodontal site of CHS patients 78.

Specific granule deficiency:

It is a rare disease which was originally described as a disease in which neutrophils lacked specific granules. But now it is clear that the defect is in the packaging of azurophilic and specific granule proteins. Specific granule proteins which are missing include lactoferrin, cobalophilin, cytochrome b, the FPR, C5a receptor, and CR3. So, because of lack of these components, neutrophils show 79-84,

  • Depressed respiratory burst activity.
  • Diminished ability to respond to chemoattractants.
  • Poor phagocytosis.
  • Atypical nuclear morphology

The packaging of defensins into azurophilic granules is also affected. So, intra-lysosomal killing is slow. The inflammatory response is also slow due to above defects. This disease may probably have autosomal recessive expression.

Morbus kostmann’s syndrome (MKS):

Morbus kostmann syndrome (MKS) is an autosomal recessive disorder characterized by severe neutropenia that results in severe bacterial infections early in life. The primary line of treatment for MKS is the administration of granulocyte colony-stimulating factor (G-CSF). Although, in MKS patients neutrophil count comes to normal after G-CSF treatment, but they still exhibit severe periodontitis. A possibility is that neutrophils and keratinocytes lack appropriate antibiotic peptides. Thus, these patients have diminished levels of α-defensins and LL-37. α- defensins is not as effective against periodontal pathogen as LL-37.

Palmoplantar hyperkeratosis:

Palmoplantar keratodermas are a group of disorders characterized by thickening of the skin on the palms of the hands and soles of the feet of affected individuals 85. We have three related diseases in this category,

  • Papillon-Lefevre syndrome (PLS).
  • Haim-Munk syndrome (HMS).
  • Non-syndromic prepubertal periodontitis (NS-PPP).

Both PLS and HMS show aggressive periodontitis and palmoplantar hyperkeratosis. HMS has additional features like hyperkeratosis, arachnodactyly, acro-osteolysis, atrophic changes in the nails and deformity of the fingers. NS-PPP shows one less feature i.e. there is no palmoplantar hyperkeratosis. HMS has been traced back to Cochin, India. In PLS, HMS and NS-PPP there is allelic variation in cathepsin c gene, which is localized to ch11q14-q21. Cathepsin c is distributed to many tissues, including leukocytes. It is important in protein degradation and proenzyme activation. It has been shown to be involved in the activation of T-cell granzymes A and B; therefore it may also be significant in the activation of neutrophil serprocidins (Granzymes-A related molecules) and neutrophil cathepsin-G (Granzyme-B related molecule).

The exact defect is still unclear, but it seems that in PLS defect lies in myeloperoxidase deficiency, low integrin expression, increased superoxide production and defective phagocytosis and chemotaxis 86. Neutrophils from individuals of PLS show decreased receptor affinity for chemotaxis such as formyl-peptides 87. Other features are,

  • Increased circulating NK cells.
  • Decreased monocyte phagocytosis.
  • Diminished lymphocyte responsiveness.
  • Periodontal connective tissue clearly shows dominated plasma cells.

Other syndromes with qualitative neutrophil defects that could predispose to periodontal destruction include Kindler syndrome and Hypotrichosis osteolysis periodontitis palmoplantar keratoderma syndrome 88.

Chronic granulomatous diseases:

It is a group of diseases characterized by the inability of the phagocytes to reduce oxygen. In this condition, there is a deficiency of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which results from a mutation in one of the four components of the NADPH oxidase complex. The most frequent form is the X-linked (XCGD), with mutations in the CYBB gene encoding gp91phox subunit. Rare subgroups are caused by mutations in CYBANCF1 or NCF2 genes encoding p22phox, p47phox or p67phox subunits respectively 89, 90. It is characterized by the presence of recurrent, indolent, pyogenic infections caused by catalase-positive bacteria. In addition, CGD patients also suffer from infections and sterile hyperinflammation in the oral cavity 91. Because the host phagocytes are unable to mount a normal respiratory burst, they have difficulty in controlling those microorganisms which do not release reduced oxygen metabolites themselves. Apparently, catalase-negative bacteria release enough hydrogen peroxide to assist neutrophils to perform oxidative killing. The inability to rapidly dispatch bacteria which gain access to the connective tissue lead to the formation of granuloma by the chronic immune cells.

The ulcerative lesion shows inflammatory cell infiltrate consisting of plasma cells, histiocytes, and occasionally, eosinophils. This is in addition to small granulomas characterized by mononuclear histiocytes and occasional multinucleated giant cells 92. Another report described chronic inflammation and non-caseating granuloma composed of many epithelioid cells, a few giant cells, edema, and dilated lymphatic vessels in the superficial dermis in the biopsy of an upper lip granulomatous cheilitis 93.

The oral and periodontal findings of CGD include severe gingivitis 94-96, periodontitis 93-96, generalized prepubertal periodontitis 97, granulomatous mucositis in the upper lip 93 and the soft palate 98, geographic tongue 99, oral candidiasis 100, and enamel hypoplasia 101.

Hyper-IgE syndrome (Job’s Syndrome):

The hyper-IgE syndrome was first described in 1966 by Davis, Wedgwood and Schaller 102. It is a rare, complex disorder that has been localized to chromosome 7q21 and is characterized by a marked elevation of IgE. The exact etiology of the hyper-IgE syndrome is unclear, but heterogeneous disorders of the immune system have variably been described. These include impaired production of IFN-γ by T-cells, defective T-helper 1 (Th1)-dependent cytokine response, a skewed Th1/Th2 cell ratio, a diminished memory T-cell populations, decreased delayed-type hypersensitivity responses, an impaired response of lymph cells to antigenic and alloantigenic stimulation 103, as well as a defective neutrophil chemotaxis 104..

The patient has chronic dermatitis, coarse faces and serious lifelong recurrent infections which result in skin abscesses remarkable in their lack of erythema (“cold” abscesses). The eczematoid dermatitis starts in the newborn period and is typically associated with and driven by Staphylococcus aureus infection. Recurrent bacterial sinusitis and otitis are common in this condition. Repeated lung infections due to S. aureus, Streptococcus pneumoniae, and Haemophilus influenza are also common and start in early childhood.

Leukocyte adhesion deficiency type-I (LAD-I):

It is characterized by the inability of individuals to express β2 subunit (CD18) which is common to leukointegrins, LFA-1, Mac-1, p150/95 and αDβ2.

  1. Leukointegrins: They are heterodimers consisting of α and β subunits. The α subunits are 4 in number (CD11a, CD11b, CD11c, and CD11d) whereas β subunit is common. So, it leads to a defective adhesion of leukocytes.
  2. LFA-1: It is important for neutrophil diapedesis and lymphocytes scanning of APC’s.
  • MAC-1: It is important for adhesion of leukocytes to endothelial cells
  1. MAC-1 and p150/95: Both of them are important for complement receptors involved in phagocytosis
  2. αDβ2: It binds to ICAM3 and is distributed to certain macrophages and lymphocytes.

These defects occur in homozygous and heterozygous forms. Homozygous form manifests as generalized aggressive periodontitis whereas heterozygous may have normal prepubertal status. Histologically, LAD-1 shows dense plasma cell infiltration of periodontal lesions with copious immunoglobulin production (which appear histologically as Russell bodies).

Clinical manifestations:

The prominent clinical features of patients with LAD-1 are recurrent bacterial infections, primarily localized to skin and mucosal surfaces. The absence of pus formation at the sites of infection is one of the hallmarks of LAD-1. At birth these patients commonly present with infection, omphalitis (inflammation of the umbilical cord stump in the neonatal newborn period) with delayed separation of the umbilical cord. Severe gingivitis and periodontitis are the major features among all patients who survive infancy. Impaired healing of traumatic or surgical wounds is also characteristic of this syndrome 98.

Leukocyte adhesion deficiency-II (LAD-II):

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Clinical manifestations:

In this case, affected children are born after uneventful pregnancies with normal height and weight. No delay in the separation of the umbilical cord is observed. Later on patients present with severe mental retardation, short stature, and a distinctive facial appearance. There is no pus formation at the site of infection. After the age of 3 years, the frequency of infections decreases and children no longer need  prophylactic antibiotics 106.

Leukocyte adhesion deficiency-III (LAD-III):

The precise molecular defect in LAD-III is still unknown and it may be the result of several different genes involved in the inside-out signaling for general integrin activation 107-109. Present evidence suggests that defects in the activation of β1, β2, and β3 integrin subunits result in an abnormal neutrophil function.

Clinical manifestations:

In few case reports described, the clinical presentation is very similar to LAD I but it also includes defects in platelet activation 110 and a severe bleeding tendency 111.

Neutrophil function in chronic and aggressive periodontitis

The research work done on neutrophil functions in periodontitis cases, particularly in aggressive periodontitis cases suggests neutrophilic dysfunction as one of the etiological factors associated with disease progression 112-114. The impaired chemotactic response of neutrophils in aggressive periodontitis patients has been proposed as one of the neutrophilic dysfunction 115. Hyperactive / “primed” neutrophils have been the focus of research for last few decades and have been proposed to be responsible for the rapid soft tissue destruction in aggressive periodontal diseases. A detailed description of neutrophil function defects in chronic and aggressive periodontitis has been given in “Chronic and aggressive periodontitis”.

Conclusion

Neutrophils make up the primary line of defense against infection and their normal function is essential to prevent and eliminate infection from the body. In the above discussion, various clinical conditions have been discussed where the normal neutrophil function is disturbed. It has been well established now that patients with a defective neutrophil number or function demonstrate rapid periodontal destruction as compared to patients with normal neutrophil functions. Hence, a thorough understanding of neutrophil structure and function is essential to understand the etiopathogenesis of periodontal diseases.

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References:

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