By U. Milok. The College of Insurance.
Allergic rhinitis is often caused by pollen order amitriptyline us, but can also be triggered by common indoor allergens including pet dander cheap amitriptyline on line, mold purchase cheapest amitriptyline and amitriptyline, dust mites amitriptyline 10mg for sale, and cockroach particles. Seasonal allergens such as pollen and mold spores are the most common causes of allergic conjunctivitis. One of the most common recommendations that we will make for treatment in those with seasonal or outdoor allergies is that of store-bought eye drops, which can help to soothe irritation and lubricate the eyes. Other causes of allergies, such as certain foods or bee stings, do not typically affect the eyes the way airborne allergens do. Adverse reactions to certain cosmetics or drugs such as antibiotic eyedrops also may cause eye allergies. Antihistamines relieve many symptoms caused by airborne allergens, such as itchy, watery eyes, runny nose and sneezing. The most common signs and symptoms of eye allergies include red eyes, swollen eyelids, itchy eyes and excessive tearing. Eyedrops frequently prescribed for eye allergies contain olopatadine hydrochloride, an ingredient that can effectively relieve symptoms associated with an allergic reaction. An allergic reaction that affects the conjunctiva, a clear layer of mucous membrane overlying the eyes, is referred to as allergic conjunctivitis. The condition is usually seasonal and is associated with hay fever The main cause is pollens, although indoor allergens such as dust mites, molds, and dander from household pets such as cats and dogs may affect the eyes year-round. Common symptoms are itchy eyes, redness, tearing and a burning sensation. There are a few common causes of allergic conjunctivitis including pollen and mold that your body is sensitive to. Everyone is not allergic to the same type of pollen, so only a specific flower might trigger an allergic reaction in your eyes. It also means that there is an increase of pollen in the air causing people to have red and irritated eyes During the springtime, many people suffer from an eye condition called allergic conjunctivitis which affects more than 20 percent of the U.S. population. Combines an antihistamine with a redness reliever to provide relief from itchy, red allergy eyes. A systematic review of 30 trials, with 17 different treatment comparisons found that all topical antihistamines and mast cell stabilizers included for comparison were effective in reducing symptoms of seasonal allergic conjunctivitis. Treatment of allergic conjunctivitis is by avoiding the allergen (e.g., avoiding grass in bloom during "hay fever season") and treatment with antihistamines , either topical (in the form of eye drops ), or systemic (in the form of tablets). Many people will treat their nasal allergy symptoms but ignore their itchy, red, watery eyes. An allergy to contact lenses , called giant papillary conjunctivitis , makes eyes sensitive and red. The usual suspects - pollen , dust mites , pet dander, feathers, and other indoor or outdoor allergens - can set off eye allergy symptoms To treat them, find out what triggers them and stay ahead of the symptoms. This reaction is usually centered in a part of the eye called the conjunctiva, which becomes inflamed when triggered by a substance that a person is especially sensitive to. An ocular allergy can happen suddenly or some time after you come in contact with the allergen. The symptoms are similar but more severe than those of allergic conjunctivitis, including intensely itchy eyes that burn and feel as if something has entered the eye to irritate it. Light sensitivity and blurred vision may be present. Common allergens affecting the eyes include, but are not limited to, pollen, ragweed, grass, mold, weeds, dust, and pet dander. Perennial allergic conjunctivitis: Less common than the seasonal condition, in the perennial form of allergic conjunctivitis, symptoms like puffy eyes occur all year round. Immunotherapy or allergy shots may be an option for relieving eye allergies if your symptoms are not controlled by avoiding allergens, using eye drops or medications. Seasonal allergic conjunctivitis (hay fever conjunctivitis) and year-round or perennial allergic conjunctivitis (atopic conjunctivitis, atopic keratoconjunctivitis) are the most common types of allergic reaction in the eyes. Eye irritation from allergies can occur when allergens in the air, such as pollen, pet dander or dust, come into contact with the thin membrane that covers the eyeball. The most common causes of allergic conjunctivitis are seasonal allergens such as pollen and mold spores. The "best" treatment overall for eye allergies is to avoid the allergic triggers - the allergens that lead to your symptoms. The diagnosis of allergic conjunctivitis is made with a history of symptoms suggestive of eye allergies, an examination by a healthcare professional with findings consistent with conjunctivitis , and, often times, allergy testing showing seasonal or perennial allergies. Seasonal allergic conjunctivitis (SAC) is the most common form of eye allergy, with grass and ragweed pollens being the most common seasonal triggers. Before the advent of modern medications, treatment for seasonal allergic conjunctivitis was limited to eye washes that would cleanse the allergen from the eye and provide short-term relief. In most parts of the United States, plant pollens are often the cause of seasonal allergic rhinitis—more commonly called hay fever. For example, to determine whether your reaction is a result of food, airborne or chemical allergens, the doctor might ask, "Have you eaten anything unusual recently?", "Have you been working or exercising vigorously outdoors?" or "Did you come into contact with anything which might have irritated your skin and eyes?" Your doctor will likely ask if you suffer from asthma , since allergies increase the risk of an asthma attack. Roughly 40 million Americans suffer from pollen allergies, also known as hay fever, allergic rhinitis or seasonal allergies. While anithistamines and topical nasal steroids can help control the symptoms of a seasonal allergy such as birch pollen allergy, these medicines do not interfere with the risk of further allergies or the development of asthma. Trees - about 1 in 4 (25%) of people with hay fever in the UK are allergic to pollen from trees, including oak, ash, cedar and birch (people with an allergy to birch often also experience an allergic reaction to apples, peaches, plums and cherries because these types of fruit contain a similar protein to birch pollen) Most people with hay fever are allergic to grass pollen, but it can also be caused by trees and weeds. Airborne pollens are responsible for causing allergy symptoms, such as runny nose, itchy eyes, nasal congestion, and sneezing. Hay fever is the most common name for pollen allergy and is most commonly caused by grass pollens, although other pollens can also trigger the symptoms. Not only are more people experiencing the symptoms of burning, itchy eyes and runny nose or congestion, allergy seasons overall — including spring and fall — are lasting as much as 27 days longer than in the past. Common symptoms associated with hay fever are nasal congestion, itching in the nose, mouth, eyes or throat, sneezing, drainage, cough, and headaches. Simultaneous exposure to allergens (such as pollens) and air pollution (such as from diesel exhaust or ozone) may increase the risk for people with asthma and allergies. Pollinosis, also known as seasonal allergic rhinitis, pollen allergy or hay fever, is the result of sensitization to pollen components. Itchy, watery eyes; sneezing; clear runny or itchy nose; and nasal congestion are the most common symptoms of a pollen allergy. As the symptoms of hay fever occur at the same time or in the same season each year, it is also known as season allergic rhinitis. Grass allergy from pollen can cause hay fever and thunderstorm asthma , with symptoms that include: When a chronic cough is not caused by a bacterial infection, allergies, or asthma, a child may need other types of treatment to address the underlying cause. Our doctors may recommend over-the-counter antihistamines and nasal steroids to relieve allergy symptoms, which can contribute to an ongoing cough in children. For children with cough-variant asthma , a breathing disorder in which coughing is the only symptom, our doctors may prescribe anti-inflammatory medicines to reduce inflammation in the airways. Asthma is more likely to develop in children who continue to wheeze after the age of 3 and have allergies such as eczema, hayfever, runny nose with a cold or whose parents have allergies. Illnesses that cause coughing like colds and the flu are passed around constantly among the public, and allergies to airborne substances like pet dander and plant pollen are very common afflictions. Histamine is responsible for runny noses, coughing, sneezing, and swelling of the nasal passages, so the patient starts experiencing cold-like symptoms even in the absence of the common cold. Cough is usually accompanied by a runny nose and nasal congestion, and these symptoms occur simultaneously when a person is suffering from a common cold or allergic reaction. Allergists have particular expertise in allergic rhinitis (or hay fever) and sinus infections, which may contribute to postnasal drainage, a common cause of chronic cough. Coughing at night with hoarseness and frequent throat clearing may be caused by postnasal drip from allergic rhinitis or sinusitis. If you are prone to asthma and allergies during summer, there are ways to control coughing and other allergy symptoms caused by humidity and rising temperatures: If your baby already has an allergy such as a diagnosed food allergy or eczema, or if you have a family history of food allergies, eczema, asthma or hay-fever, you may need to be particularly careful when introducing foods, so talk to your GP or health visitor first. If your child has symptoms of an allergic reaction, follow the food allergy action plan your doctor gave you. A breastfeeding elimination diet can be helpful if your baby is overly fussy and might have a milk protein allergy or intolerance to other foods that you are eating.
The first branch of the aortic arch should be the left subclavian artery discount amitriptyline 10 mg without prescription, then 25 Vascular Rings 295 Fig buy amitriptyline australia. Double aortic arch: The ascending aorta bifurcates into two arches which course from the anterior ascending aorta toward the posterior descending aorta on either side of the midline structures of trachea and esophagus order 75mg amitriptyline visa, thus encir- cling them the left carotid artery before the arch heads rightward best amitriptyline 10mg, however, in this anomaly; the left subclavian artery does not emerge from where it is expected as the first branch but much later from the distal part of the distal aortic arch. Therefore, the first branch is the left carotid artery, followed by the right carotid artery and then the right subclavian artery. The left subclavian artery emerges from the Diverticulum of Kommerell, a slightly larger blood vessel which emerges from the distal right- sided aortic arch, the Diverticulum of Kommerell courses to the left, crossing the midline behind the esophagus and then giving rise to the left subclavian artery and the ductus arteriosus. The ductus arteriosus continues leftward till it joins the base of the left pulmonary artery. The encircling vascular vessels around the esophagus and trachea are composed of the following: • Anteriorly by the ascending aorta. The latter is anchored to the heart anteriorly through the main pulmonary artery, thus completing the vascular ring. Vascular sling: This anomaly is technically not a ring since it does not encircle the trachea and esophagus. Instead, the left pulmonary artery which normally emerges from the main pulmonary artery arises from the proximal right pulmonary artery, just right of the tracheobronchial bifurcation. The left pulmonary artery courses leftward behind the distal trachea and in front of the esophagus to reach the left lung hilum. Right aortic arch with aberrant left subclavian artery with left-sided ductus arteriosus. The esophagus and trachea are encircled by the ascending aorta, aortic arch, diverticulum of Kommerell, and the ductus arteriosus Fig. Vascular sling: The left pulmonary artery emerges in an anomalous fashion from the right pulmonary artery then courses leftward behind the distal trachea and in front of the esophagus to reach the left lung hilum 25 Vascular Rings 297 Pathophysiology The exact anatomical features of vascular rings are typically difficult to imagine as it involves understanding of the spacial anatomy of great vessels and their branches as they encircle the esophagus and trachea. On the other hand, the pathophysiological changes they cause are more straightforward. Vessels arranged in an abnormal fashion, completing a circle around the trachea and esophagus eventually cause constriction of these tubular structures (esophagus and trachea) leading to difficulty in air flow through the trachea leading to stridor. Pathological constriction of the trachea eventually interferes with normal processes of breath- ing and clearing secretions from the lower respiratory tract leading to superim- posed infections. Constriction of esophagus occurs in most cases; however, symptoms of feeding difficulties tend to be less prominent than respiratory symptoms. Respiratory symptoms worsen with feeding and apnea lasting for few seconds may be noted. Patients with double aortic arch present early in infancy as the constriction caused by the double aortic arch is worse. Children with right aortic arch with aberrant left subclavian artery may present later in childhood. Dysphagia is a complaint of older children since it cannot be verbalized by infants; however, worsening respiratory symptoms is more prominent in infants. Children may assume a back arching, neck extending position to keep trachea patent. Chest Radiography The chest X-ray may give a hint to vascular abnormality through observing a right aortic arch. The findings in this image are highly suggestive, though not diagnostic of vascular ring. Electrocardiography This is normal in children with vascular ring as abnormal vascular arrangement does not impact the cardiovascular hemodynamics. It is not unusual in many such cases that a poorly performed echocardiography misin- terpreted as normal causes delay of diagnosis. In double aortic arch, the echocardiographer first notices that there is a right aortic arch with only two brachiocephalic branches, closer examination shows another aortic arch, to the left and again with only two brachiocephalic branches. A challenge to diagnosing double aortic arch is when the left aortic arch is atretic since it is not visible by echocardiography without blood coursing through it. Right aortic arch with aberrant left subclavian artery and left-sided ductus arteriosus is suspected when the aortic arch is noted to be rightward with the first branch being the left carotid artery (rather than the left subclavian artery). Examination of the distal arch shows a branch which starts of as being somewhat large, coursing from right to left, then becoming smaller in caliber to give the left subclavian artery. The larger first portion of this artery reflects the fact that it starts as the diverticulum of Kommerell which gives off the ductus arteriosus, then the subclavian artery. The capability of producing 3D images of the vascular anatomy, upper airway, and esophagus is truly spectacular in providing accurate diagnosis. Management Management of these anomalies is surgical to relief compression of the upper airway structures. Double aortic arch is relieved through ligation and resection of one of the aortic arches, typically the left as it tends to be smaller. The ductus arteriosus or ligamentum must be resected in cases of right aortic arch with 300 Ra-id Abdulla aberrant left subclavian artery. In the rare cases of pulmonary sling, the left pulmonary artery is resected at its base and reimplanted from the distal main pul- monary artery, thus relieving the pressure over the right main bronchus and distal trachea. Clinical Scenarios Case 1 A 3-month-old girl, product of full term gestation presents to a pediatrician’s office because of respiratory distress and bouts of cyanosis noted during feeding. The mother believes that the child has always had these respiratory symptoms, exacer- bated by agitation and feeding with worsening of symptoms over the past 2 weeks. Physical examination is unremarkable other than the evidence of moderate respiratory distress. This showed normal cardiac silhouette, no evidence of bronchopulmonary pathology and a suggestion of a right aortic arch. The right aortic arch is suggestive of a vascular ring due to double aortic arch or right aortic arch with aberrant left subclavian artery. Echocardiography confirmed the diagnosis of double aortic arch, the right aortic arch was dominant, therefore surgery was performed though a left thoracotomy and the left aortic arch was ligated and resected. The child’s symptoms improved significantly postoperatively and complete resolution of symptoms was noted in a follow-up visit 3 months later. The child is suspected to have reactive airway disease and was admitted three times over the past 4 months for increasing respiratory distress associated with wheezing. On examination, the child appeared to be in moderate respiratory distress, he sat down on mother’s lap with slightly extended neck with no cyanosis. Cardiac auscultation was within normal limits, no significant Hepatomegaly was detected. Chest X-ray was not significant for any pulmonary disease, cardiac silhouette was normal in size and there was evidence of right aortic arch. In view of stridor, repeated previous hospitalization and atypical features for reactive airway disease bronchoscopy was performed which showed a pulsatile mass constricting the posterior and left aspects of the tracheal lumen. Echocardiography was not informative because of poor echo window and lack of child’s cooperation; however, right aortic arch was confirmed. Surgery was performed through a lateral thoracotomy and the ligamentum was resected causing relief of tracheal compression. The child’s symptoms improved, however, did not completely resolve except after 4–6 months. Delayed resolution is to be expected in view of anatomical changes of the trachea due to prolonged compression. Chapter 26 Congenital Abnormalities of Coronary Arteries Russell Robert Cross and Daniel E. Felten Key Facts • Congenital coronary artery anomalies are due to abnormal origin. Although echocardiography is helpful in making this diag- nosis, cardiac catheterization and angiography may be needed to ensure normal origin of coronary arteries. Felten Key Facts (continued) • Abnormal origin of left main coronary artery from the pulmonary artery is corrected by reimplanting anomalous coronary artery into the aorta, or creating a baffle to direct blood flow from the aortic root to the coronary artery originating from the pulmonary artery (Takeuchi procedure). There are many different coronary artery abnormalities, but they can generally be divided into two main groups that influence timing and type of symptoms at presentation: coronary arteries arising from the pulmonary artery or coronary arteries arising from the wrong aortic sinus. The former group is nearly always symptomatic and presents early in life with symptoms of dilated cardiomyo- pathy. On the other hand, anomalies in the latter are often asymptomatic, but may present catastrophically as sudden death in teenagers. Incidence It is estimated that 2–5% of individuals in the general population have a coronary artery anomaly, but of these, only a fraction are clinically significant. On the other hand, it is variously estimated that 10–20% of sudden death in teenagers and young adults is the result of an anomalous coronary. This makes identification of the rare clinically significant coronary artery anomaly important but challenging.
Interestingly order 50mg amitriptyline free shipping, while periodontal tissues are directly exposed to a microbial challenge even both health and disease conditions purchase amitriptyline 25 mg without a prescription, dental pulp features comprise a special situation where the tissue is enclosed by a rigid cheap amitriptyline 75mg line, mineralized tissue shell buy generic amitriptyline pills, and thus the microbial challenge only will reach the host tissue after significant enamel and dentin matrix degradation, or in other words, in already established pathological process. While the mineralized structure may present an initial protective role, in the course of pathological process the tubular structure of dentin confers significant permeability properties on the tissue (Pashley et al. After dental tissue damage by caries lesions, odontoblasts are the first pulp cells to encounter both products of the infectious process, including the invading pathogens and their components, as well as detecting dentine matrix constituents released during demineralization. Although odontoblasts provide barrier function by protecting the underlying tissue from the invading bacteria, they are also immunocompetent and capable of coordinating an inflammatory response (Veerayutthwilai et al. Progression of the carious infection deeper into the underlying dental tissue results in changes in the composition of the bacterial biofilm (Takahashi et al. Certainly, further molecular interactions between bacteria and stem cells at the core of the pulp arise, resulting in exacerbation of inflammatory events. It is because of their ability to proliferate, migrate and synthesize several Inflammation, Chronic Diseases and Cancer – 228 Cell and Molecular Biology, Immunology and Clinical Bases components of the periodontium, and also participate in both protective and destructive mechanism that prevents periodontitis or impede its progression, and initiates lesions and promotes progressive disease by various biological mechanisms, respectively (Benatti et al. In addition to the soft connective tissue elements, alveolar bone loss is a key structure of periodontal and periapical environments. Bone homeostasis depends on the maintenance of a delicate equilibrium between bone resorption by osteoclasts and bone formation by osteoblasts. It is important to make clear that tissue homeostasis represents a delicate balance between anabolic and catabolic activities, and that a wide range of stimuli can disrupt this balance and compromise the tissue integrity. Along such stimuli, inflammation-related molecules can result in pathological changes in periodontal, periapical and pulpar tissues, as discussed in the next section. However, it is important to consider that even in clinical health conditions, the periodontium continuously expresses cytokines, chemokines and cell adhesion molecules, associated with a basal level of inflammation, thought to be responsible for providing protection against bacterial challenge without resulting in tissue damage. Indeed, as previously cited, periodontal tissues are directly exposed to a microbial challenge even in healthy subjects. To cope with such microbial stimulation, the periodontium has a highly orchestrated expression of select innate host defence mediators (Darveau, 2010). Periodontal tissue, unlike the intestine, does not have a large mucous layer to prevent contact between the microbial community and the epithelial cell surface (Bosshardt & Lang, 2005, Darveau, 2010). In fact, although both periodontal and intestinal tissues are in close proximity to polymicrobial communities, it seems that they use two completely different strategies to contend with the constant presence of microbial stimulation. The intestinal epithelium is a single layer of cells connected by tight junctions that channels bacteria and their components to the highly specialized Peyers patches, where a localized, fully developed lamina propria can recognize microorganisms and respond accordingly The Role of Chemokines and Cytokines in the Pathogenesis of Periodontal and Periapical Lesions: Current Concepts 229 (Darveau, 2010, Duerkop et al. Innate host protective mechanisms are coupled with regenerative and biomechanical signalling systems, resulting in tissue homeostasis. In this context, the transition from a healthy-related to a disease-related inflammatory condition seems to be associated with quantitative and qualitative changes in the host inflammatory immune response, whose characteristics have been investigated usually in a pathological context, which will be discussed in the sequence. The balance between pro- and anti-inflammatory mediators determines the outcome of resorption in bone destructive diseases, as in periodontitis (Garlet et al. However, before specific discussion on host response to periodontal and periapical diseases outcome modulation, it is important to review the molecular pathways associated with periodontal and periapical tissues destruction. The integrity of bone tissues depends on the maintenance of a delicate equilibrium between osteoclasts and osteoblasts. It has long been assumed that the host defense against microbial invasion and subsequent tissue destruction involves both innate and adaptive immunity cytokines. We are going to discuss both immune response mechanisms, separately, in this chapter. Classic inflammatory cytokines role in periodontal and periapical inflammatory lesions As previously discussed in this chapter, the presence of pathogens is required, but not sufficient for bone inflammatory diseases initiation, being the host response a critical determinant of periodontal and periapical tissues breakdown (Graves, 2008, Nair, 2004). The innate host response initially involves the recognition of microbial components as “danger signals” by host cells and the subsequent production of inflammatory mediators. This signalling cascade involves activation of transcription factors and the subsequent inflammatory cytokines expression, leukocyte migration and osteoclastogenesis (Lima et al. However, recent studies from mouse models point to important roles of cytokines in the control of periodontal infection. Curiously, the individual absence of innate immunity cytokines attenuates inflammatory bone loss; however their simultaneous inhibition results in more effective protection leading to almost complete remission of bone loss rate (Sartori et al. In addition to a direct action toward bone resorption, innate immune cytokines also interfere with the coupled bone formation process (Behl et al. In fact, recent studies confirmed the early hypothesis that proinflammatory cytokines inhibit osteogenic differentiation (Ding et al. T helper cytokines role in periodontal and periapical inflammatory lesions Complementarily to the innate immune response, periodontal and endodontic bacteria result in mobilization of adaptive immunity mechanisms. After activation, mature dendritic cells express co-stimulatory molecules and produce distinct patterns of cytokines that will determine the subsequent polarization and activation of antigen specific lymphocytes (Cutler & Jotwani, 2004). As a general rule, immune responses mediated by T cells polarized into a Th1-type phenotype are characteristically cellular and pro-inflammatory, while Th2 cells are associated with humoral immunity and present anti-inflammatory properties (Jankovic et al. Under normal condition, proinflammatory mechanisms must be controlled in order to prevent excessive tissue destruction and promote autoimmune processes. The in vitro data support a previous hypothesis that Th1 cells are associated with the stable lesions while Th2 cells are associated with disease progression (Gemmell et al. In fact, B cell deletion was recently demonstrated to prevent bone loss in mice after oral P. The protective role for Th2- biased humoral immunity also refers to the prevention of alveolar bone loss after immunization protocols, which are usually associated with increase in serum immunoglobulin levels (Zhang, et al. Accordingly, a longitudinal human study demonstrated that serum levels of IgG antibodies against A. Indeed, while the association of Th2 cells with inflammatory diseases outcome remains controversial, Tregs have been described as a protective T cell subset concerning the tissue damage in periodontal and periapical environment. Tregs seem to be essential for the maintenance of peripheral tolerance and to control the immune response (Kotake et al. Subsequently to the discovery of Tregs subsets, the identification of a Th17 subset that present effector antagonic roles for Treg-suppressive cells (Appay et al. Th17 cells develop through cytokine signals distinct from, and antagonized by, products of the Th1 and Th2 lineages (Appay et al. In consequence, Th17 cells are thought to exacerbate inflammatory diseases by activating adjacent cells to produce inflammatory mediators, generating therefore a positive loop for inflammatory reaction amplification that leads to lesion exacerbation. Recently, it has been shown the involvement of others cytokines and Th subsets than Th1, Th2, Tregs and Th17 in the complex process of inflammatory diseases development and progression (Brand et al. However, the discovery of new T cell subsets lead to a more complex scenario regarding the role of cytokines in periapical inflammatory diseases pathogenesis. In fact, the Th1/Th2 and Th17/Tregs paradigms provided interesting frameworks, but further studies are still required to integrate them in a string theory to unravel the destructive and protective role of cytokines from the tissue destruction viewpoint. Although the lipid mediators do not fit in the classic definition of cytokines (usually comprising proteins, peptides or glycoproteins), they may modulate or be modulated by them. However, recent reports suggest that the concept of “protective and destructive” mediators in the control of periodontal and periapical infection is an obviously simplified model, and that cytokines may present dual and apparently conflicting protective or destructive roles. Hence, a different perspective is that the spatial orientation of the inflammatory infiltrate to the bone and the periodontal ligament is an important component of determining whether the destructive influence is reversible as in the case of gingivitis or irreversible as in the case of periodontitits and pulp necrosis (Graves et al. Chemokines as determinants of host response nature Leukocytes are an essential part of the host’s inflammatory response and are fundamental to antibacterial defense (Bellingan, 2000, Kantarci et al. Chemokines are a family of potent chemotatic cytokines that regulate the trafficking and recruitment of Inflammation, Chronic Diseases and Cancer – 238 Cell and Molecular Biology, Immunology and Clinical Bases leukocytes to distant sites of inflammation (Zlotnik & Yoshie, 2000). The fine tuning of the regulation of the chemokine system is essential for host homeostasis and defense, and its abnormal expression is often associated with pathological processes (Garin & Proudfoot, 2011). There is a great deal of redundancy and binding promiscuity between chemokine ligands and their receptors because some chemokines can bind multiple receptor subtypes, and some receptors can bind multiple chemokines (Murphy et al. Although most chemokine receptors recognize more than one chemokine, they are almost always restricted to a single subclass. Engagement of chemokine receptors with their respective ligands affects leukocyte migration by regulation of cytoskeletal re-arrangement, integrin-dependent adhesion, as well as by the binding and detachment of cells from their substrate (Silva et al, 2007). Among the mediators potentially involved in leukocyte migration to periodontal and periapical environment, chemokines have been investigated with special interest (Silva et al. Chemokines are found in gingival tissue and crevicular fluid and are produced by a number of cell types in the periodontium, such as fibroblasts, endothelial cells, macrophages, osteoclasts, epithelial cells, polymorphonuclear leukocytes, monocytes, lymphocytes, and mast cells and exert their effects locally in paracrine or autocrine fashion (Baggiolini, 2001, Traves & Donnelly, 2005). Some chemokines have important proinflammatory effects and are related to periodontal tissue destruction that involves the stimulation of bone resorption and induction of tissue damage. Chemokines can also affect the recruitment, differentiation, or fusion of precursor cells to form osteoclasts or enhance osteoclast survival (Pradeep et al.