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Join our two-day hands-on workshop on porcelain veneers at Ivoclar Academy, Gurgaon, Delhi, India.
👉Dates: 27th and 28th October.
👉Limited to 15 participants only.
👉WhatsApp 8700383548 to register for the next batch.

To register, here is the website details – https://tmc.gov.in/m_conference_new/Conference/Onlinereg?confid=24290
Intensive microbiologic, immunologic, and morphologic research investigations, especially during the past decade, have shown that colonization of tooth surface by pathogenic bacteria is accompanied by humoral and cellular defense mechanisms of the organism not only during the more advanced stage of infection, but also throughout the initial stages. Penetration of these complex defenses, which is usually of limited duration, disturbs the equilibrium of the system and results in disease. Within the dental pulp, this biologic equilibrium has to do with the balanced calcium and phosphate ion exchange during the continuous demineralization and remineralization of the enamel and exposed dentin. As long as a disease process is reversible, as is incipient caries, the capacity for progression and regression is present. Carious breakdown means that enamel is being demineralized by acidogenic plaque more rapidly than it can be remineralized. In its early stages, the caries has become a chronic destructive process, in which irreversible structural changes will preclude any further remission.
Looking at the dynamics of demineralization and remineralization, and the etiology of caries against the epidemiologic background, and comparing them with the results of therapy, a pattern of active disease spurts alternating with resting phases emerges. During these periods of remission, the chronic destructive process is not reversed, but is only brought to a standstill. This concept of progression and stagnation ( Socransky et al. 1984) is strongly influenced by the defensive capability of the organism.
Progression is defined by invasion of caries into dentin with inflammation and loss of connective tissue. Stagnation means the defenses are increased, there are defensive inflammatory cells in the tissues, and connective tissue is being replaced by secondary dentin or granulation tissue. Histologically, this ever-changing dynamic process in carious teeth is recorded over the years through deposition and destruction of dentin.
For the practitioner, the obvious questions that arise are how to classify the histopathologic condition of the pulp and the apical periodontal tissues, and how to initiate treatment that is appropriate, considering the background of stagnation or progression. Based upon clinical findings, differentiations are made between a clinically sound pulp, reversible pulpitis, irreversible pulpitis, a necrotic pulp, and apical periodontitis. These distinctions are based solely upon clinical observations; generally, a correlation between certain symptoms and a specific pathologic entity cannot be expected. Making the distinction between reversible and irreversible inflammations of the pulpal tissues can be a diagnostic problem, because they can present similar clinical symptoms. Histologically, the diagnosis of acute inflammation is based upon the predominance of neutrophilic granulocytes. However, this diagnostic picture does not always coincide with the appearance of pain symptoms because neutrophilic granulocytes can also be found in cases where there is no pain ( Langeland 1981, Lin and Langeland 1981 b, Lin et al. 1984 ).
Caries begins with microscopic demineralization of the affected enamel or cementum surface. As it progresses, the enamel first becomes chalky, then its surface is broken through. In this stage, the caries is easy to detect, but has frequently progressed so far that extensive restorative and endodontic treatment in necessary. More difficult to diagnose, on the other hand, are lesions that are in their early stages and dentinal lesions with macroscopically intact surfaces.
Epidemiologic studies have shown that – coincident with a general decrease in caries prevalence in industrialized countries – the occlusal surfaces of the permanent molars of children and young adults are the surfaces most frequently attacked by caries. In contrast to fissure caries, proximal and smooth surface caries is much less frequent. Radiographically evident incipient lesions in enamel of the proximal surfaces have likewise shown a decline. In adults, the probability that these lesions would penetrate further has increased, and this has caused the proportion of proximal caries to rise again.
During clinical examination using explorer many carious lesions with cavity go undiagnosed, so for their proper diagnosis bitewing radiographs, and fiberoptic transillumination (FOTI) are used. Bitewing radiographs are still the method of choice for the diagnosis of approximal caries, and account for the detection of approximately three-fourths of dentinal carious lesions ( Mileman and van der Weele 1990, Noar and Smith 1990). Studies found that where there is a dentinal lesion, there is a surface that has been broken through, which precludes any chance for remineralization (Marthaler and Germann 1970; Bille and Thylstrup 1982; Mejare and Malmgren 1986). Even though the actual extent of caries is underestimated with the radiograph, it may be concluded that the specificity, that is, the ability to recognize sound teeth as sound, is approximately 95% ( Mileman and van der Weele 1990). As far as caries diagnosis is concerned more sensitive X-ray films seem to be the equal of earlier films as far as caries diagnosis is concerned but as they produce same degree of contrast with significantly less radiation, their use is now highly recommended. Preventive measures can impede further penetration and even promote remineralization, provided that the enamel surface has not yet been disrupted.
The progression of caries can be monitored with periodic radiographs. Their interval depends, among other things, upon the individual’s susceptibility to caries. Patients at high risk of caries should be radiographed every year while those at very low risk need only be radiographed every 2-4 years. The time in which it takes caries to penetrate the enamel of a mature permanent molar in a patient with good oral hygiene can exceed 5 years. This offers the opportunity to post-pone invasive restorative treatment and to observe whether the caries progresses or regresses. The rate at which penetration progresses can be estimated by comparing radiographs produced at different times by a standardized technique. Recently erupted teeth, on the other hand, demonstrate a markedly reduced penetration time (Marthaler and Wiesner 1973, Shwarz et al. 1984).
In order to minimize overlapping of the images of approximating tooth surfaces, a film holder is recommended. A deviation of the horizontal angle of the X-ray tube by only a few degrees will result in a substantial decrease in correct diagnoses. Radiolucency in dentin should be treated as invasive only if there is also an unmistakable radiolucency in the enamel region. The radiograph should be inspected carefully under magnification and away from the influence of any light coming from the sides.
FOTI can be used in addition to bitewing radiographs if there is no interference from adjacent interproximal fillings that are other than tooth colored. More than 70% of dentinal lesions in anterior teeth can be detected by means of FOTI. Dentinal lesions in posterior teeth, however, can be differentiated only with great difficulty ( Pieper and Schurade 1987, Choski et al. 1994 ).


Reference – Color Atlas of Dental Medicine
ENDODONTOLGY
Rudolf Beer, Michael A. Baumann, and Syngcuk Kim
Navigating the Antibiotic Puzzle in Maxillofacial Space Infections
Ah, the world of maxillofacial space infections, where microbes dance in the shadows, and antibiotics become our knights in shining armor. But, my dear readers, the antibiotic quest is no simple tale, for it’s a matter of choosing the right weapon against the unseen invaders.
🧫 Microbial Dance: The Cast of Characters
Antibiotics play a crucial role in the management of maxillofacial space infections. These infections can be caused by a wide variety of aerobic and anaerobic microorganisms (Mehedi et al., 2019). The choice of antibiotics should be based on the causative microorganisms and their susceptibility to different antimicrobial agents (Mehedi et al., 2019).
📋 Antibiotic Casting Call: The Right Players
In general, the main empiric antibiotics used for the treatment of oral and maxillofacial infections are amoxicillin-clavulanic acid, metronidazole, and erythromycin (Lee et al., 2022). However, it is important to note that the resistance to amoxicillin in dental infections can range from 9% to 54% (Lee et al., 2022).
🏥 Strategic Timing: Perioperative Antibiotics
In the management of maxillofacial space infections, the use of perioperative antibiotics is recommended to prevent postoperative infections (Lauder et al., 2010). The current standard of care is to administer antibiotics within 2 hours before surgery, as this has been shown to reduce the rates of surgical site infections (Lauder et al., 2010). However, the use of additional antibiotics outside the perioperative timeframe does not reduce the rate of postoperative infections (Lauder et al., 2010). It is worth noting that the use of additional antibiotics may be warranted in cases of severe facial trauma with multiple open fracture wounds (Lauder et al., 2010).
🕶️ The Antibiotic Hero: Clindamycin Takes Center Stage
In terms of antibiotic efficacy, a study conducted by found that clindamycin was the most effective single antibiotic, with a sensitivity rate of 90% in cases of orofacial space infections (Mehedi et al., 2019). Other effective single antibiotics included erythromycin (50%) and azithromycin (40%) (Mehedi et al., 2019). However, it is important to note that most orofacial space infections are caused by mixed microorganisms, making it difficult to treat them with a single empirical antibiotic (Mehedi et al., 2019).
🦠 Antibiotic-Resistant Drama: A Growing Plot Twist
The emergence of antibiotic-resistant bacteria is a growing concern in the management of maxillofacial infections. It has been reported that the overuse, abuse, and misuse of antibiotics contribute to the development of antibiotic-resistant bacteria (Yuvaraj, 2015). However, clinical observations have shown that the presence of penicillin-resistant strains in mixed microflora of odontogenic maxillofacial infections does not adversely affect the outcome of treatment when penicillin is prescribed as an adjunct to surgical drainage (Yuvaraj, 2015).
💊 Beyond Antibiotics: Multifaceted Strategies
In addition to antibiotic therapy, other treatment modalities may be used in the management of maxillofacial space infections. These include surgical drainage of the abscess, removal of the source of infection (such as extraction or endodontic therapy of the offending tooth), and the use of herbal anti-edematous agents to reduce post-operative swelling (Dongol et al., 2022; Dar-Odeh et al., 2018).
🔍 In Conclusion: The Script for Success
As the final act approaches, remember that the script for success depends on understanding the microbial ensemble and their antibiotic preferences. Perioperative antibiotics are the opening act, but the choice should be tailored to the situation. Keep an eye on the looming specter of antibiotic-resistant bacteria and let responsible stewardship guide the way.
RESEARCH ARTICLES WITH DOWNLOADABLE LINKS
REFERENCES
Dar-Odeh, N., Abu-Hammad, S., & Abu-Hammad, O. (2018). Herbal anti-edematous agents for certain cases of facial cellulitis of odontogenic origin. clinical recommendation.. The International Arabic Journal of Antimicrobial Agents, 8(3). https://doi.org/10.3823/825 Dongol, A., Bhattarai, N., Yadav, A., Acharya, P., Mahato, V., & Jaisani, M. (2022). Microbial flora and their antibiotic susceptibility in oral and maxillofacial infections at bpkihs: a prospective observational study. Journal of Bp Koirala Institute of Health Sciences, 5(1), 9-14. https://doi.org/10.3126/jbpkihs.v5i1.43381 Lauder, A., Jalisi, S., Spiegel, J., Stram, J., & Devaiah, A. (2010). Antibiotic prophylaxis in the management of complex midface and frontal sinus trauma. The Laryngoscope, 120(10), 1940-1945. https://doi.org/10.1002/lary.21081 Lee, H., Moon, S., Oh, J., Choi, H., Park, S., Kim, T., … & You, J. (2022). Eskape pathogens in oral and maxillofacial infections. Journal of Oral Medicine and Pain, 47(1), 52-61. https://doi.org/10.14476/jomp.2022.47.1.52 Mehedi, A., Chowdhury, G., Rab, A., & Haider, I. (2019). Evaluation of efficiency of conventional empirical antimicrobial regimen for the management of maxillofacial fascial space infection. Journal of Armed Forces Medical College Bangladesh, 11(2), 47-54. https://doi.org/10.3329/jafmc.v11i2.39823 Yuvaraj, V. (2015). Maxillofacial infections of odontogenic origin: epidemiological, microbiological and therapeutic factors in an indian population. Indian Journal of Otolaryngology and Head & Neck Surgery, 68(4), 396-399. https://doi.org/10.1007/s12070-015-0823-x
Sections show buccal mucosa in which there is mild epithelial atrophy with parakeratosis. The pattern of epithelial maturation is regular and the overall architecture is preserved. The rete processes are flattened and bands of hyaline collagen best seen in Van Geison stained sections are present in the lamina propria. A mild chronic inflammatory infiltrate is present in the subepithelial tissue.
Our adventure starts with a visit to the microscopic realm of the buccal mucosa – the inner lining of the cheek. Imagine a bustling cityscape with layers of epithelial cells, each playing its role in maintaining the oral harmony. But wait, something’s not quite right here!
🔬 Clue 1: The Atrophy Enigma
The buccal mucosa seems to be undergoing a transformation – a mild epithelial atrophy. It’s as if the cells are shrinking, losing some of their vitality. Parakeratosis is in play too, where these cells are holding onto their nuclei longer than they should. It’s like they’re not quite ready to grow up and shed their immature ways.
📜 Clue 2: The Architectural Anomaly
Despite the changes, the overall architectural blueprint of the buccal mucosa remains intact. The maturation of the epithelial cells follows a regular pattern, almost like well-practised dancers performing a choreographed routine. The rete processes – the finger-like projections that interlock the layers – appear flatter than usual. It’s as if they’re tired and can’t stand as tall as they used to.
🔍 Clue 3: The Mysterious Collagen Chronicles
Ah, now for a fascinating twist! Van Geison stained sections reveal bands of hyaline collagen lurking in the depths of the lamina propria – the supporting layer beneath the epithelium. These collagen bands are like secretive cobwebs, weaving a mysterious tale of their own. Their presence hints at something more profound beneath the surface.
🔥 Clue 4: The Inflammatory Intrigue
As our investigation deepens, we stumble upon an unexpected guest – a mild chronic inflammatory infiltrate. It’s almost like a small group of protesters voicing their concerns beneath the epithelial cityscape. What could they be protesting? What’s causing this subtle turmoil?
🚀 The Grand Reveal: Unveiling Submucous Fibrosis
Now, my fellow detectives, armed with our clues and insights, it’s time for the big reveal! The answer to this intriguing riddle is none other than Submucous Fibrosis.
🕵️♂️ Unraveling the Mystery
Submucous Fibrosis is a condition often linked to the chewing of paan (betel), a common practice in certain cultures. In this condition, dense collagenous bands sneakily weave their way into the lamina propria – that’s the collagen we spotted earlier! These bands tighten their grip, causing limitations in mouth opening and even trouble with swallowing.
But wait, there’s more! The potential consequences get even more serious. With these collagenous infiltrators running amok, there’s a risk of dysplasia – that’s abnormal cell growth – and even the development of oral cancer.

A 65-year-old man went through some serious stuff. 🙌 He had a mandibular rim resection and neck dissection to tackle squamous-cell carcinoma in the floor of his mouth and ventral tongue. 🦠 The pathologist’s notes spill the beans – the tumor was mainly hanging out in the mouth floor, measuring 28mm wide and 11mm deep. And guess what? Out of 48 lymph nodes from the neck dissection, 5 were playing host to some sneaky squamous-cell carcinoma guests, 2 even decided to venture out of their capsules! 🏃♂️💥 So, what’s the verdict?
So, in fancy doctor lingo aka Union for International Cancer Control, they call it pT2 when the tumor’s between 2 and 4cm big, and pN2b when you got a bunch of nodes involved but none are bigger than 6cm. 🤷♂️
Nose is richly supplied by both the external and internal carotid systems, both on the septum and the lateral walls. NASAL SEPTUM Internal Carotid System – Branches of Ophthalmic Artery External Carotid System LATERAL WALL Internal Carotid System – Branches of Ophthalmic Artery External Carotid System LITTLE’S AREA Situated in the anterior inferior part of […]