**What is the Role of Pediatricians on Oral Health?**

Cigdem Elbek Cubukcu *Uludag University, School of Medicine, Consultation Unit of Oral Diseases, Turkey*

### **1. Introduction**

136 Complementary Pediatrics

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Good oral health and dentition is important for efficient mastication, speaking and cosmetically for smiling. If left untreated, dental pathologies can lead to pain and infection, reduced growth and development, speech disorders, and high treatment costs. Chronic infection around one or more teeth can result in damage to localized structures, such as the developing permanent teeth. Children who are medically compromised (such as being immunocompromised from a disease and/or therapy) are at increased risk of developing systemic complications from dental infections which can be fatal. Therefore, the author focuses on the role of the general pediatrician in promoting the importance of good oral health for all children and in particular those children receiving cancer therapy. Etiology, assessment, and prevention of dental caries and oral mucositis are presented, evidence based where available.

### **2. Dental caries development**

Dental caries has historically been considered one of the most important global oral health burdens. It is still a major health problem in both developing and developed countries. 60-90 % of school-aged children are affected by the disease (Petersen, 2003). At present, the distribution and severity of dental caries vary in different parts of the world and within the same region or country. In permanent dentition, when dental caries experience is expressed as Significant Caries Index (SiC), the determined values are relatively high both for America region (SiC = 4.8) and the European region (SiC = 5.3) whereas the experience is lower in most African countries (SiC = 3.4) (World Health Organization [WHO], 2011). In developing countries, the prevalence rates of dental caries and its experience are now tending to increase probably due to the increasing consumption of sugars and inadequate exposure to fluorides. Conversely, a decline in caries has been observed in most developed countries as a result of a number of public health measures, including effective use of fluorides, together with changing living conditions, lifestyles and improved self-care practices. However, it must be emphasized that *dental caries as a disease of children has not been eradicated, but only controlled to a certain degree.*

#### **2.1 Etiology of dental caries**

Dental caries is a process that may take place on any tooth surface in the oral cavity where dental plaque (biofilm) is allowed to develop over a period of time. Plaque formation is a

What is the Role of Pediatricians on Oral Health? 139

**Upper Primary Teeth Development Chart**  Upper Teeth When tooth emerges When tooth falls out Central incisor 8 to 12 months 6 to 7 years Lateral incisor 9 to 13 months 7 to 8 years Canine (cuspid) 16 to 22 months 10 to 12 years First molar 13 to 19 months 9 to 11 years Second molar 25 to 33 months 10 to 12 years **Lower Primary Teeth Development Chart**  Lower Teeth When tooth emerges When tooth falls out Second molar 23 to 31 months 10 to 12 years First molar 14 to 18 months 9 to 11 years Canine (cuspid) 17 to 23 months 9 to 12 years Lateral incisor 10 to 16 months 7 to 8 years Central incisor 6 to 10 months 6 to 7 years Table 1. Eruption and exfoliation timetable of primary human dentition. The first teeth begin to break through the gums at about 6 months of age. Usually, the first two teeth to erupt are the two bottom central incisors (the two bottom front teeth). Next, the top four front teeth emerge. After that, other teeth slowly begin to fill in, usually in pairs -- one each side of the upper or lower jaw -- until all 20 teeth (10 in the upper jaw and 10 in the lower jaw) have

> **Upper Permanent Teeth Development Chart**  Upper Teeth When tooth emerges Central incisor 7 to 8 years Lateral incisor 8 to 9 years Canine (cuspid) 11 to 12 years

(first bicuspid) 10 to 11 years

First molar 6 to 7 years Second molar 12 to 13 years Third molar (wisdom teeth) 17 to 21 years **Lower Permanent Teeth Development Chart**  Lower Teeth When tooth emerges

Second premolar (second bicuspid) 10 to 12 years

Third molar (wisdom tooth) 17 to 21 years Second molar 11 to 13 years First molar 6 to 7 years

Second premolar (second bicuspid) 11 to 12 years

(first bicuspid) 10 to 12 years Canine (cuspid) 9 to 10 years Lateral incisor 7 to 8 years Central incisor 6 to 7 years Table 2. Eruption and exfoliation timetable of permanent human dentition. Permanent teeth begin to come in around the age of 6.

First premolar

First premolar

first to emerge; in others, the incisors are the first to emerge.

natural, physiological process. It is an example of a biofilm which means a community of microorganisms attached to a surface. The bacteria in the plaque are always metabolically active. Some of them are capable of fermenting a suitable dietary carbohydrate substrate (such as the sugars sucrose and glucose), to produce acid. The acid produced causes the plaque pH to fall to below 5 within 1-3 minutes. Repeated falls in pH may result in demineralization of the tooth surface in time. However, the acid is neutralized by saliva, so the pH increases and mineral may be regained. This is called remineralization. The cumulative results of de- and remineralization processes may be a loss of mineral and a carious lesion can be seen. Alternatively, the changes may be so slight that a carious lesion never becomes apparent (Kidd, 2005). *The formation of the biofilm and its metabolic activity cannot be prevented, but dental caries formation can be controlled, its progression in enamel tissue can be arrested and even advanced carious lesions (in dentin) may become inactive.*

#### **2.2 Factors known to influence increased dental caries risk**

Socio-economic factors or circumstances may influence increased caries risk. Factors such as social deprivation, unemployment, lower socio-economic status, low knowledge, low education of parents, and no regular dental check-ups are directly related to dental caries resulting in more cariogenic food consumption, less good oral hygiene, saliva problems (medications), and reduced fluoride support (WHO, 1994).

General health may also indicate increased caries risk. Some general diseases such as Sjögren's Syndrome or their treatments (medicines) affect saliva secretion. Also, the conditions can result in more cariogenic food and in less good oral hygiene (WHO, 2003).

Medicines can interfere with dental caries in two ways by leading to voluminous plaqueformation (containing fermentable carbohydrates) and by leading to a change in saliva production and composition. Medicines classified as follows have been proposed to cause xerostomia (oral dryness): antispasmodic, antidepressant, antipsychotic, skeletal muscle relaxant, parkinsonism therapy, antiarrythmic, antihistamine, appetite depressant, anticonvulsant, anxiolytic, antihypertensive, and diuretic. *Oral dryness is the third most common side-effect from using medicines* (Moore, 2008)*.*

Diet is one of the key factors for dental caries and will be discussed in detail on section 4.1.

### **3. Assessment of dental development and referral for dental problems**

Accurate chronologies of primary (deciduous) teeth calcifications as well as permanent dentition in particular first permanent molars are of clinical significance to the pediatricians (Table 1 and 2). It is often necessary to explain to parents the time sequence of calcification in utero and during infancy. The common observation of tetracycline pigmentation, developmental enamel defects, and generalized hereditary anomalies can be explained if the calcification schedule is known.

#### **3.1 Chronologic development and eruption of the teeth**

Evidence of development of the human tooth can be observed as early as the sixth week of embryonic life. Its life starts with initiation (bud stage) and follows with proliferation (cap stage), histodifferentiation and morphodifferentiation (bell stage), apposition, and

natural, physiological process. It is an example of a biofilm which means a community of microorganisms attached to a surface. The bacteria in the plaque are always metabolically active. Some of them are capable of fermenting a suitable dietary carbohydrate substrate (such as the sugars sucrose and glucose), to produce acid. The acid produced causes the plaque pH to fall to below 5 within 1-3 minutes. Repeated falls in pH may result in demineralization of the tooth surface in time. However, the acid is neutralized by saliva, so the pH increases and mineral may be regained. This is called remineralization. The cumulative results of de- and remineralization processes may be a loss of mineral and a carious lesion can be seen. Alternatively, the changes may be so slight that a carious lesion never becomes apparent (Kidd, 2005). *The formation of the biofilm and its metabolic activity cannot be prevented, but dental caries formation can be controlled, its progression in enamel tissue*

Socio-economic factors or circumstances may influence increased caries risk. Factors such as social deprivation, unemployment, lower socio-economic status, low knowledge, low education of parents, and no regular dental check-ups are directly related to dental caries resulting in more cariogenic food consumption, less good oral hygiene, saliva problems

General health may also indicate increased caries risk. Some general diseases such as Sjögren's Syndrome or their treatments (medicines) affect saliva secretion. Also, the conditions can result in more cariogenic food and in less good oral hygiene (WHO, 2003). Medicines can interfere with dental caries in two ways by leading to voluminous plaqueformation (containing fermentable carbohydrates) and by leading to a change in saliva production and composition. Medicines classified as follows have been proposed to cause xerostomia (oral dryness): antispasmodic, antidepressant, antipsychotic, skeletal muscle relaxant, parkinsonism therapy, antiarrythmic, antihistamine, appetite depressant, anticonvulsant, anxiolytic, antihypertensive, and diuretic. *Oral dryness is the third most*

Diet is one of the key factors for dental caries and will be discussed in detail on section 4.1.

Accurate chronologies of primary (deciduous) teeth calcifications as well as permanent dentition in particular first permanent molars are of clinical significance to the pediatricians (Table 1 and 2). It is often necessary to explain to parents the time sequence of calcification in utero and during infancy. The common observation of tetracycline pigmentation, developmental enamel defects, and generalized hereditary anomalies can be explained if the

Evidence of development of the human tooth can be observed as early as the sixth week of embryonic life. Its life starts with initiation (bud stage) and follows with proliferation (cap stage), histodifferentiation and morphodifferentiation (bell stage), apposition, and

**3. Assessment of dental development and referral for dental problems**

*can be arrested and even advanced carious lesions (in dentin) may become inactive.*

**2.2 Factors known to influence increased dental caries risk**

(medications), and reduced fluoride support (WHO, 1994).

*common side-effect from using medicines* (Moore, 2008)*.*

**3.1 Chronologic development and eruption of the teeth**

calcification schedule is known.

Table 1. Eruption and exfoliation timetable of primary human dentition. The first teeth begin to break through the gums at about 6 months of age. Usually, the first two teeth to erupt are the two bottom central incisors (the two bottom front teeth). Next, the top four front teeth emerge. After that, other teeth slowly begin to fill in, usually in pairs -- one each side of the upper or lower jaw -- until all 20 teeth (10 in the upper jaw and 10 in the lower jaw) have come in by the time the child is 2 ½ to 3 years old.

Table 2. Eruption and exfoliation timetable of permanent human dentition. Permanent teeth begin to come in around the age of 6. In some children, the first permanent molars are the first to emerge; in others, the incisors are the first to emerge.

What is the Role of Pediatricians on Oral Health? 141

a temporary painful condition which relieves within a few days. The eruption process may be hastened if the child is allowed to chew on a clean teething object. Using finger press technique upon where the tooth has been emerging will subside the probably fretful condition. The application of a nonirritating topical anesthetic may bring in temporary relief in the child has been experiencing extreme difficulty during the teeth eruption (Sood &

• A general rule of thumb is that for every 6 months of life, approximately 4 teeth will

• Teeth in both jaws usually erupt in pairs -- one on the right and one on the left Primary teeth are smaller in size and whiter in color than the permanent teeth that will

• By the time a child is 2 to 3 years of age, all primary teeth should have erupted Shortly after age 4, the jaw and facial bones of the child begin to grow, creating spaces between the primary teeth. This is a perfectly natural growth process that provides the

• Between the ages of 6 and 12, a mixture of both primary teeth and permanent teeth

• They help attain good nutrition (missing or carious teeth make it difficult to chew

• They help give a healthy start to the permanent teeth (caries and infection in baby teeth

A bluish purple, elevated area of tissue called an *eruption hematoma* rarely develops a few weeks before the eruption of a primary or permanent tooth. It is actually a blood-filled cyst. It occurs most frequently in the primary second molar or the first permanent molar regions. The condition usually develops as a result of trauma to the soft tissue during mastication. The condition is self-limited and usually subsides in a few days following the break-through of the crown. Therefore, the treatment of the hematoma is rarely necessary. In order to expose the crown, surgical incision of the gingival tissue may rarely be needed (Tsiklakis &

The eruption sequestrum is seen occasionally at the time of eruption of the first permanent molar. It may develop from either osteogenic (Starkey & Shafer, 1963) or odontogenic tissue (Watkins, 1975; Pridds & Price, 1984). Regardless of its origin, the condition is usually of

If baby teeth fall out after a couple of years, why is it important to care for them?

can cause dark spots on the permanent teeth developing beneath it).

Sood, 2010).

erupt

follow

Patsakas, 1989).

**3.2.2 Eruption sequestrum**

reside in the mouth

Primary teeth eruption facts for the pediatricians:

• Girls generally precede boys in tooth eruption • Lower teeth usually erupt before upper teeth

necessary space for the larger permanent teeth to emerge.

• They reserve space for their permanent counterparts

• They give the face its normal appearance • They aid in the development of clear speech

causing children to reject foods)

**3.2.1 Eruption hematoma (eruption cyst)**

calcification (AlQahtani et al., 2010). Ameloblasts will form enamel whereas odontoblasts will form dentin tissue. Following completion of all these stages the tooth will erupt. Primary teeth will shed (exfoliate) to their permanent successors. Although many theories have been advanced (Marks Jr., 1996; Philbrick et al., 1998; Wise et al., 2002), the factors responsible for the eruption of the teeth are not fully understood. The factors that have been related to the eruption of teeth include elongation of the root, forces exerted by the vascular tissues around and beneath the root, growth of the alveolar bone, growth of dentin, growth and pull of the periodontal membrane, hormonal influences (pituitary growth hormone, thyroid hormone, and parathyroid hormone-related protein), presence of a viable dental follicle, pressure from the muscular action, and resorption of the alveolar crest. A review article by Wise et al (Wise et al., 2002) focused on the molecular signals that initiate tooth eruption. They stated that tooth eruption is a complex and tightly regulated process involving cells of the tooth organ and surrounding alveolus. Mononuclear cells (osteoclast precursors) must be engaged into the dental follicle prior to the onset of eruption. These cells will turn into osteoclasts which resorb alveolar bone, and create an eruption pathway for the tooth to exist its bony container. Interaction of osteoblasts, osteoclasts and dental follicle involve a complex interplay of regulatory genes. It should be remembered that the time of eruption of both primary and permanent teeth varies greatly and variations of 6 months on either side of the usual eruption date may be considered normal for a given child. Demirjian and Levesque (1980) investigated a large sample of 5437 radiographs from a homogenous French-Canadian population, their analysis showed the similarity in timing between sexes for the early stages of tooth development (crown formation). However, their data indicated the importance of sexual dimorphism during the period of root development which girls were more advanced than boys by an average of 0.35 year for four teeth. For the stages of root development the mean difference between the sexes for all teeth was 0.54 year. The largest difference was for the canine (0.90 year). A study by Proffit and Fraizer-Bowers (2009) reviews the mechanism and control of tooth eruption. Finally an extensive review by Almonaitiene et al. (2010) analyzed the factors influencing permanent teeth eruption. Readers who wish to obtain more information about the details of the tooth eruption process are referred to these review articles.

#### **3.2 Teething and difficult eruption**

In general, the eruption of primary teeth comes before by increased salivation, and the child would want to put the hands and fingers into the mouth. Some young children become daytime restlessness, an increase in the amount of finger sucking or rubbing of the gum, an increase in drooling and some loss of appetite during the time of eruption of the primary teeth. *These observations may be the only indication that the teeth will soon erupt (*Macknin et al., 2000; Feldens et al., 2010)*.* However, in some children a pronounced change in the mucosa often with small hemorrhages could be expected (Tasanen, 1968). Many conditions including croup, diarrhea, fever, convulsions, and primary herpetic gingivostomatitis have been *incorrectly* attributed to eruption (Dally, 1996). Leung (1989) reported that serious mistakes could be made in the care of infants and toddlers if their symptoms were ascribed to teething without completion of a thorough diagnostic evaluation and resulted in the overlooking of significant systemic disturbances. *Because of the tooth eruption is a normal physiologic process, the association with fever and systemic disturbances are not justified*. Inflammation of the gingival tissues before complete eruption of the tooth crown may cause

calcification (AlQahtani et al., 2010). Ameloblasts will form enamel whereas odontoblasts will form dentin tissue. Following completion of all these stages the tooth will erupt. Primary teeth will shed (exfoliate) to their permanent successors. Although many theories have been advanced (Marks Jr., 1996; Philbrick et al., 1998; Wise et al., 2002), the factors responsible for the eruption of the teeth are not fully understood. The factors that have been related to the eruption of teeth include elongation of the root, forces exerted by the vascular tissues around and beneath the root, growth of the alveolar bone, growth of dentin, growth and pull of the periodontal membrane, hormonal influences (pituitary growth hormone, thyroid hormone, and parathyroid hormone-related protein), presence of a viable dental follicle, pressure from the muscular action, and resorption of the alveolar crest. A review article by Wise et al (Wise et al., 2002) focused on the molecular signals that initiate tooth eruption. They stated that tooth eruption is a complex and tightly regulated process involving cells of the tooth organ and surrounding alveolus. Mononuclear cells (osteoclast precursors) must be engaged into the dental follicle prior to the onset of eruption. These cells will turn into osteoclasts which resorb alveolar bone, and create an eruption pathway for the tooth to exist its bony container. Interaction of osteoblasts, osteoclasts and dental follicle involve a complex interplay of regulatory genes. It should be remembered that the time of eruption of both primary and permanent teeth varies greatly and variations of 6 months on either side of the usual eruption date may be considered normal for a given child. Demirjian and Levesque (1980) investigated a large sample of 5437 radiographs from a homogenous French-Canadian population, their analysis showed the similarity in timing between sexes for the early stages of tooth development (crown formation). However, their data indicated the importance of sexual dimorphism during the period of root development which girls were more advanced than boys by an average of 0.35 year for four teeth. For the stages of root development the mean difference between the sexes for all teeth was 0.54 year. The largest difference was for the canine (0.90 year). A study by Proffit and Fraizer-Bowers (2009) reviews the mechanism and control of tooth eruption. Finally an extensive review by Almonaitiene et al. (2010) analyzed the factors influencing permanent teeth eruption. Readers who wish to obtain more information about the details of the tooth eruption

In general, the eruption of primary teeth comes before by increased salivation, and the child would want to put the hands and fingers into the mouth. Some young children become daytime restlessness, an increase in the amount of finger sucking or rubbing of the gum, an increase in drooling and some loss of appetite during the time of eruption of the primary teeth. *These observations may be the only indication that the teeth will soon erupt (*Macknin et al., 2000; Feldens et al., 2010)*.* However, in some children a pronounced change in the mucosa often with small hemorrhages could be expected (Tasanen, 1968). Many conditions including croup, diarrhea, fever, convulsions, and primary herpetic gingivostomatitis have been *incorrectly* attributed to eruption (Dally, 1996). Leung (1989) reported that serious mistakes could be made in the care of infants and toddlers if their symptoms were ascribed to teething without completion of a thorough diagnostic evaluation and resulted in the overlooking of significant systemic disturbances. *Because of the tooth eruption is a normal physiologic process, the association with fever and systemic disturbances are not justified*. Inflammation of the gingival tissues before complete eruption of the tooth crown may cause

process are referred to these review articles.

**3.2 Teething and difficult eruption**

a temporary painful condition which relieves within a few days. The eruption process may be hastened if the child is allowed to chew on a clean teething object. Using finger press technique upon where the tooth has been emerging will subside the probably fretful condition. The application of a nonirritating topical anesthetic may bring in temporary relief in the child has been experiencing extreme difficulty during the teeth eruption (Sood & Sood, 2010).

Primary teeth eruption facts for the pediatricians:

If baby teeth fall out after a couple of years, why is it important to care for them?

#### **3.2.1 Eruption hematoma (eruption cyst)**

A bluish purple, elevated area of tissue called an *eruption hematoma* rarely develops a few weeks before the eruption of a primary or permanent tooth. It is actually a blood-filled cyst. It occurs most frequently in the primary second molar or the first permanent molar regions. The condition usually develops as a result of trauma to the soft tissue during mastication. The condition is self-limited and usually subsides in a few days following the break-through of the crown. Therefore, the treatment of the hematoma is rarely necessary. In order to expose the crown, surgical incision of the gingival tissue may rarely be needed (Tsiklakis & Patsakas, 1989).

#### **3.2.2 Eruption sequestrum**

The eruption sequestrum is seen occasionally at the time of eruption of the first permanent molar. It may develop from either osteogenic (Starkey & Shafer, 1963) or odontogenic tissue (Watkins, 1975; Pridds & Price, 1984). Regardless of its origin, the condition is usually of

What is the Role of Pediatricians on Oral Health? 143

*interfere with breastfeeding or not hypermobile, no intervention is necessary. Consultation with a pediatric dentist is strongly recommended in order to evaluate the preferred treatment and for differential diagnosis.* Eruption of teeth during the neonatal period causes fewer problems. These teeth can usually be maintained even tough root development is limited (Figure 1).

Fig. 1. Intraoral view showing a natal teeth and Riga-Fede disease (quoted from

of the literature. *Dent Traumatol* 26, 6, Dec, 490-5.)

**3.4 Epstein pearls, bohn nodules, and dental lamina cysts**

**3.5 Local and systemic factors that influence tooth eruption**

is recommended for appropriate treatment.

Padmanabhan et al. (2010) Neonatal sublingual traumatic ulceration - case report & review

Small, white or grayish white lesions on the alveolar mucosa of the newborn are identified as inclusion cysts. They are classified as the following three types according to their location in oral cavity: Epstein pearls are formed along the midpalatine raphe. Bohn nodules are formed along the buccal and lingual aspects of the dental ridges and on the palate away from the raphe. Dental lamina cysts are found on the crest of the maxillary and mandibular ridges. These lesions are usually multiple but do not increase in size. No treatment is indicated since the lesions will spontaneously be shed a few weeks after birth. These lesions

may be incorrectly diagnosed as the natal teeth (Fromm, 1967; Cetinkaya et al., 2011).

Local factors which influence tooth eruption are ankylosed primary and permanent teeth, and ankylosis of primary molars with absence of permanent successors. Local factors generally cause delayed teeth eruption (Ertugrul et al., 2002). Referral to a pediatric dentist

General factors associated with altered tooth eruption are Down syndrome (Trisomy 21 syndrome), cleidocranial dysplasia, congenital hypothyroidism (Cretinism), juvenile hypothyrodism, hypopituitarism, and achondroplastic dwarfism. Sporadic delayed eruption of teeth frequently occurs in children with Down syndrome. The first primary teeth may not appear until 2 years of age, and the dentition may not be complete until 5 years of age. The eruption generally follows an abnormal sequence and some of the primary teeth may be retained until 15 years of age (Jara et al., 1993; Ondarza et al., 1997). The prevalence and severity of early onset periodontal disease in children with Down syndrome are much

little or no clinical significance. As the tooth erupts, the fragment will sequestrate. However, it can be removed if it causes local irritation.

#### **3.2.3 Ectopic eruption**

A variety of local factors such as arch length inadequacy may influence a tooth to erupt or try to erupt in an abnormal position (Gupta et al, 2011).

#### **3.3 Natal and neonatal teeth (prematurely erupted primary teeth)**

The normal eruption of the primary teeth typically begins at six months of age. Natal teeth (teeth present at birth) and neonatal teeth (teeth that erupt during the first 30 days) are usually benign conditions (Cunha et al., 2001). Whatever the conditions they are, both of them considered as early eruption of primary teeth. Spouge and Feasby believe that the terms *natal teeth* and *neonatal teeth* constitute a relatively artificial distinction. Therefore, they have suggested that the terms *mature* and *immature* are more in keeping with the varying prognoses associated with such teeth in clinical point of view (Spouge & Feasby, 1966). The incidence of natal teeth ranges from 1:2000 to 1:3500 live births (Seminario & Ivancakova, 2004). The exact etiology is unknown. Infection, febrile states, trauma, malnutrition, superficial position of the tooth germ, hormonal stimulation and maternal exposure to environmental toxins has been implicated as causative factors (Cunha et al., 2001). It has been previously reported that heavily exposures to polychlorinated biphenyls and dibenzofurans caused to born infants with natal teeth in Taiwan (Gladen et al., 1990). However, Alaluusa et al. (2002) did not find any association between milk levels of polychlorinated biphenyls and dibenzofurans, and the occurrence of natal teeth. Early eruption of primary teeth might occur as a hereditary transmission of an autosomal dominant gene. A positive familial history has been reported in 8-62 % of natal teeth cases (Zhu & King, 1995). Natal teeth are present in 2 % of infants with unilateral cleft lip and palate and 10 % of infants with bilateral cleft lip and palate (de Almeida & Gomide, 1996). Natal teeth have been reported in association with syndromes such as Ellis-van Creveld, Jadassohn-Lewandowsky, Hallerman-Streiff, craniofacial dysostosis, steacystoma multiplex, Sotos, Wiedemann-Rautenstrauch, Meckel-Gruber and Pierre Robin (Seminario & Ivancakova, 1992; Uzamis et al., 1999; Marakoglu et al., 2004).

The most commonly affected teeth are the lower primary central incisors (85 %), followed by the maxillary incisors (11%), mandibular canines and molars (3 %), and maxillary canines and molars (1 %). Natal teeth usually occur in pairs (Zhu & King, 1995). However, an unusual case of an infant with fourteen natal teeth was reported by Masatomi et al. (1991). Natal teeth might resemble normal primary teeth in size and shape; however, the teeth are often smaller, conical and yellowish, and have hypoplastic enamel and dentin with poor or absent root development. Most prematurely erupted primary teeth are mobile because of limited root development. Some teeth may be supernumerary or mobile to the extent that there is danger of displacement of the tooth and possible aspiration. In such cases the removal (extraction) of the tooth is indicated. However, Zhu and King (1995) did not find any reported cases of aspirated natal or neonatal teeth in the literature. In some cases sharp incisal edge of the teeth may cause sublingual ulceration of the infant (Riga-Fede disease) or laceration of the mothers' breasts. If the teeth with rough edges are not hypermobile or not supernumerary; smoothing the sharp incisal edges of teeth or the placement of round smooth composite resin over the incisal edges is indicated. *However, if the tooth does not*

little or no clinical significance. As the tooth erupts, the fragment will sequestrate. However,

A variety of local factors such as arch length inadequacy may influence a tooth to erupt or

The normal eruption of the primary teeth typically begins at six months of age. Natal teeth (teeth present at birth) and neonatal teeth (teeth that erupt during the first 30 days) are usually benign conditions (Cunha et al., 2001). Whatever the conditions they are, both of them considered as early eruption of primary teeth. Spouge and Feasby believe that the terms *natal teeth* and *neonatal teeth* constitute a relatively artificial distinction. Therefore, they have suggested that the terms *mature* and *immature* are more in keeping with the varying prognoses associated with such teeth in clinical point of view (Spouge & Feasby, 1966). The incidence of natal teeth ranges from 1:2000 to 1:3500 live births (Seminario & Ivancakova, 2004). The exact etiology is unknown. Infection, febrile states, trauma, malnutrition, superficial position of the tooth germ, hormonal stimulation and maternal exposure to environmental toxins has been implicated as causative factors (Cunha et al., 2001). It has been previously reported that heavily exposures to polychlorinated biphenyls and dibenzofurans caused to born infants with natal teeth in Taiwan (Gladen et al., 1990). However, Alaluusa et al. (2002) did not find any association between milk levels of polychlorinated biphenyls and dibenzofurans, and the occurrence of natal teeth. Early eruption of primary teeth might occur as a hereditary transmission of an autosomal dominant gene. A positive familial history has been reported in 8-62 % of natal teeth cases (Zhu & King, 1995). Natal teeth are present in 2 % of infants with unilateral cleft lip and palate and 10 % of infants with bilateral cleft lip and palate (de Almeida & Gomide, 1996). Natal teeth have been reported in association with syndromes such as Ellis-van Creveld, Jadassohn-Lewandowsky, Hallerman-Streiff, craniofacial dysostosis, steacystoma multiplex, Sotos, Wiedemann-Rautenstrauch, Meckel-Gruber and Pierre Robin (Seminario &

The most commonly affected teeth are the lower primary central incisors (85 %), followed by the maxillary incisors (11%), mandibular canines and molars (3 %), and maxillary canines and molars (1 %). Natal teeth usually occur in pairs (Zhu & King, 1995). However, an unusual case of an infant with fourteen natal teeth was reported by Masatomi et al. (1991). Natal teeth might resemble normal primary teeth in size and shape; however, the teeth are often smaller, conical and yellowish, and have hypoplastic enamel and dentin with poor or absent root development. Most prematurely erupted primary teeth are mobile because of limited root development. Some teeth may be supernumerary or mobile to the extent that there is danger of displacement of the tooth and possible aspiration. In such cases the removal (extraction) of the tooth is indicated. However, Zhu and King (1995) did not find any reported cases of aspirated natal or neonatal teeth in the literature. In some cases sharp incisal edge of the teeth may cause sublingual ulceration of the infant (Riga-Fede disease) or laceration of the mothers' breasts. If the teeth with rough edges are not hypermobile or not supernumerary; smoothing the sharp incisal edges of teeth or the placement of round smooth composite resin over the incisal edges is indicated. *However, if the tooth does not*

it can be removed if it causes local irritation.

try to erupt in an abnormal position (Gupta et al, 2011).

**3.3 Natal and neonatal teeth (prematurely erupted primary teeth)**

Ivancakova, 1992; Uzamis et al., 1999; Marakoglu et al., 2004).

**3.2.3 Ectopic eruption**

*interfere with breastfeeding or not hypermobile, no intervention is necessary. Consultation with a pediatric dentist is strongly recommended in order to evaluate the preferred treatment and for differential diagnosis.* Eruption of teeth during the neonatal period causes fewer problems. These teeth can usually be maintained even tough root development is limited (Figure 1).

Fig. 1. Intraoral view showing a natal teeth and Riga-Fede disease (quoted from Padmanabhan et al. (2010) Neonatal sublingual traumatic ulceration - case report & review of the literature. *Dent Traumatol* 26, 6, Dec, 490-5.)


**6. Information content and axiomatic properties**

Since the pioneer work by Wang and Kerre [1], researchers have examined the axiomatic properties (i.e., the six axioms listed in Section 2) of fuzzy number ranking methods. The intent of this section is to discuss how the information content for ranking can influence the axiomatic properties in the context of our ranking approach. One key message is that the satisfaction of axioms depends on the selection of information that is deemed relevant to FNR. If more information is selected and considered for ranking, the ranking method is more likely to violate the axioms. This message is aligned with the topic of information basis in the analysis of the Arrow's Impossibility Theorem [39, 40].

#### **6.1 Analysis of Axiom 4**

Axiom 4 somewhat dictates the ranking of non-overlapping fuzzy numbers. If we only consider representative x-values for ranking (i.e., no range, membership ratio and discount factors), our ranking procedure will directly follow the results from Ban and Coroianu [28], and it will thus satisfy Axiom 4. However, if range and membership ratio are considered as relevant information for ranking, Axiom 4 can be violated, and the reason is given below.

Axiom 4 only focuses on the boundary values without considering any distributional information (e.g., range and membership). When multiple attributes are considered for ranking, Axiom 4 can be violated by strengthening the distributional aspect of the inferior fuzzy number (in view of Axiom 4). For example, we have *FO*2≽*FO*1 in case o (see **Table 5**) according to Axiom 4, no matter how small of membership ratio of *FO*2. However, when we consider range and membership ratio, we obtain *FO*1≽*FO*2 (see **Table 6**), which violates Axiom 4. Notably, the logic of such violation can be held whenever we deem membership ratio as relevant information for FNR, regardless of the details of the ranking procedures.

Notably, this discussion is not about rejecting Axiom 4. Instead, we want to explain one logical tension with Axiom 4. That is, Axiom 4 dictates some ranking of fuzzy numbers based on their boundary values only, and this opens a chance for the information of range and membership ratio to violate Axiom 4. Alternately, if we choose the index class by [28], representative x-values will be the only information considered for ranking, and the information of range (for example) will become irrelevant for FNR. In other words, if we consider that FNR should involve trade-off with multiple attributes in addition to representative x-value, Axiom 4 could be violated in some situations.


*5.1. IEEE*−*13 Bus URDN*

5.1.1. Fundamental Power Flow Solution for Accuracy Test

The proposed three-phase FPFA is examined on IEEE−13 bus unbalanced test feeder without interfacing of D-STATCOM device. Figure 7 shows the IEEE−13 bus feeder and its data is collected from [31]. 5000 kVA and 4.16 kV are the chosen base values for this network. The FPFA is taken 5 iterations for its convergence with tolerance for convergence is 10−4 . The comparison of obtained power flow solution with IEEE solution and errors in voltage magnitudes and phase angles at every bus are presented in Table 4. Table 5 presents the comparison of obtained power loss with the IEEE losses. Insignificant values of maximum errors of 0.0005 p.u and 0.010o for voltage magnitudes and phase angles are observed in Table 6. So that, in terms of accuracy the test results are consistent with IEEE results.

**Figure 7.** IEEE 13 Bus URDN.

**Table 4.** Fundamental voltage solution for IEEE−13 bus URDN.

**Table 5.** Power loss in IEEE−13 bus URDN.

**Table 6.** Power loss in IEEE−13 bus URDN.


**1.4 Tendon reflexes and H-reflexes of the proximal muscles**

The L3-4 posterior roots can be studied with the patellar reflex (**Figure 4a** and **b**), and the adductor reflex [6]. The adductor tendon reflex can be evoked by ipsilateral tap to the medial epicondyle of the femur. Surprisingly, this reflex may also be elicited easily by tap to several sites of the lower extremity: for instance contralateral patellar tap, as well as ipsi- and contralateral anterior superior iliac spine tap. On the contrary, patellar tendon reflex was obtained only by ipsilateral tap to the patellar tendon. H-reflex of the adductor muscle (latency 16.4 ms, SD 1.6) is obtained by percutaneous

**41**

**Figure 3.**

*Calibration as above.*

*Recording of Proprioceptive Muscle Reflexes in the Lower Extremity*

stimulation of the obturator nerve at the level of pubic tubercle. Even a mediumlatency reflex, "late polysynaptic reflex response" of more than 50 ms was described in the adductor muscle [6]. However, these methods are rarely used in routine ENMG studies. The H-reflex of the quadriceps femoris muscle is readily recorded by stimulation of the femoral nerve [4], but we have not gained any experience with this method. The Achilles tendon reflex may also be recorded with surface electrodes on the triceps surae muscle. This recording was not used in routine ENMG studies. We should also

*A. M-response of the right peroneus longus muscle in a patient aged 80 with a right L5 root syndrome: Right L5 compression in MRI, positive needle EMG finding in the right L5 paraspinal muscle, F-response latency asymmetrically prolonged in the right extensor digitorum brevis muscle but bilaterally normal in the abductor hallucis muscles. Stimulation of the common peroneal nerve at the fibular head. Latency of the M-response 3.9 ms. The H-reflex cannot be elicited in spite of changes of the stimulation intensity 3.0-11.7 mA (submaximal and supramaximal). Calibration: 8 ms/div and 5 mV/div. No medium latency reflexes (see Figure 9). The tibialis posterior nerve was evidently not coactivated with the stimulation of the common peroneal nerve, there was only plantar dorsiflexion. B. M-response and H-reflex (arrow) of the left peroneus longus muscle of the patient. Latency of the M-response 4.0 ms and H-reflex 31.2 ms. stimulation intensity 3.1-14.4 mA.*

remember that the tendon reflex and H-reflex have distinct differences [7].

*DOI: http://dx.doi.org/10.5772/intechopen.95575*

*Recording of Proprioceptive Muscle Reflexes in the Lower Extremity DOI: http://dx.doi.org/10.5772/intechopen.95575*

#### **Figure 3.**

*Proprioception*

**Figure 2.**

*observed (not shown).*

**40**

of the given muscle [4], but we have found it too difficult for routine use. No H-reflex for the L5-level was described for clinical use in root syndromes. We have tried to measure H-reflexes of the peroneus longus and extensor hallucis longus muscles, but these measurements were hampered by volume conduction of reflexes of the triceps surae muscle. However, H-reflex of the peroneus longus muscle can be confirmed by recording it with EMG needle electrode (**Figure 2**). The peroneus longus H-reflex may disappear in the symptomatic side of a patient with unilateral L5 root syndrome (**Figure 3**). Problems with volume conduction are

*H-reflex of peroneus longus, 32 years old male. Stimulation with 2 cm bipolar surface electrode to common peroneal nerve at the fibular head causing clear ankle dorsiflexion; ten concurrent stimulations with increasing stimulation current. Simultaneous recording of peroneus longus with both surface electrodes (interelectrode distance ca 3 cm), a 30 G concentric needle electrode, and soleus with surface electrodes (interelectrode distance ca 3 cm). Note the typical appearance of H-wave, latency 32 ms (vertical line), reaching its maximal amplitude before M-wave (contrary to the performance of F-responses) and appearance of H-wave solely on peroneus longus and not on soleus. 2 mV/div, 8 ms/div. A similar recording with surface electrodes on the lateral gastrocnemius muscle was also performed and no reflex response of this muscle was*

The L3-4 posterior roots can be studied with the patellar reflex (**Figure 4a** and **b**), and the adductor reflex [6]. The adductor tendon reflex can be evoked by ipsilateral tap to the medial epicondyle of the femur. Surprisingly, this reflex may also be elicited easily by tap to several sites of the lower extremity: for instance contralateral patellar tap, as well as ipsi- and contralateral anterior superior iliac spine tap. On the contrary, patellar tendon reflex was obtained only by ipsilateral tap to the patellar tendon. H-reflex of the adductor muscle (latency 16.4 ms, SD 1.6) is obtained by percutaneous

**1.4 Tendon reflexes and H-reflexes of the proximal muscles**

discussed at the end of this chapter.

*A. M-response of the right peroneus longus muscle in a patient aged 80 with a right L5 root syndrome: Right L5 compression in MRI, positive needle EMG finding in the right L5 paraspinal muscle, F-response latency asymmetrically prolonged in the right extensor digitorum brevis muscle but bilaterally normal in the abductor hallucis muscles. Stimulation of the common peroneal nerve at the fibular head. Latency of the M-response 3.9 ms. The H-reflex cannot be elicited in spite of changes of the stimulation intensity 3.0-11.7 mA (submaximal and supramaximal). Calibration: 8 ms/div and 5 mV/div. No medium latency reflexes (see Figure 9). The tibialis posterior nerve was evidently not coactivated with the stimulation of the common peroneal nerve, there was only plantar dorsiflexion. B. M-response and H-reflex (arrow) of the left peroneus longus muscle of the patient. Latency of the M-response 4.0 ms and H-reflex 31.2 ms. stimulation intensity 3.1-14.4 mA. Calibration as above.*

stimulation of the obturator nerve at the level of pubic tubercle. Even a mediumlatency reflex, "late polysynaptic reflex response" of more than 50 ms was described in the adductor muscle [6]. However, these methods are rarely used in routine ENMG studies. The H-reflex of the quadriceps femoris muscle is readily recorded by stimulation of the femoral nerve [4], but we have not gained any experience with this method. The Achilles tendon reflex may also be recorded with surface electrodes on the triceps surae muscle. This recording was not used in routine ENMG studies. We should also remember that the tendon reflex and H-reflex have distinct differences [7].

#### **Figure 4.**

*a. Electrical recording of the patellar reflex, 33 years old male. Stimulation with tendon hammer electrically connected to EMG-machine. Recording is triggered by a strike to prepatellar tendon. Recording in the rectus femoris muscle with both concentric needle electrode (30 G) and surface electrodes and an accelerometer connected to tibia. Three separate recordings of same stimulation protocol. 7-10 superimposed responses. Patellar reflex at ca 20 ms. 20 ms/div. b. Electrical recording of the patellar reflex, responses shown in a.*

**43**

*Recording of Proprioceptive Muscle Reflexes in the Lower Extremity*

A medium latency reflex response (60-80 ms) of the soleus muscle can be recorded by supramaximal stimulus of the common peroneal nerve, which causes powerful twitch contraction of the peroneal muscles [8] (**Figure 5a**). Originally this reflex response was considered to use low-threshold muscle afferents and a transcranial loop, possibly involving the primary motor cortex and the supplementary motor area [9]. Later on it was demonstrated that the medium-latency reflex response of the soleus muscle to stretch does not involve a long reflex loop [10]. Soleus stretch resulting from unexpected perturbation during human walking elicits both short and medium latency reflex responses. It was concluded by cooling, ischaemia and tizanidine studies that the afferent receptors of the short latency component are Ia afferents and those of the medium latency component are

By stimulation of the common peroneal nerve at the fibular neck, only the medium latency reflex response can be recorded in electroneurography of the human soleus muscle [8] (**Figure 5a**). It was observed that stimulation of the common peroneal nerve results in long lasting (up to 200 ms) soleus H-reflex depression [12]. On the contrary, by stimulation of the posterior tibial nerve at the popliteal space, no medium latency reflex response can be recorded from the

**1.6 Calculations of conduction velocities and the role of β-efferents in the**

the upper extremity [13] and 48 m/s in the lower extremity [7].

The distances between the stimulation and recording sites were measured when the responses depicted in **Figure 5a** were recorded. The afferent pathway for H-reflex latency 27.0 ms was 640 mm between the stimulation site at the popliteal space, and L1 spinal level. Respectively, the distance of the efferent pathway between L1 spinal level and the estimated motor point of the soleus muscle was 750 mm. Considering that the synaptic delay in the spinal cord is about 1 ms [7] we can conjecture that the afferent conduction time from the stimulation site to the spinal cord is 11 ms and the efferent conduction time is 15 ms. The respective conduction velocities are for Ia afferents 58 m/s and for α motor efferents 50 m/s. These values match well with the recordings of Ia afferent conduction velocity 64 m/s and α motor conduction velocity 56 m/s of the median nerve [13], assuming that the respective values are slightly slower in the lower than in the upper extremity. The more distally recorded Ia afferent conduction velocity between the popliteal fossa and ankle is 56 m/s [7]. Cutaneous afferents are slower than Ia afferents, 61 m/s in

A similar calculation may be performed for the medium latency reflex latency 62 ms. The distance from the proximal part of the soleus muscle (site of the most proximal muscle spindles) to the L1 spinal level was 670 mm, and the distance from L1 to the motor point of the soleus muscle was 750 mm. The estimated afferent conduction time is 30 ms and the efferent conduction time 31 ms, the spinal synaptic delay time was again estimated to be 1 ms. By these values we may calculate, that the afferent conduction velocity for II-afferent pathway is 22 m/s, and for the efferent conduction velocity is 24 m/s. This afferent conduction velocity matches well with the II-afferent conduction velocity 21 m/s observed in the lower extremity [14]. But the efferent conduction velocity 24 m/s is far too slow for the α motor efferent pathway, which was calculated to be 50 m/s in the H-reflex arch (see above).

*DOI: http://dx.doi.org/10.5772/intechopen.95575*

**1.5 Medium latency reflex responses**

II-afferents, respectively [11].

anterior tibial muscle [8].

**medium latency reflexes**

## **1.5 Medium latency reflex responses**

*Proprioception*

**42**

**Figure 4.**

*a. Electrical recording of the patellar reflex, 33 years old male. Stimulation with tendon hammer electrically connected to EMG-machine. Recording is triggered by a strike to prepatellar tendon. Recording in the rectus femoris muscle with both concentric needle electrode (30 G) and surface electrodes and an accelerometer connected to tibia. Three separate recordings of same stimulation protocol. 7-10 superimposed responses. Patellar reflex at ca 20 ms. 20 ms/div. b. Electrical recording of the patellar reflex, responses shown in a.*

A medium latency reflex response (60-80 ms) of the soleus muscle can be recorded by supramaximal stimulus of the common peroneal nerve, which causes powerful twitch contraction of the peroneal muscles [8] (**Figure 5a**). Originally this reflex response was considered to use low-threshold muscle afferents and a transcranial loop, possibly involving the primary motor cortex and the supplementary motor area [9]. Later on it was demonstrated that the medium-latency reflex response of the soleus muscle to stretch does not involve a long reflex loop [10]. Soleus stretch resulting from unexpected perturbation during human walking elicits both short and medium latency reflex responses. It was concluded by cooling, ischaemia and tizanidine studies that the afferent receptors of the short latency component are Ia afferents and those of the medium latency component are II-afferents, respectively [11].

By stimulation of the common peroneal nerve at the fibular neck, only the medium latency reflex response can be recorded in electroneurography of the human soleus muscle [8] (**Figure 5a**). It was observed that stimulation of the common peroneal nerve results in long lasting (up to 200 ms) soleus H-reflex depression [12]. On the contrary, by stimulation of the posterior tibial nerve at the popliteal space, no medium latency reflex response can be recorded from the anterior tibial muscle [8].

## **1.6 Calculations of conduction velocities and the role of β-efferents in the medium latency reflexes**

The distances between the stimulation and recording sites were measured when the responses depicted in **Figure 5a** were recorded. The afferent pathway for H-reflex latency 27.0 ms was 640 mm between the stimulation site at the popliteal space, and L1 spinal level. Respectively, the distance of the efferent pathway between L1 spinal level and the estimated motor point of the soleus muscle was 750 mm. Considering that the synaptic delay in the spinal cord is about 1 ms [7] we can conjecture that the afferent conduction time from the stimulation site to the spinal cord is 11 ms and the efferent conduction time is 15 ms. The respective conduction velocities are for Ia afferents 58 m/s and for α motor efferents 50 m/s. These values match well with the recordings of Ia afferent conduction velocity 64 m/s and α motor conduction velocity 56 m/s of the median nerve [13], assuming that the respective values are slightly slower in the lower than in the upper extremity. The more distally recorded Ia afferent conduction velocity between the popliteal fossa and ankle is 56 m/s [7]. Cutaneous afferents are slower than Ia afferents, 61 m/s in the upper extremity [13] and 48 m/s in the lower extremity [7].

A similar calculation may be performed for the medium latency reflex latency 62 ms. The distance from the proximal part of the soleus muscle (site of the most proximal muscle spindles) to the L1 spinal level was 670 mm, and the distance from L1 to the motor point of the soleus muscle was 750 mm. The estimated afferent conduction time is 30 ms and the efferent conduction time 31 ms, the spinal synaptic delay time was again estimated to be 1 ms. By these values we may calculate, that the afferent conduction velocity for II-afferent pathway is 22 m/s, and for the efferent conduction velocity is 24 m/s. This afferent conduction velocity matches well with the II-afferent conduction velocity 21 m/s observed in the lower extremity [14]. But the efferent conduction velocity 24 m/s is far too slow for the α motor efferent pathway, which was calculated to be 50 m/s in the H-reflex arch (see above).

#### **Figure 5.**

*a. the tibial H-reflex of the soleus muscle elicited with submaximal stimuli, minimum latency 27.0 ms. The stimulation was changed to the common peroneal nerve at the knee joint and supramaximal stimuli elicited the medium latency reflexes of soleus, minimum latency 62.0 ms (vertical line). The" M-response" was reflected from the pretibial muscles. For calculations of the afferent and efferent conduction velocities of the reflex responses* see text*. Calibration: 10 ms/div, 2 mV/div. A voluntary healthy subject, male, age 31 y, height 166 cm. b. H-reflex of the median nerve (2 uppermost sweeps), latency 15,5 ms (arrow), stimulation: Median nerve at the elbow, recording with surface electrodes on the forearm flexors. The stimulation was changed to the radial nerve at the spiral groove (2 middle responses). When the stimulus was turned to supramaximal value, medium latency reflex responses, latency 30.5 ms, were elicited (vertical line, 5 lowermost sweeps) from the forearm flexors. Calibration: 8 ms/div, 2 mV/div. A voluntary healthy subject, male, age 31 y, height 166 cm.*

**45**

**Figure 6.**

*Recording of Proprioceptive Muscle Reflexes in the Lower Extremity*

This fact justifies the hypothesis that the efferent pathway of the medium latency reflexes consists of skeletofusimotor β motor fibres, which are thinner and slower

Ib afferent nerve fibres from Golgi tendon organs are slightly smaller than those of Ia afferents [11]. The electrically evoked excitatory postsynaptic potential may be curtailed by the inhibitory postsynaptic potential of only slightly longer latency than the excitatory postsynaptic potential [7]. There is a Ib inhibitory volley from the Golgi tendon organs, which originate from the proximal tendon insertion of the anterior tibial muscle, elicited by the strong contraction of the muscle by stimulation of the posterior tibial nerve at the popliteal space. This inhibitory volley may reach the spinal cord and prevent the occurrence of the medium latency reflex response. The lack of medium latency reflex was pointed out in this muscle [8]. Unexpected perturbation during walking elicits short- and medium-latency soleus reflex responses [11]. However, soleus stretch, caused by electric stimulation of the common peroneal nerve and powerful contraction of the pretibial muscles, elicits only a medium-latency reflex response of the soleus muscle. It may be considered that the Ia reciprocal inhibitory influence [7] plays a role in inhibition of the soleus

The forearm flexor muscles (for example m. flexor carpi radialis and m. flexor digitorum superficialis) show H-reflexes, when the median nerve is stimulated at the elbow [4]. When the stimulation is changed to the radial nerve at the spiral groove, a medium reflex response may be recorded at the same site than the median H-reflex (**Figure 5B**). Thus, the respective reflex responses seem to be elicited in

*The" reflex" response of the anterior tibial muscle (latency 27.4 ms), recorded by the stimulation of the posterior tibial nerve at the popliteal fossa. Superficially it may be reminiscent to a myotatic reflex of the anterior tibial muscle, but in reality it is the H-reflex of the triceps surae muscle, volume conducted to the recording site (compare with the H-reflex recording in Figure 4). The" M-response" points out the direct*

*activation of the triceps surae muscle. Calibration: 8 ms/div, 2 mV/div.*

than α motor fibres. β motor efferents have been observed in man [15].

**1.7 The possible influence of inhibitory pathways on the reflex responses**

*DOI: http://dx.doi.org/10.5772/intechopen.95575*

short-latency reflex response in this situation.

**1.8 Comparison with the upper extremity**

*Proprioception*

**44**

**Figure 5.**

*a. the tibial H-reflex of the soleus muscle elicited with submaximal stimuli, minimum latency 27.0 ms. The stimulation was changed to the common peroneal nerve at the knee joint and supramaximal stimuli elicited the medium latency reflexes of soleus, minimum latency 62.0 ms (vertical line). The" M-response" was reflected from the pretibial muscles. For calculations of the afferent and efferent conduction velocities of the reflex responses* see text*. Calibration: 10 ms/div, 2 mV/div. A voluntary healthy subject, male, age 31 y, height 166 cm. b. H-reflex of the median nerve (2 uppermost sweeps), latency 15,5 ms (arrow), stimulation: Median nerve at the elbow, recording with surface electrodes on the forearm flexors. The stimulation was changed to the radial nerve at the spiral groove (2 middle responses). When the stimulus was turned to supramaximal value, medium latency reflex responses, latency 30.5 ms, were elicited (vertical line, 5 lowermost sweeps) from the forearm flexors. Calibration: 8 ms/div, 2 mV/div. A voluntary healthy subject, male, age 31 y, height 166 cm.*

This fact justifies the hypothesis that the efferent pathway of the medium latency reflexes consists of skeletofusimotor β motor fibres, which are thinner and slower than α motor fibres. β motor efferents have been observed in man [15].


**5. Conclusions**

The microwave-based vegetation water content index, Emissivity Di fference Vegetation Index (EDVI) has a close connection to the evapotranspiration process in forests [26–29] and responses to precipitation process dynamically [69]. In this study, we designed an algorithm for forest LE estimation driven by EDVI from an advanced microwave scanning radiometer for EOS (AMSR-E), vegetation fraction information derived from a moderate-resolution imaging spectroradiometer (MODIS), net radiation flux derived from clouds and earth's radiation energy system (CERES), which are all on the Aqua satellite, and the associated parameters of atmospheric states from the European Centre for Medium-Range Weather Forecasts (ECMWF).

The satellite inputs and the results of this algorithm are validated against the in situ measurements at three ChinaFLUX sites located at the Dinghushan (DHS) covered by subtropical evergreen broad-leaved forest, Qianyanzhou (QYZ) covered by subtropical plantation forest, and Changbaishan (CBS) covered by temperate deciduous mixed forest from 2003 to 2005. Validation results show that the mean correlation coe fficients (R) between instantaneous LEcal and LEobs in the study years of DHS, QYZ and CBS are 0.62, 0.82 and 0.83 with small bias errors of +23.08 Wm−2, +10.69 Wm−2 and −15.57 Wm−2, respectively. These biases were well kept within 16% of the in situ measurements for three sites. At a monthly scale, the R between LEcal and LEobs can reach 0.84, 0.88, and 0.95 at DHS, QYZ, and CBS, with bias of +14.3%, −0.3%, and −12.9%, respectively. Validation results can be further improved after removing the samples in severely rainy days.

Our method is also validated under di fferent cloudy sky conditions. The results indicate that EDVI-based LEcal have stable performances with good accuracy under cloudy sky for all three forests. Slopes of fit lines are close to 1.0 and the bias are less than 35 Wm−2 (26%) for di fferent cloud cover. A good temporal correlation between LEcal and LEobs under clear and cloudy skies is indicated by the R of 0.62–0.80. These results indicate that this EDVI-based LE algorithm, using only satellite and reanalysis datasets as inputs, has great potential for estimating LE at large scale in forest areas under cloudy sky in China.

The extensive application and improvement of our algorithm is warranted in more di fferent biome types. Potential improvements can be achieved by (i) taking into account the evaporation components from bare soil and canopy-intercepted water, (ii) considering the inhomogeneity within the satellite field of view at microwave regions and (iii) extending the current LE estimation from one point to the regional scale.

**Author Contributions:** Conceptualization, Y.W. and R.L.; Methodology, Y.W. and R.L.; Validation, Y.W.; Writing—original draft preparation, Y.W.; Writing—review and editing, Y.W. and R.L.; Supervision, R.L., Q.M., L.Z., G.Y. and Y.B. All authors discussed the results and revised the manuscript.

**Funding:** This work was funded by the National Natural Science Foundation of China NSFC (Grant No. 41675022, 41375148, 41830104), National Key R&D Program on Monitoring, Early Warning and Prevention of Major Natural Disasters under grant (Grant No. 2017YFC1501402), Belmont Forum and JPI-Climate Collaborative Research Action with NSFC (Grant No.<PHONE_NUMBER>7), the "Hundred Talents Program" of the Chinese Academy of Sciences, the "Hundred Talents Program" of Anhui Province, and the Jiangsu Provincial 2011 Program (Collaborative Innovation Center of Climate Change).

**Acknowledgments:** We thank the anonymous reviewers and members of the editorial team for their helpful comments and valuable suggestions which have helped us greatly improve the manuscript. We thank Zongting Gao, in Institute of Meteorological Sciences of Jilin Province, Jilin Provincial Key Laboratory of Changbai Mountain Meteorology & Climate Change, Laboratory of Research for Middle-High Latitude Circulation and East Asian Monsoon in Changchun, for his significant help in data processing and data analysis in this work.

**Conflicts of Interest:** The authors declare no conflict of interest.


**Abstract**

Nowadays, sugar\*free food is very popular because of its low calorie value. So food industries make use of various artificial sweeteners of low calorie as an alternative to high calorie sugars and they provide low glycemic response. The U.S. Food and Drug Administration has approved artificial sweeteners such as saccharin, acesulfame-K, sucralose, aspartame, etc. as per acceptable daily intake value (ADI) value, but these artificial sweeteners that breakdown products during metabolism in turn are known to have health and metabolic effects. Hence, in this work, we will discuss about artificial sweeteners, types, and their metabolic and health effects.

**Keywords:** artificial sweeteners, adverse effects, potential toxicity


**Conflict of interest**

The authors have declared no conflict of financial interest.

*Application of Carbon Nanomaterials Decorated Electrochemical Sensor for Analysis… DOI: http://dx.doi.org/10.5772/intechopen.96538*


**Discrete-Time Fractional-Order Systems: Modeling and Stability Issues Discrete-Time Fractional-Order Systems: Modeling and Stability Issues**

Saïd Guermah, Saïd Djennoune and Maâmar Bettayeb Saïd Djennoune and Maâmar Bettayeb Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/51983