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No Causal Link between Periodontal and Heart Disease

Dental blog article written April 16, 2012

After a review of over 500 journal articles and studies, the American Heart Association (AHA) has again released a statement in its April 18 (2012) issue of Circulation that it does not support the finding of a causative link between periodontal disease and atherosclerotic vascular disease.

A consensus on the position is held by the ADA Council on Scientific Affairs, the AHA, including infectious disease specialists, cardiologists, and dentists.  Many doctors have long suspected a causative link between heart disease and periodontal disease for decades, as have others in the medical community.

Although there appears to be a strong association between the two conditions, past studies have not accounted for common risk factors between periodontal and heart disease, such as age, smoking, and diabetes mellitus.

Both conditions do produce common clinical markers of inflammation, such as C-reactive protein.  Periodontal treatment has been shown to reduce systemic inflammation, and thus levels of inflammatory markers.  However, that does not in any way guarantee heart disease reduction or reversal.

The same day, the American Academy of Periodontology (AAP) released its position:

“While current research does not yet provide evidence of a causal relationship between the two diseases, scientists have identified biologic factors, such as chronic inflammation, that independently link periodontal disease to the development or progression of cardiovascular disease in some patients.”

As practitioners, we need to be certain our patients are not absorbing unwarranted conclusions from the media, while also getting out the word on the many health benefits of improved dental hygiene and maintenance.

Leeway Space in Primary Dentition

Dental question written for National Dental Board Exam review course.

 

Which of the following pertains to Leeway Space in the primary dentition?

  1. The size difference in the posterior segments of both arches.
  2. The four maxillary permanent incisors are 7.6 mm wider than the primary incisors
  3. The four mandibular permanent incisors are 6.0 mm wider than the primary incisors
  4. Most arches do have somewhat wider spaces mesial to the maxillary canines and distal to the mandibular canines.
  5. The distance (in millimeters) from the facial surface of the maxillary incisors to the facial surface of the mandibular incisors when teeth are in occlusion

 

 

Answer & Explanation:                                                     

The answer is 1.

The size difference in the posterior segments of both arches is termed the Leeway Space. The combined length of the primary canine, first primary molar and second primary molar are, on average, 1.7 mm greater on each side of the mandibular arch than that of their permanent successors (canine, first premolar, and second premolar). In the maxillary arch, the primary teeth are only .9 mm greater than their permanent counterparts.

The four maxillary permanent incisors are 7.6 mm larger than the primary incisors (Choice 2) is incorrect. However; it is an important observation in evaluating space analysis during the incisor transition years (from ages 6 to 8). Taken with the observation that the four mandibular permanent incisors are 6.0 mm larger than the primary incisors, (Choice 3), these inverse size differentials have been termed the “incisor liability”.

In (Choice 4), the fact that most arches have somewhat noticeably wider spaces mesial to the maxillary canines and distal to the mandibular canines has nothing to do with the Leeway Space. Instead, these observations are termed “primate spaces”. Primate space ranges from 0 mm to 10 mm in the maxillary arch, with an average of 4 mm. The primate space range in the mandible is from 0 mm to 6 mm, with a mean of 3 mm. The primate spaces are of interest because they are utilized when the wider permanent incisors of both arches erupt.

(Choice 5) is also false. The distance (in millimeters) from the facial surface of the maxillary incisors to the facial surface of the mandibular incisors (when teeth are in occlusion) is the definition of “horizontal overjet”.

 

References:

Mathewson, R.J., Primosch, R.E. (1995). Fundamentals of Pediatric Dentistry (3rd Edition). US. Quintessence Publishing.

Lymph Node Drainage

Medical question written for the National Dental Board Exam review course.

 

Through which chain of lymph nodes will a severe infection of a maxillary tooth abscess drain?

  1. Submental
  2. Submandibular
  3. Retropharyngeal
  4. Infrahyoid
  5. Jugulodigastric

 

Answer & Explanation:

The answer is 2.

The submandibular lymph nodes are part of the superficial horizontal ring of lymph drainage. Structures that drain to it include the submental nodes (which are also part of the superficial horizontal ring), cheek, nose, upper lip, maxillary teeth, vestibular gingivae, the hard palate mucosa and gingivae, posterior floor of the mouth, and the lateral aspects of the anterior two thirds of the tongue. The submandibular nodes then drain to nodes of the deep cervical chain, paralleling the right and left internal jugular veins. In our example, a maxillary tooth could drain to vessels through the infraorbital canal and then pass into a submandibular node, next passing to a jugulodigastric node of the deep cervical nodes.

The general schematic of lymph node chain layout can be grouped into three main chains. There is a horizontal ring of superficial nodes, a horizontal ring of deep nodes, and a pair of vertical chains of deep cervical nodes (bilateral). The superficial horizontal ring contains the submental and submandibular lymph nodes, and slightly deeper parotid nodes which include superficial deep preauricular nodes and retroauricular mastoid occipital nodes. The deep horizontal ring includes retropharyngeal, paratracheal, pretracheal, prelaryngeal, and infrahyoid nodes. Finally, the deep cervical vertical chain consists of the jugulodigastric, jugular-omohyoid, and other cervical chain nodes.

The submental lymph node (Choice 1) is incorrect. Along with the submandibular lymph node, the submental lymph node is the other member of the superficial horizontal ring. The lower lip, chin, tongue tip, and anterior floor of the mouth drain to it. The submental nodes subsequently drain to the submandibular nodes of the superficial horizontal ring and to the jugulo-omohyoid nodes of the deep cervical vertical chain.

The retropharyngeal nodes (Choice 3) is also incorrect.  The retropharyngeal nodes lie within the retropharyngeal space, which is the fascial space between the pharynx wall and the prevertebral fascia of the vertebral unit. These nodes receive drainage from the posterior nasal cavity, nasopharynx, soft palate, middle ear, and external auditory meatus. They drain into the upper group of the deep cervical nodes.

The infrahyoid nodes (Choice 4) is also incorrect. The infrahyoid nodes receive drainage from the larynx, trachea, pharynx, and esophagus. They also drain into the upper group of the deep cervical nodes.

The jugulodigastric nodes (Choice 5) is also incorrect. As part of the deep cervical vertical chain, they receive drainage from the superficial horizontal ring of nodes and the deep horizontal ring of nodes. On the left side, the jugular trunk joins the thoracic duct or may enter the junction of the subclavian vein and internal jugular vein independently. On the right side, the jugular trunk joins the subclavian and broncomediastinal lymph trunks. These may join to form a common right lymphatic duct that empties to the right subclavian and internal jugular veins.

 

References:

Putz, R. & Pabst, R. (1997). Sobatta, Atlas of Human Anatomy Volume 1, Head, Neck, and Upper Limb (12th Edition). Munchen, Germany. Williams and Wilkins.

Liebgott, B. (2001). The Anatomical Basis of Dentistry (2nd Edition). US. Mosby & Co.

Embryological Development of the Tongue

Medical question written for a National Board Dental Exam test site.

Which of the following statements about embryologic development of the tongue are true?

A.  The tongue develops from the first branchial arch.
B.  Occipital somites migrate into the floor of the mouth to form the musculature of the tongue.
C.  The tongue’s somatic, sensory, and special sensory afferent nerves, and musculature arise together from the first and second branchial arches.
D.  The second branchial arch retains importance during development.
E.  The tongue begins to develop at 9 weeks.

Answer & Explanation:

The answer is B.

The tongue begins to develop at about four weeks. The pharyngeal arches meet in the midline beneath the primitive mouth. Local proliferation of the mesenchyme then gives rise to a number of swellings in the floor of the mouth. A midline swelling, the hypobranchial eminence, develops from the third arch mesenchyme. The first arch develops lingual swellings, along with a central tuberculum impar. The hypobranchial eminence overgrows the second arch, forms the root of the tongue, and fuses with the lingual swellings and the tuberculum impar. It also gives rise to the mucosal covering the root and posterior third of the tongue.

The tongue separates from the floor of the mouth by a downgrowth of ectoderm around its periphery that subsequently degenerates to form the lingual sulcus and gives the tongue mobility. The muscles of the tongue have a different origin: they arise from the occipital somites that migrate forward into the tongue area, carrying the hypoglossal nerve XII.

Each branchial arch has the same basic architecture. The inner aspect is covered by endoderm (ectoderm in the case of the first arch because it forms in front of the buccopharyngeal membrane, which delineates the junction of stomatodeum ectoderm with the foregut endoderm). The outer surface is covered by ectoderm. The central core consists of mesenchyme derived from the lateral plate mesoderm, which is surrounded by mesenchyme derived from the neural crest. The neural crest mesenchyme (also termed echtomesenchyme) condenses to form a bar of cartilage, the arch cartilage.

Each arch also contains an artery and a nerve. The nerve consists of a motor and a sensory component. The sensory nerve has two branches. One branch supplies the epithelium covering the anterior half of that arch. Another branch passes forward to supply the epithelium covering the posterior half of the preceding arch. The nerve of the first branchial arch contains the fifth cranial nerve. The second arch contains the seventh nerve. The third arch contains the ninth cranial nerve. Thus, the first arch musculature gives rise to the muscles of mastication that are innervated by the trigeminal nerve V, and the second arch gives rise to the muscles of facial expression that are innervated by the facial nerve VII.

(Choice A) is incorrect. The tongue develops from the first three branchial arches although the second arch ceases to be of importance. The third arch mesenchyme rapidly overgrows the second arch.

(Choice C) is incorrect. Because the mucosa of the anterior two thirds of the tongue is derived from the first arch, it is supplied by the arch’s trigeminal nerve V. Similarly, the mucosa of the posterior third of the tongue is derived from the third arch supplied by this arch’s hypoglossal nerve IX. These two nerves supply general sensory nerves only; special sensory taste nerves are supplied by facial nerve VII via the chora tympani.

The second branchial arch (Choice D) does not remain important during the remainder of the tongue’s development after the tongue’s mucosal covering has been formed from the first and third branchial arches.

The tongue begins to develop (Choice E) at four weeks. By the ninth week, the tongue is elevated and has begun growing forward.

References:

Putz, R. & Pabst, R. (1997). Sobatta, Atlas of Human Anatomy Volume 1, Head, Neck, and Upper Limb (12th Edition). Munchen, Germany. Williams and Wilkins.

Liebgott, B. (2001). The Anatomical Basis of Dentistry (2nd Edition). US. Mosby & Co.

Ten Cate, A.R. (1998). Oral Histology: Development, Structure, and Function (5th Edition). US. Mosby-Year Book Company.

Streptococcus tigurinis says, “Hello world”

Dental blog article written October 23, 2012

A newly discovered and named bacterium has been discovered: Streptococcus tigurinus.  It closely resembles other Streptococcus strains that colonize the oral cavity.  It was isolated from multiple blood cultures of patients suffering from endocarditis, meningitis, and spondylodiscitis.  It is believed that bleeding gums may have been the likely point of entry into these patients’ bloodstreams.

Gene sequencing studies proved the new bacterium to be a member of the Steptococcus mitis group (one of the Bad Boy Gangs of Dentistry).  However, since it does not correspond to any known species, it is thus believed to be a new (to man) species.  Strep mitis, a regular inhabitant of the mouth, is implicated in many of the above mentioned diseases after being isolated from the bloodstream of patients with these diseases.

Studying this bacterium and its strategies for causing disease is expected to shed light on other species, as well as indicate drug designs that hopefully stymie this and related bacterium.  Andrea Zbinden, MD, led the study and further reading can be found at the International Journal of Systematic and Evolutionary Microbiology:

ijs.sgmjournals.org/content/early/2012/01/16/ijs.0.038299-0

Parting the “Acid Curtain”

Dental blog article written April 12, 2012

New (and old) evidence indicates the body is much more active in fighting and preventing caries from within the tooth than previously believed possible.

Recent research findings indicate that the tooth is more than just a passive entity during the decay process. The “acid attack” explanation of caries has held currency for decades, with good reason …. attacks by acid do result in cavitation. But there is clearly more to the story than acid acting on a tiny spot of the tooth surface. Any excessive presence of acid(s) in the oral cavity leads to poor oral health of varying degrees. Nearly every day there is another finding that links poor oral health to body-wide systemic disease processes.

Many of the tooth’s dentinal defense mechanisms were uncovered and characterized quite some time ago by researchers at Loma Linda dental school, Ralph Steinman (DDS, MS) and John Leonora (PhD, Endocrinology), as early as the 1960s.¹ For years, their findings met with strong resistance by many wedded to the uncomplicated “Acid Curtain” theory of caries.

Today, there is renewed interest in dentinal physiology, as dental researchers are beginning to look at carious disease from the pulpal (dentinal fluid) side, instead of attributing decay to simple acidic destruction of the tooth’s surface. Another reason for renewed interest in the inner workings of dentin is the growing understanding of dentinal fluid transport. This knowledge is essential in the development of new restorative materials. The time is right to explore the architecture of dentinal tissue and its regulation.

The dominant acid-destruction paradigm that has prevailed since the 1940s for explaining enamel decay also applies to dentinal decay. This is because enamel and dentin share the same hydroxyapatite crystal hard tissue constituents (albeit in different percentages of composition with enamel having a higher crystal content than dentin). Advanced enamel destruction almost inevitably leaves the underlying dentin openly exposed to the hostile environment of the oral cavity.
Hyroxyapatite crystalline structure is composed of tightly packed molecules of calcium, phosphate, and hydroxyl ions of the formula Ca10(PO4)6(OH)2. This same structure is also found in bone.

The effect of acids on enamel’s hydroxyapatite crystalline structure is well understood, and it is characterized as demineralization at the tooth’s surface. In other words, enamel destruction is treated as a chemical event confined to the oral cavity and limited in scope to the local site of acid attack. Acid’s high proton concentration in solution reacts with the crystalline molecule’s hydroxyl and unprotonated phosphate groups and dissolves the crystalline structure.

Numerous events and stages are required in order to successfully form two sets of human teeth. Specialized cells lay down collagen matrix-like scaffolding during amelogenesis and dentinogenesis (starting at week 13 in human embryogenesis). Cells dedicated to laying down these scaffolds, known as ameloblasts and odontoblasts, respectively, form each tooth under a fascinating, elaborately orchestrated series of genetically regulated steps.

Ameloblasts lay down a collagen matrix that will shortly be mineralized to form enamel rods. Odontoblasts elaborate slightly different patterns of collagen matrices that will be mineralized as dentinal tubules. Vesicles of calcium phosphate ions are delivered to these matrices and the mineralization process is set in motion – largely as a passive chemical event driven by local differences in ion concentration and precipitation – once localized nucleating centers have been created.

Hydroxyapatite crystal can be strengthened when a native hydroxyl group is replaced with fluoride. This “improved” crystal (referred to as fluorapatite) is then less vulnerable to acid attack because it has a higher energy requirement for its dissociation. Fluoride is approximately the same size as the hydroxyl group and does not appreciably distort the crystal’s packed structure. Unlike the hydroxyl group it replaced, the fluoride atom will remain intact and the molecule undisturbed when exposed to moderate acid exposure in the mouth.

During tooth formation, while rods and tubules are being mineralized, fluoride can be incorporated into the developing tooth structure, if it is made available. For adults, incorporation of fluoride is only possible topically upon the tooth’s outer surface, since the tooth’s deepest structures were completed long ago. There is no way for an adult to gain access to deeper layers of tissue via fluoridation.

Acids of any source may demineralize the hydroxyapatite crystal of enamel and dentin, provided the pH is low enough. To be clear, we can distinguish between carious cavitation caused as a result of bacterial metabolism acid products and noncarious cavitation caused by the presence of acids not of bacterial origination. Common acids of this category include dietary sources such as soda drinks, fruit juices, and milk. An important nondietary source can be the body’s own digestive acids. When introduced into the oral cavity, stomach acid from bulimia and GERD demineralize enamel, leaving behind a characteristic pattern of cavitation and destruction in their wake.

Acids produced by bacterial metabolism are special, however, because the bacteria themselves elicit an immune response from the host. Bacteria is often in continual and intimate contact with the tooth at the lesion if plaque has been allowed to form. It is now obvious why two important dental treatment modalities involve both the physical removal of plaque as well as the introduction of fluoride treatment in order to “harden” the tooth’s remaining surface.

While having a lower hydroxyapatite content than enamel, the dentinal layer of the tooth is living tissue. Its soft tissue component within hard tissue dentinal tubules includes odontoblasts, dentinal fluid, and innervation with nonmylinated nerve fibers (as anyone who has ever had a toothache will vividly recall)!

Mechanoreceptors on these nerve endings are exquisitely sensitive to changes in dentinal fluid movements registered within the affected dentinal tubules. For example, a change in osmolarity in the oral cavity (such as the introduction of sugar) immediately induces dentinal fluid movement, activating the mechanoreceptors’ ion channels. This results in pain that is characteristic to the nature of the insult, especially in the case of heat or cold. This characteristic pain response provides important diagnostic symptoms that give the clinician insight to the severity of damage to the pulp. Or, in the case of a chronic lesion, there may be no response to either temperature extreme, usually indicating pulpal necrosis or a chronic lesion.

Through dentinal tubules, the body brings host defenses to bear on what happens to be a very small piece of real estate in the case of decay. Today it is recognized that caries are not merely a surface phenomenon of an acid attack on a passive rock in the mouth. Thanks to countless advances in molecular biology and immunology, cariology is being revisited with the body’s full host defenses and dentinal behavior in mind.

[1] Early on, Ralph Steinman (DDS, MS) and John Leonora (PhD, Endocrinology) investigated dentinal fluid transport and its physiological mechanisms at Loma Linda University School of Dentistry. During decades of collaboration, they established DFT regulation by a parotid-hypothalamic axis.