Journal of Dental Pathology and Medicine
Open Access

Periodontal disease; Gingivitis; Periodontitis; Dental biofilm; Host response; Diagnosis; Risk factors; Periodontal therapy; Oral microbiome; Regenerative treatment; Precision dentistry

Introduction

Periodontal disease, also known as gum disease, encompasses two main conditions, gingivitis and periodontitis. Gingivitis is the milder, reversible form characterized by inflammation of the gingival tissues without bone loss [1]. In contrast, periodontitis involves the progressive destruction of the periodontal ligament and alveolar bone, leading to tooth mobility and potential tooth loss [2].

The prevalence of periodontal disease is high, affecting nearly 50% of adults globally, with severe cases observed in around 10-15% of the population. Periodontitis is also associated with systemic conditions such as cardiovascular disease, diabetes, and adverse pregnancy outcomes [3]. Periodontal disease is a prevalent chronic inflammatory condition that compromises the integrity of the periodontium—the specialized tissues that surround and support the teeth [4]. It is a leading cause of tooth loss in adults and poses significant public health concerns due to its high prevalence and association with systemic diseases such as cardiovascular disease, diabetes mellitus, and adverse pregnancy outcomes [5]. The disease spectrum ranges from the reversible inflammation of the gingiva (gingivitis) to the more severe and irreversible destruction of periodontal tissues (periodontitis). The development of periodontal disease is primarily initiated by the accumulation of dental plaque—a complex biofilm of microbial communities [6]. However, the progression from gingival inflammation to periodontitis is significantly influenced by the host’s immune response, environmental and behavioral factors, and genetic susceptibility. Risk factors such as tobacco smoking, poor oral hygiene, stress, and systemic conditions play a crucial role in disease initiation and progression [7]. In recent years, significant advancements have been made in understanding the pathophysiology of periodontal disease, aided by innovations in diagnostic technology and therapeutic interventions. Despite this progress, early diagnosis and effective management remain challenging due to the disease's asymptomatic nature in early stages and its complex etiology. An interdisciplinary and individualized approach is essential for the successful prevention and treatment of periodontal disease [8].

This paper aims to provide a comprehensive review of the etiology, diagnostic modalities, and current management strategies of periodontal disease. It also discusses emerging therapies and highlights the importance of integrating modern technologies into clinical practice to enhance patient outcomes.

The primary etiological

The primary etiological factor in periodontal disease is dental plaque, a biofilm composed of bacteria, salivary proteins, and food debris. Key periodontal pathogens include:

• Porphyromonas gingivalis
• Tannerella forsythia
• Aggregatibacter actinomycetemcomitans
• Treponema denticola

These bacteria release endotoxins, proteases, and virulence factors that trigger inflammation and destruction of periodontal tissues.

Periodontal tissue destruction is largely due to the host's inflammatory response rather than direct bacterial action. The immune response involves:

• Pro-inflammatory cytokines, IL-1β, IL-6, and TNF-α
• Matrix metalloproteinases (MMPs), enzymes that degrade collagen and extracellular matrix
• Oxidative stress, production of reactive oxygen species (ROS), exacerbating tissue damage
• Genetics, variations in genes encoding cytokines (e.g., IL-1, IL-6) may influence susceptibility

Smoking, a significant risk factor, smokers have a higher prevalence of severe periodontitis and reduced treatment response.

Diabetes mellitus, periodontal disease is more severe and progresses faster in diabetic patients due to impaired immune response and increased inflammation.

• Gingival recession and attachment loss
• Periodontal pockets (>4 mm)
• Tooth mobility and migration
• Halitosis (bad breath)

The 2018 classification system categorizes periodontitis based on,

• Stage, severity (I to IV)
• Grade, rate of progression (A to C)
• Extent, localized, generalized, or molar-incisor distribution

Diagnosis

• Periodontal probing, measures pocket depth and clinical attachment loss (CAL)
• Bleeding on probing (BOP), indicator of inflammation
• Tooth mobility and furcation involvement
• Intraoral periapical (IOPA) X-rays, detect bone loss
• Cone-beam computed tomography (CBCT), provides three-dimensional evaluation of bone morphology
• PCR and DNA-based assays identify specific periodontal pathogens
• Salivary biomarker analysis (e.g., MMP-8, IL-1β) aids in disease monitoring

Scaling and Root Planing (SRP), mechanical debridement of subgingival plaque and calculus.

• Systemic, amoxicillin + metronidazole for aggressive periodontitis.
• Local, chlorhexidine or tetracycline gel in deep pockets.

Laser Therapy, reduces bacterial load and promotes healing.

Host Modulation Therapy, sub-antimicrobial dose doxycycline (SDD) inhibits MMPs and reduces inflammation.

Flap Surgery, access surgery to clean deep pockets and reshape bone.

Guided Tissue Regeneration (GTR), uses barrier membranes to promote new attachment formation.

Bone Grafts, indicated for osseous defects to regenerate lost bone.

Periodontal Plastic Surgery, corrects gingival recession and improves aesthetics.

Probiotics, promote a beneficial oral microbiome and reduce pathogenic bacteria.

Host Immunotherapy, monoclonal antibodies targeting pro-inflammatory cytokines.

Gene Therapy, emerging techniques targeting genetic factors influencing periodontal disease.

Stem Cell Therapy, use of mesenchymal stem cells for periodontal regeneration.

Periodontal-systemic connection

Periodontitis has been linked to several systemic conditions,

Cardiovascular disease, increased inflammatory markers contribute to atherosclerosis.

Diabetes mellitus, periodontitis worsens glycemic control and vice versa.

Adverse pregnancy outcomes, preterm birth and low birth weight linked to maternal periodontitis.

Oral hygiene practices, twice-daily brushing, interdental cleaning, and mouth rinses.

Professional maintenance, periodontal maintenance therapy (PMT) every 3–6 months.

Risk factor control, smoking cessation, glycemic control, and stress management.

Conclusion

Periodontal disease is a prevalent and complex condition influenced by microbial, genetic, and environmental factors. Early diagnosis and a comprehensive treatment approach, including both non-surgical and surgical interventions, are critical for successful management. Regular maintenance therapy is essential to prevent disease recurrence and ensure long-term oral health. Emerging therapies hold promise for improved regenerative outcomes and disease modulation. Periodontal disease remains a major burden in dental health, with profound implications for both oral and systemic health. A comprehensive understanding of its multifactorial etiology including microbial, immunological, genetic, and environmental influences is critical for effective prevention and management. Diagnostic advancements now allow for earlier and more precise detection, while treatment strategies have shifted toward a patient-centered, multifaceted approach that combines mechanical, pharmacological, and behavioral interventions.

As our knowledge deepens and technologies evolve, the future of periodontal care lies in precision medicine, where interventions are tailored based on individual risk profiles and biological responses. Continued research, interprofessional collaboration, and public health initiatives will be pivotal in reducing the global impact of periodontal disease and promoting lifelong oral health.